Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN.
A chronic form of glomerulonephritis characterized by deposits of predominantly IMMUNOGLOBULIN A in the mesangial area (GLOMERULAR MESANGIUM). Deposits of COMPLEMENT C3 and IMMUNOGLOBULIN G are also often found. Clinical features may progress from asymptomatic HEMATURIA to END-STAGE KIDNEY DISEASE.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
A type of glomerulonephritis that is characterized by the accumulation of immune deposits (COMPLEMENT MEMBRANE ATTACK COMPLEX) on the outer aspect of the GLOMERULAR BASEMENT MEMBRANE. It progresses from subepithelial dense deposits, to basement membrane reaction and eventual thickening of the basement membrane.
Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.
An autoimmune disease of the KIDNEY and the LUNG. It is characterized by the presence of circulating autoantibodies targeting the epitopes in the non-collagenous domains of COLLAGEN TYPE IV in the basement membranes of kidney glomeruli (KIDNEY GLOMERULUS) and lung alveoli (PULMONARY ALVEOLI), and the subsequent destruction of these basement membranes. Clinical features include pulmonary alveolar hemorrhage and glomerulonephritis.
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.
Represents 15-20% of the human serum immunoglobulins, mostly as the 4-chain polymer in humans or dimer in other mammals. Secretory IgA (IMMUNOGLOBULIN A, SECRETORY) is the main immunoglobulin in secretions.
Autoantibodies directed against cytoplasmic constituents of POLYMORPHONUCLEAR LEUKOCYTES and/or MONOCYTES. They are used as specific markers for GRANULOMATOSIS WITH POLYANGIITIS and other diseases, though their pathophysiological role is not clear. ANCA are routinely detected by indirect immunofluorescence with three different patterns: c-ANCA (cytoplasmic), p-ANCA (perinuclear), and atypical ANCA.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).
The thin membranous structure supporting the adjoining glomerular capillaries. It is composed of GLOMERULAR MESANGIAL CELLS and their EXTRACELLULAR MATRIX.
A dysgammaglobulinemia characterized by a deficiency of IMMUNOGLOBULIN A.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
A condition characterized by severe PROTEINURIA, greater than 3.5 g/day in an average adult. The substantial loss of protein in the urine results in complications such as HYPOPROTEINEMIA; generalized EDEMA; HYPERTENSION; and HYPERLIPIDEMIAS. Diseases associated with nephrotic syndrome generally cause chronic kidney dysfunction.
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
A darkly stained mat-like EXTRACELLULAR MATRIX (ECM) that separates cell layers, such as EPITHELIUM from ENDOTHELIUM or a layer of CONNECTIVE TISSUE. The ECM layer that supports an overlying EPITHELIUM or ENDOTHELIUM is called basal lamina. Basement membrane (BM) can be formed by the fusion of either two adjacent basal laminae or a basal lamina with an adjacent reticular lamina of connective tissue. BM, composed mainly of TYPE IV COLLAGEN; glycoprotein LAMININ; and PROTEOGLYCAN, provides barriers as well as channels between interacting cell layers.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.
Presence of blood in the urine.
Inflammation of any part of the KIDNEY.
A clinicopathological syndrome or diagnostic term for a type of glomerular injury that has multiple causes, primary or secondary. Clinical features include PROTEINURIA, reduced GLOMERULAR FILTRATION RATE, and EDEMA. Kidney biopsy initially indicates focal segmental glomerular consolidation (hyalinosis) or scarring which can progress to globally sclerotic glomeruli leading to eventual KIDNEY FAILURE.
Immune complex disease caused by the administration of foreign serum or serum proteins and characterized by fever, lymphadenopathy, arthralgia, and urticaria. When they are complexed to protein carriers, some drugs can also cause serum sickness when they act as haptens inducing antibody responses.
The layer of EXTRACELLULAR MATRIX that lies between the ENDOTHELIUM of the glomerular capillaries and the PODOCYTES of the inner or visceral layer of the BOWMAN CAPSULE. It is the product of these two cell types. It acts as a physical barrier and an ion-selective filter.
An IgG autoantibody against the ALTERNATIVE PATHWAY C3 CONVERTASE, found in serum of patients with MESANGIOCAPILLARY GLOMERULONEPHRITIS. The binding of this autoantibody to C3bBb stabilizes the enzyme thus reduces the actions of C3b inactivators (COMPLEMENT FACTOR H; COMPLEMENT FACTOR I). This abnormally stabilized enzyme induces a continuous COMPLEMENT ACTIVATION and generation of C3b thereby promoting the assembly of MEMBRANE ATTACK COMPLEX and cytolysis.
Smooth muscle-like cells adhering to the wall of the small blood vessels of the KIDNEY at the glomerulus and along the vascular pole of the glomerulus in the JUXTAGLOMERULAR APPARATUS. They are myofibroblasts with contractile and phagocytic properties. These cells and their MESANGIAL EXTRACELLULAR MATRIX constitute the GLOMERULAR MESANGIUM.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
A condition characterized by the presence of abnormal quantities of CRYOGLOBULINS in the blood. Upon cold exposure, these abnormal proteins precipitate into the microvasculature leading to restricted blood flow in the exposed areas.
Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.
A mouse substrain that is genetically predisposed to the development of systemic lupus erythematosus-like syndrome, which has been found to be clinically similar to the human disease. It has been determined that this mouse strain carries a mutation in the fas gene. Also, the MRL/lpr is a useful model to study behavioral and cognitive deficits found in autoimmune diseases and the efficacy of immunosuppressive agents.
A group of differentiation surface antigens, among the first to be discovered on thymocytes and T-lymphocytes. Originally identified in the mouse, they are also found in other species including humans, and are expressed on brain neurons and other cells.
Abnormal immunoglobulins, especially IGG or IGM, that precipitate spontaneously when SERUM is cooled below 37 degrees Celsius. It is characteristic of CRYOGLOBULINEMIA.
Inflammation of the interstitial tissue of the kidney. This term is generally used for primary inflammation of KIDNEY TUBULES and/or surrounding interstitium. For primary inflammation of glomerular interstitium, see GLOMERULONEPHRITIS. Infiltration of the inflammatory cells into the interstitial compartment results in EDEMA, increased spaces between the tubules, and tubular renal dysfunction.
Infections with bacteria of the genus STREPTOCOCCUS.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
Pathological processes of the KIDNEY or its component tissues.
A kidney disease with no or minimal histological glomerular changes on light microscopy and with no immune deposits. It is characterized by lipid accumulation in the epithelial cells of KIDNEY TUBULES and in the URINE. Patients usually show NEPHROTIC SYNDROME indicating the presence of PROTEINURIA with accompanying EDEMA.
The principle immunoglobulin in exocrine secretions such as milk, respiratory and intestinal mucin, saliva and tears. The complete molecule (around 400 kD) is composed of two four-chain units of IMMUNOGLOBULIN A, one SECRETORY COMPONENT and one J chain (IMMUNOGLOBULIN J-CHAINS).
Inbred NZB mice are a strain of laboratory mice that spontaneously develop an autoimmune disease similar to human systemic lupus erythematosus (SLE), characterized by the production of autoantibodies, immune complex deposition, and glomerulonephritis.
A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the NASAL MUCOSA; BUCCAL MUCOSA; and conjunctival mucosa.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.
A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.
Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.
A multisystemic disease of a complex genetic background. It is characterized by inflammation of the blood vessels (VASCULITIS) leading to damage in any number of organs. The common features include granulomatous inflammation of the RESPIRATORY TRACT and kidneys. Most patients have measurable autoantibodies (ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES) against neutrophil proteinase-3 (WEGENER AUTOANTIGEN).
A systemic non-thrombocytopenic purpura caused by HYPERSENSITIVITY VASCULITIS and deposition of IGA-containing IMMUNE COMPLEXES within the blood vessels throughout the body, including those in the kidney (KIDNEY GLOMERULUS). Clinical symptoms include URTICARIA; ERYTHEMA; ARTHRITIS; GASTROINTESTINAL HEMORRHAGE; and renal involvement. Most cases are seen in children after acute upper respiratory infections.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
Creatinine is a waste product that's generated from muscle metabolism, typically filtered through the kidneys and released in urine, with increased levels in blood indicating impaired kidney function.
An immunologic deficiency state characterized by selective deficiencies of one or more, but not all, classes of immunoglobulins.
A non-fibrillar collagen found in the structure of BASEMENT MEMBRANE. Collagen type IV molecules assemble to form a sheet-like network which is involved in maintaining the structural integrity of basement membranes. The predominant form of the protein is comprised of two alpha1(IV) subunits and one alpha2(IV) subunit, however, at least six different alpha subunits can be incorporated into the heterotrimer.
A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 1.11.1.7.
A genus of snakes of the family VIPERIDAE. About 30 species are currently recognized, found in southeast Asia and adjacent island chains. The Okinawa habu frequently enters dwellings in search of rats and mice; the Chinese habu is often found in suburban and agricultural areas. They are quite irritable. (Moore: Poisonous Snakes of the World, 1980, p136)
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
Laboratory tests used to evaluate how well the kidneys are working through examination of blood and urine.
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.
The urea concentration of the blood stated in terms of nitrogen content. Serum (plasma) urea nitrogen is approximately 12% higher than blood urea nitrogen concentration because of the greater protein content of red blood cells. Increases in blood or serum urea nitrogen are referred to as azotemia and may have prerenal, renal, or postrenal causes. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.
A febrile disease occurring as a delayed sequela of infections with STREPTOCOCCUS PYOGENES. It is characterized by multiple focal inflammatory lesions of the connective tissue structures, such as the heart, blood vessels, and joints (POLYARTHRITIS) and brain, and by the presence of ASCHOFF BODIES in the myocardium and skin.
Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
A primary systemic vasculitis of small- and some medium-sized vessels. It is characterized by a tropism for kidneys and lungs, positive association with anti-neutrophil cytoplasmic antibodies (ANCA), and a paucity of immunoglobulin deposits in vessel walls.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.
Disease having a short and relatively severe course.
The extracellular moiety of the POLYMERIC IMMUNOGLOBULIN RECEPTOR found alone or complexed with IGA or IGM, in a variety of external secretions (tears, bile, colostrum.) Secretory component is derived by proteolytic cleavage of the receptor during transcytosis. When immunoglobulins IgA and IgM are bound to the receptor, during their transcytosis secretory component becomes covalently attached to them generating SECRETORY IMMUNOGLOBULIN A or secretory IMMUNOGLOBULIN M.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.
The protein components of ferritins. Apoferritins are shell-like structures containing nanocavities and ferroxidase activities. Apoferritin shells are composed of 24 subunits, heteropolymers in vertebrates and homopolymers in bacteria. In vertebrates, there are two types of subunits, light chain and heavy chain. The heavy chain contains the ferroxidase activity.
The processes triggered by interactions of ANTIBODIES with their ANTIGENS.
A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.
Highly differentiated epithelial cells of the visceral layer of BOWMAN CAPSULE of the KIDNEY. They are composed of a cell body with major CELL SURFACE EXTENSIONS and secondary fingerlike extensions called pedicels. They enwrap the KIDNEY GLOMERULUS capillaries with their cell surface extensions forming a filtration structure. The pedicels of neighboring podocytes interdigitate with each other leaving between them filtration slits that are bridged by an extracellular structure impermeable to large macromolecules called the slit diaphragm, and provide the last barrier to protein loss in the KIDNEY.
Serum proteins with an electrophoretic mobility that falls between ALPHA-GLOBULINS and GAMMA-GLOBULINS.
A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.
An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed)
The transference of a kidney from one human or animal to another.
'Rats, Inbred Lew' is a strain of laboratory rat that is widely used in biomedical research, known for its consistent genetic background and susceptibility to certain diseases, which makes it an ideal model for studying the genetic basis of complex traits and disease processes.
A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.
Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies.
A form of necrotizing non-granulomatous inflammation occurring primarily in medium-sized ARTERIES, often with microaneurysms. It is characterized by muscle, joint, and abdominal pain resulting from arterial infarction and scarring in affected organs. Polyarteritis nodosa with lung involvement is called CHURG-STRAUSS SYNDROME.
An important soluble regulator of the alternative pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It is a 139-kDa glycoprotein expressed by the liver and secreted into the blood. It binds to COMPLEMENT C3B and makes iC3b (inactivated complement 3b) susceptible to cleavage by COMPLEMENT FACTOR I. Complement factor H also inhibits the association of C3b with COMPLEMENT FACTOR B to form the C3bB proenzyme, and promotes the dissociation of Bb from the C3bBb complex (COMPLEMENT C3 CONVERTASE, ALTERNATIVE PATHWAY).
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Group of systemic vasculitis with a strong association with ANCA. The disorders are characterized by necrotizing inflammation of small and medium size vessels, with little or no immune-complex deposits in vessel walls.
Elements of limited time intervals, contributing to particular results or situations.
Removal of plasma and replacement with various fluids, e.g., fresh frozen plasma, plasma protein fractions (PPF), albumin preparations, dextran solutions, saline. Used in treatment of autoimmune diseases, immune complex diseases, diseases of excess plasma factors, and other conditions.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A species of gram-positive, coccoid bacteria isolated from skin lesions, blood, inflammatory exudates, and the upper respiratory tract of humans. It is a group A hemolytic Streptococcus that can cause SCARLET FEVER and RHEUMATIC FEVER.
Substances that are recognized by the immune system and induce an immune reaction.
A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.
Globulins are a group of simple proteins, found in blood plasma and other bodily fluids, which are insoluble in water but soluble in saline solutions and are involved in various biological functions such as immune response, transport, and enzyme regulation.
A 206-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c (749-954), and C3dg (955-1303) in the presence COMPLEMENT FACTOR H.
Disorder characterized by a vasculitic syndrome associated with exposure to an antigen such as a drug, infectious agent, or other foreign or endogenous substance. Its pathophysiology includes immune complex deposition and a wide range of skin lesions. Hypersensitivity or allergy is present in some but not all cases.
A double-walled epithelial capsule that is the bulbous closed proximal end of the kidney tubular system. It surrounds the cluster of convoluted capillaries of KIDNEY GLOMERULUS and is continuous with the convoluted PROXIMAL KIDNEY TUBULE.
Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
Serum globulins that migrate to the gamma region (most positively charged) upon ELECTROPHORESIS. At one time, gamma-globulins came to be used as a synonym for immunoglobulins since most immunoglobulins are gamma globulins and conversely most gamma globulins are immunoglobulins. But since some immunoglobulins exhibit an alpha or beta electrophoretic mobility, that usage is in decline.
Antibodies produced by a single clone of cells.
Cell surface receptors that bind to and internalize SECRETED PHOSPHOLIPASES A2. Although primarily acting as scavenger receptors, these proteins may also play a role in intracellular signaling. Soluble forms of phospholipase A2 receptors occur through the action of proteases and may a play a role in the inhibition of extracellular phospholipase activity.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. It is produced by LEUKOCYTES of both monocyte and lymphocyte lineage and by FIBROBLASTS during tissue injury. It has specificity for CCR2 RECEPTORS.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
A PREDNISOLONE derivative with similar anti-inflammatory action.
'Blood Protein Disorders' refer to conditions characterized by an abnormal amount, structure, or function of proteins present in the blood, including immunoglobulins, coagulation factors, complement components, and transport proteins, which can lead to various clinical manifestations such as immune dysfunction, bleeding disorders, or metabolic imbalances.
Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.
A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.
The presence of albumin in the urine, an indicator of KIDNEY DISEASES.
Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.
An encapsulated lymphatic organ through which venous blood filters.
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.
A polymorphonuclear leukocyte-derived serine protease that degrades proteins such as ELASTIN; FIBRONECTIN; LAMININ; VITRONECTIN; and COLLAGEN. It is named for its ability to control myeloid cell growth and differentiation.
Pathological processes of the KIDNEY without inflammatory or neoplastic components. Nephrosis may be a primary disorder or secondary complication of other diseases. It is characterized by the NEPHROTIC SYNDROME indicating the presence of PROTEINURIA and HYPOALBUMINEMIA with accompanying EDEMA.
The classes of immunoglobulins found in any species of animal. In man there are nine classes that migrate in five different groups in electrophoresis; they each consist of two light and two heavy protein chains, and each group has distinguishing structural and functional properties.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.

Exposed peptide core of IgA1 hinge region in IgA nephropathy. (1/761)

BACKGROUND: The human IgA1 hinge region is a very unique O-linked glycopeptide, and its sialylation and galactosylation recently were reported to be defective in the serum IgA1 derived from patients with IgA nephropathy (IgAN). This study was performed to examine the underglycosylation of the IgA1 hinge region and consequent exposure of the peptide core in IgAN. METHODS: A polyclonal antibody against a synthetic human IgA1 hinge peptide, PVPSTPPTP SPSTPPTPSPS, (anti-sHP ab) was raised in rabbits and shown specifically to recognize the IgA1 which was treated with neuraminidase, beta-galactosidase and alpha-N-acetylgalactosaminidase. The reactivity of the anti-sHP ab against the purified serum IgA1 was compared among the following three groups: 39 patients with IgAN, 30 patients with other renal diseases (ORD) and 21 healthy controls (HC) using an enzyme-linked immunosorbent assay. RESULTS: The reactivity was significantly higher in the IgAN group (mean +/- SD of OD 490 nm: 0.327 +/- 0.059) than in the ORD group (0.274 +/- 0.043, P=0.0002) and in the HC group (0.265 +/- 0.037, P<0.0001). No significant difference was observed between the latter two groups. The frequency of positive cases (> mean +/- 2SD of HC) was 46.2% (18/39) in the IgAN group, 6.7% (2/30) in the ORD group and 0% (0/21) in the HC group. CONCLUSIONS: It was suggested that the peptide core of the IgA1 hinge region is exposed aberrantly by a defective N-acetylgalactosaminylation and plays a possible role in the pathogenesis of IgAN.  (+info)

Ambulatory blood pressure monitoring and progression in patients with IgA nephropathy. (2/761)

BACKGROUND: Hypertension is a recognized marker of poor prognosis in IgA nephropathy. METHODS: The present study investigated the prevalence of white-coat hypertension, the diurnal rhythm of blood pressure (BP), the effectiveness of antihypertensive drug therapy, and the effect of the above on the progression of the kidney disease in IgA nephropathy. One hundred twenty-six IgA nephropathy patients were selected consecutively for 24-h ambulatory blood pressure monitoring (ABPM). Fifty-five patients were normotensive and 71 were treated hypertensives. Their antihypertensive drugs were angiotensin-converting enzyme inhibitors (ACEI) alone or in combination with calcium-channel blockers (CCB). RESULTS: The mean night-time BP of normotensives (108+/-9/67+/-6 mmHg) was significantly lower than their day-time BP (125+/-8/82+/-7 mmHg, P<0.05). There was no significant difference between the mean day-time and night-time BP in hypertensive patients (125+/-9/82+/-7 mmHg vs 128+/-10/85+/-9 mmHg). The circadian variation of BP was preserved ('dippers') in 82% of the normotensive and 7% of the hypertensive patients (P<0.001). There were 10 'white-coat hypertensives' among the patients classified as normotensives with ABPM (mean office blood pressure 149+/-7/96+/-8 mmHg, 24-h blood pressure 127+/-6/83+/-5 mmHg, P<0.05) and 14 among treated hypertensives (mean office BP 152+/-8/98+/-6 mmHg, 24-h BP 130+/-4/85+/-8 mmHg, P<0.05). There was no difference in mean day-time BP among normotensive and treated hypertensive patients (125+/-8/81+/-5 mmHg vs 128+/-10/85+/-9 mmHg). Hypertensives had significantly higher night-time BP (125+/-9/85+/-9 mmHg) than normotensives (108+/-9/67+/-6 mmHg, P<0.001). There was no difference in serum creatinine levels among the different groups at the time of the ABPM. However, thirty-six+/-4.1 months after the ABPM, hypertensive patients (n=52) had higher serum creatinine levels (124+/-32 micromol/l) than at the time of the ABPM (101+/-28 micromol/l). The serum creatinine of normotensive patients (n=43) did not change during the follow-up period. 'Non-dipper' normotensives (n=10) had significantly higher serum creatinine levels at the end of the follow-up period than at its beginning (106+/-17 micromol/l vs 89+/-18 micromol/l, P<0.05). There was no increase in serum creatinine of 'dipper' normotensives. The mean serum creatinine of 'white-coat hypertensives' was significantly higher at the end of the study period than at its beginning. CONCLUSIONS: There is no diurnal blood pressure variation in most of the hypertensive IgA nephropathy patients. ACEI and CCB treatment have better effect on day-time than night-time hypertension. The lack of the circadian rhythm and 'white-coat hypertension' seems to accelerate the progression of IgA nephropathy.  (+info)

Decreased IgA1 response after primary oral immunization with live typhoid vaccine in primary IgA nephropathy. (3/761)

INTRODUCTION: Patients with primary IgA nephropathy (IgAN) have an increased level of immunological memory to certain parenteral recall antigens. We recently found a deficient IgA1 immune response after intranasal challenge with a neo-antigen: cholera toxin subunit B. In the present study, we assessed the specific IgA1 and IgA2 antibody response in plasma, peripheral blood cells and mucosal secretions after primary enteral immunization. METHODS: Twenty eight IgAN patients, 26 patients with non-immunological renal disease and 32 healthy subjects were immunized orally with three sequential doses of live, attenuated, Salmonella typhi Ty21a. The humoral immune response in body fluids and antibody synthesis by circulating B cells was assessed in specific ELISAs and ELIPSAs respectively. RESULTS: Oral immunization resulted in significantly (P<0.0001) increased IgM, IgG, IgA, IgA1 and IgA2 responses in all groups, both in plasma and in circulating B cells in vitro. The IgA1 response in plasma was significantly (P<0.05) lower in IgAN patients, while no significant differences in IgM (P=0.36), IgG (P= 0.79) or IgA2 (P=0.45) responses were found as compared with matched control groups. The amount of IgA1 synthesized by circulating B cells tended to be lower in IgAN patients. No significant IgA response after oral immunization with S. typhi Ty21a was found in saliva (P=0.11) or tears (P=0.10). CONCLUSIONS: These data suggest an IgA1 hyporesponsiveness in patients with IgAN that is not only apparent after primary challenge of the nasal-associated lymphoid tissue but also after presentation to the gut. Previous results after parenteral recall immunization may be explained by assuming that IgAN patients require more frequent and/or longer exposure to IgA1-inducing antigens on their mucosal surfaces before they reach protective mucosal immunity. As a consequence, overproduction of IgA1 antibodies occurs in the systemic compartment, accompanied by an increased number of IgA1 memory cells.  (+info)

ACE inhibition and ANG II receptor blockade improve glomerular size-selectivity in IgA nephropathy. (4/761)

Protein trafficking across the glomerular capillary has a pathogenic role in subsequent renal damage. Despite evidence that angiotensin-converting enzyme (ACE) inhibitors improve glomerular size-selectivity, whether this effect is solely due to ANG II blocking or if other mediators also play a contributory role is not clear yet. We studied 20 proteinuric patients with IgA nephropathy, who received either enalapril (20 mg/day) or the ANG II receptor blocker irbesartan (100 mg/day) for 28 days in a randomized double-blind study. Measurements of blood pressure, renal hemodynamics, and fractional clearance of neutral dextran of graded sizes were performed before and after 28 days of treatment. Both enalapril and irbesartan significantly reduced blood pressure over baseline. This reduction reached the maximum effect 4-6 h after drug administration but did not last for the entire 24-h period. Despite transient antihypertensive effect, proteinuria was effectively reduced by both treatments to comparable extents. Neither enalapril nor irbesartan modified the sieving coefficients of small dextran molecules, but both effectively reduced transglomerular passage of large test macromolecules. Theoretical analysis of sieving coefficients showed that neither drug affected significantly the mean pore radius or the spread of the pore-size distribution, but both importantly and comparably reduced the importance of a nonselective shunt pathway. These data suggest that antagonism of ANG II is the key mechanism by which ACE inhibitors exert their beneficial effect on glomerular size-selective function and consequently on glomerular filtration and urinary output of plasma proteins.  (+info)

Deletion polymorphism of the angiotensin converting enzyme gene predicts persistent proteinuria in Henoch-Schonlein purpura nephritis. (5/761)

OBJECTIVE: To study the influence of deletion/insertion polymorphism in the 16th intron of the angiotensin converting enzyme (ACE) gene on clinical manifestations of Henoch-Schonlein purpura nephritis. STUDY DESIGN: Cross sectional study. ACE gene polymorphism was determined in patients (4-15 years old at onset) with Henoch-Schonlein purpura nephritis (n = 40) and compared with that in patients with IgA nephropathy (n = 79). MAIN OUTCOME MEASURES: ACE genotypes, systemic blood pressures, urine protein excretion rate, haematuria, creatinine clearance, serum ACE activities. RESULTS: The initial clinical manifestations of both Henoch-Schonlein purpura nephritis and IgA nephropathy were no different among homozygotes for insertion (II) and deletion (DD), and heterozygotes (ID) for the ACE gene. In patients with Henoch-Schonlein purpura nephritis, the incidence of moderate to heavy proteinuria at four and eight years after onset was more than five times higher in the DD genotype than in the II or ID genotypes. No such trend was seen in patients with IgA nephropathy. The number of patients with Henoch-Schonlein purpura nephritis in whom proteinuria resolved at four and eight years after onset was significantly lower in the DD genotype compared with the II genotype, whereas no differences were detected among the three different genotypes in patients with IgA nephropathy. Plasma ACE activities in patients with the DD genotype were significantly higher than in those with non-DD genotypes. CONCLUSIONS: The ACE DD genotype predicts persistent proteinuria in Henoch-Schonlein purpura nephritis. The proteinuria might be related to a defective angiotensin system which is genetically determined by the D/I polymorphism.  (+info)

Enhanced expression of L-selectin on peripheral blood lymphocytes from patients with IgA nephropathy. (6/761)

To investigate the homing characteristics of T and B lymphocytes which could explain the abnormal partition of IgA-producing cells in tonsils and bone marrow from patients with IgA nephropathy (IgAN), the expression of leucocyte adhesion molecules (CD11a, CD29, CD49d, CD62L, CD31) was assessed using flow cytometry on peripheral blood leucocytes from patients with biopsy-proven IgAN and controls. Higher proportions of T and B lymphocytes expressing higher amounts of L-selectin, as well as higher proportions of B cells expressing more CD31 were evidenced in IgAN patients. Conversely, serum levels of sCD62L were not different from controls, but significantly higher than serum levels in patients suffering from other renal diseases. We hypothesize that this over-expression of CD62L and CD31 may be involved in an enhanced efficiency of lymphoid cells homing to lymphoid tissues in this disease.  (+info)

Does circulating erythropoietin reflect progression of IgA nephropathy? Comparison with urinary N-acetyl-beta-D-glucosaminidase. (7/761)

BACKGROUND: Recent reports describe that erythropoietin (Epo) is produced by peritubular interstitial fibroblast-like cells in response to a hypoxic stimulus. We studied serum Epo levels as a possible marker of tubulointerstitial damage in the progression of IgA nephropathy (IgAN), in comparison with urinary (u-) levels of N-acetyl-beta-D-glucosaminidase (NAG), which is mainly derived from proximal tubular cells and is used as a marker of tubular damage. METHODS: Thirty-eight patients with IgA nephropathy (IgAN) with relatively preserved renal function (serum creatinine: sCr, 0.5-2.2 mg/dl) were examined. The severity of glomerulosclerosis and interstitial fibrosis of the renal biopsy tissue was expressed by semiquantitative grading scores. Clinical parameters including serum creatinine (sCr), blood pressures, and 24-h proteinuria levels were obtained at the renal biopsy. Epo was measured by a radioimmunoassay (RIA) of sera obtained in the morning and u-NAG was measured by colorimetric method of 24-h urine samples. RESULTS: The mean Epo level of the patients (17.7+/-6.3 mU/ml) was not different from the control level (19.3+/-3.7 mU/ml). There were no significant correlations between Epo levels and red blood cell (RBC) counts, haematocrit (Hct), or haemoglobin (Hb) levels. The mean u-NAG level of the patients (6.7+/-6.2 U/gCr) was significantly higher than the control level (1.9+/-0.5 U/gCr). There was an inverse quantitative correlation between Epo and u-NAG levels in the patients (P<0.02). The u-NAG levels showed quantitative positive correlations with sCr (P<0.001), u-proteins (P<0.001), systolic (SBP) (P<0.001), and diastolic blood pressures (DBP) (P<0.05). Conversely, Epo levels were inversely correlated with sCr, SBP and DBP (each P<0.05). The patients with higher u-proteins (>2.0 g/day) showed significantly decreased Epo levels (P<0.05) than those with lower u-proteins (<2.0 g/day). The both scores of glomerulosclerosis and interstitial fibrosis were positively correlated with the u-NAG levels (each P<0.001), but were not correlated with the Epo levels. CONCLUSIONS: The significant correlation between u-NAG and serum Epo levels suggests that tubular damage and interstitial cell dysfunction are associated each other in the progression of IgAN. Serum Epo levels bearing inverse correlations with sCr, blood pressure levels and heavy proteinuria seem to reflect clinical severity of IgAN, whereas u-NAG can be more useful progression marker of IgAN bearing correlations with both clinical and histological findings.  (+info)

Underglycosylation of IgA1 hinge plays a certain role for its glomerular deposition in IgA nephropathy. (8/761)

This study was performed to isolate and investigate the IgA1 that could accumulate in glomeruli (glomerulophilic IgA1). IgA1 was fractionated by the electric charge and the reactivity to Jacalin. Serum IgA1 of IgA nephropathy patients was separated and fractionated using a Jacalin column and subsequent ion-exchange chromatography. The fractions were divided into three groups of relatively cationic (C), neutral (N), and anionic (A). IgA1 was also divided into Jacalin low (L), intermediate (I), and high (H) affinity fractions by serial elution using 25, 100, and 800 mM galactose. The left kidneys of Wistar rats were perfused with 2, 5, or 10 mg of each group of IgA1. The rats were sacrificed 15 min, 30 min, 3 h, or 24 h after the perfusion. The accumulation of each IgA1 in the glomeruli was then observed by immunofluorescence. The IgA1 of the fractions N and H separated by the two methods was definitely accumulated in the rat glomeruli with a similar pattern. The electrophoresis revealed that the macromolecular IgA1 was increased in fraction H compared with other fractions. Therefore, Jacalin high-affinity IgA1(fraction H) was applied on a diethylaminoethyl column and divided into electrically cationic (HC), neutral (HN), and anionic (HA). Only the asialo-Galbeta1,3GalNAc chain was identified in the fraction HN IgA1 by gas-phase hydrazinolysis. Furthermore, the IgA1 fraction was strongly recognized by peanut agglutinin, Vicia Villosa lectins, and antisynthetic hinge peptide antibody. These results indicated that the IgA1 molecules having the underglycosylated hinge glycopeptide played a certain role in the glomerular accumulation of IgA1 in IgA nephropathy.  (+info)

Glomerulonephritis is a medical condition that involves inflammation of the glomeruli, which are the tiny blood vessel clusters in the kidneys that filter waste and excess fluids from the blood. This inflammation can impair the kidney's ability to filter blood properly, leading to symptoms such as proteinuria (protein in the urine), hematuria (blood in the urine), edema (swelling), hypertension (high blood pressure), and eventually kidney failure.

Glomerulonephritis can be acute or chronic, and it may occur as a primary kidney disease or secondary to other medical conditions such as infections, autoimmune disorders, or vasculitis. The diagnosis of glomerulonephritis typically involves a combination of medical history, physical examination, urinalysis, blood tests, and imaging studies, with confirmation often requiring a kidney biopsy. Treatment depends on the underlying cause and severity of the disease but may include medications to suppress inflammation, control blood pressure, and manage symptoms.

Membranoproliferative Glomerulonephritis (MPGN) is a type of glomerulonephritis, which is a group of kidney disorders characterized by inflammation and damage to the glomeruli, the tiny blood vessels in the kidneys responsible for filtering waste and excess fluids from the blood.

MPGN is specifically characterized by thickening of the glomerular basement membrane and proliferation (increased number) of cells in the mesangium, a region within the glomerulus. This condition can be primary or secondary to other diseases such as infections, autoimmune disorders, or monoclonal gammopathies.

MPGN is typically classified into three types based on the pattern of injury seen on electron microscopy: Type I, Type II (Dense Deposit Disease), and Type III. Each type has distinct clinical features, laboratory findings, and treatment approaches. Symptoms of MPGN may include hematuria (blood in urine), proteinuria (protein in urine), hypertension (high blood pressure), edema (swelling), and eventually progress to chronic kidney disease or end-stage renal disease if left untreated.

IGA glomerulonephritis (also known as Berger's disease) is a type of glomerulonephritis, which is a condition characterized by inflammation of the glomeruli, the tiny filtering units in the kidneys. In IgA glomerulonephritis, the immune system produces an abnormal amount of IgA antibodies, which deposit in the glomeruli and cause inflammation. This can lead to symptoms such as blood in the urine, protein in the urine, and swelling in the legs and feet. In some cases, it can also lead to kidney failure. The exact cause of IgA glomerulonephritis is not known, but it is often associated with other conditions such as infections, autoimmune diseases, and certain medications.

A kidney glomerulus is a functional unit in the nephron of the kidney. It is a tuft of capillaries enclosed within a structure called Bowman's capsule, which filters waste and excess fluids from the blood. The glomerulus receives blood from an afferent arteriole and drains into an efferent arteriole.

The process of filtration in the glomerulus is called ultrafiltration, where the pressure within the glomerular capillaries drives plasma fluid and small molecules (such as ions, glucose, amino acids, and waste products) through the filtration membrane into the Bowman's space. Larger molecules, like proteins and blood cells, are retained in the blood due to their larger size. The filtrate then continues down the nephron for further processing, eventually forming urine.

Membranous glomerulonephritis (MGN) is a kidney disorder that leads to the inflammation and damage of the glomeruli, which are the tiny blood vessels in the kidneys responsible for filtering waste and excess fluids from the blood. In MGN, the membrane that surrounds the glomerular capillaries becomes thickened and damaged due to the deposit of immune complexes, primarily composed of antibodies and antigens.

The onset of membranous glomerulonephritis can be either primary (idiopathic) or secondary to various underlying conditions such as autoimmune diseases (like systemic lupus erythematosus), infections (hepatitis B or C, syphilis, endocarditis), medications, or malignancies.

The symptoms of membranous glomerulonephritis may include:

1. Proteinuria - the presence of excess protein, specifically albumin, in the urine. This can lead to nephrotic syndrome, characterized by heavy protein loss in urine, edema (swelling), hypoalbuminemia (low blood albumin levels), and hyperlipidemia (high blood lipid levels).
2. Hematuria - the presence of red blood cells in the urine, which can be visible or microscopic.
3. Hypertension - high blood pressure.
4. Edema - swelling in various body parts due to fluid retention.
5. Nephrotic range proteinuria (protein loss greater than 3.5 grams per day) and/or nephritic syndrome (a combination of hematuria, proteinuria, hypertension, and kidney dysfunction) can be observed in some cases.

The diagnosis of membranous glomerulonephritis typically involves a thorough medical history, physical examination, urinalysis, blood tests, and imaging studies. A definitive diagnosis often requires a kidney biopsy to assess the glomerular structure and the nature of the immune complex deposits. Treatment depends on the underlying cause and severity of the disease and may include corticosteroids, immunosuppressants, blood pressure management, and supportive care for symptoms like edema and proteinuria.

Immune complex diseases are medical conditions that occur when the immune system produces an abnormal response to certain antigens, leading to the formation and deposition of immune complexes in various tissues and organs. These immune complexes consist of antibodies bound to antigens, which can trigger an inflammatory reaction and damage the surrounding tissue.

Immune complex diseases can be classified into two categories: acute and chronic. Acute immune complex diseases include serum sickness and hypersensitivity vasculitis, while chronic immune complex diseases include systemic lupus erythematosus (SLE), rheumatoid arthritis, and membranoproliferative glomerulonephritis.

The symptoms of immune complex diseases depend on the location and extent of tissue damage. They can range from mild to severe and may include fever, joint pain, skin rashes, kidney dysfunction, and neurological problems. Treatment typically involves medications that suppress the immune system and reduce inflammation, such as corticosteroids, immunosuppressants, and anti-inflammatory drugs.

Anti-glomerular basement membrane (anti-GBM) disease, also known as Goodpasture's disease, is a rare autoimmune disorder in which the body produces antibodies that attack the glomerular basement membrane (GBM), a component of the filtering units (glomeruli) in the kidneys. This leads to inflammation and damage to the glomeruli, causing hematuria (blood in urine), proteinuria (protein in urine), and potentially kidney failure. In some cases, anti-GBM disease may also affect the lungs, leading to coughing up blood (hemoptysis). The exact cause of anti-GBM disease is not fully understood, but it is believed to be related to both genetic and environmental factors. Treatment typically involves a combination of immunosuppressive therapy and plasma exchange.

Proteinuria is a medical term that refers to the presence of excess proteins, particularly albumin, in the urine. Under normal circumstances, only small amounts of proteins should be found in the urine because the majority of proteins are too large to pass through the glomeruli, which are the filtering units of the kidneys.

However, when the glomeruli become damaged or diseased, they may allow larger molecules such as proteins to leak into the urine. Persistent proteinuria is often a sign of kidney disease and can indicate damage to the glomeruli. It is usually detected through a routine urinalysis and may be confirmed with further testing.

The severity of proteinuria can vary, and it can be a symptom of various underlying conditions such as diabetes, hypertension, glomerulonephritis, and other kidney diseases. Treatment for proteinuria depends on the underlying cause and may include medications to control blood pressure, manage diabetes, or reduce protein loss in the urine.

Immunoglobulin A (IgA) is a type of antibody that plays a crucial role in the immune function of the human body. It is primarily found in external secretions, such as saliva, tears, breast milk, and sweat, as well as in mucous membranes lining the respiratory and gastrointestinal tracts. IgA exists in two forms: a monomeric form found in serum and a polymeric form found in secretions.

The primary function of IgA is to provide immune protection at mucosal surfaces, which are exposed to various environmental antigens, such as bacteria, viruses, parasites, and allergens. By doing so, it helps prevent the entry and colonization of pathogens into the body, reducing the risk of infections and inflammation.

IgA functions by binding to antigens present on the surface of pathogens or allergens, forming immune complexes that can neutralize their activity. These complexes are then transported across the epithelial cells lining mucosal surfaces and released into the lumen, where they prevent the adherence and invasion of pathogens.

In summary, Immunoglobulin A (IgA) is a vital antibody that provides immune defense at mucosal surfaces by neutralizing and preventing the entry of harmful antigens into the body.

Antineutrophil cytoplasmic antibodies (ANCAs) are a type of autoantibody that specifically target certain proteins in the cytoplasm of neutrophils, which are a type of white blood cell. These antibodies are associated with several types of vasculitis, which is inflammation of the blood vessels.

There are two main types of ANCAs: perinuclear ANCAs (p-ANCAs) and cytoplasmic ANCAs (c-ANCAs). p-ANCAs are directed against myeloperoxidase, a protein found in neutrophil granules, while c-ANCAs target proteinase 3, another protein found in neutrophil granules.

The presence of ANCAs in the blood can indicate an increased risk for developing certain types of vasculitis, such as granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA), and microscopic polyangiitis (MPA). ANCA testing is often used in conjunction with other clinical findings to help diagnose and manage these conditions.

It's important to note that while the presence of ANCAs can indicate an increased risk for vasculitis, not everyone with ANCAs will develop the condition. Additionally, ANCAs can also be found in some individuals without any associated disease, so their presence should be interpreted in the context of other clinical findings.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Lupus nephritis is a type of kidney inflammation (nephritis) that can occur in people with systemic lupus erythematosus (SLE), an autoimmune disease. In lupus nephritis, the immune system produces abnormal antibodies that attack the tissues of the kidneys, leading to inflammation and damage. The condition can cause a range of symptoms, including proteinuria (protein in the urine), hematuria (blood in the urine), hypertension (high blood pressure), and eventually kidney failure if left untreated. Lupus nephritis is typically diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment may include medications to suppress the immune system and control inflammation, such as corticosteroids and immunosuppressive drugs.

The glomerular mesangium is a part of the nephron in the kidney. It is the region located in the middle of the glomerular tuft, where the capillary loops of the glomerulus are surrounded by a network of extracellular matrix and mesangial cells. These cells and matrix play an important role in maintaining the structure and function of the filtration barrier in the glomerulus, which helps to filter waste products from the blood.

The mesangial cells have contractile properties and can regulate the flow of blood through the capillaries by constricting or dilating the diameter of the glomerular capillary loops. They also play a role in immune responses, as they can phagocytize immune complexes and release cytokines and growth factors that modulate inflammation and tissue repair.

Abnormalities in the mesangium can lead to various kidney diseases, such as glomerulonephritis, mesangial proliferative glomerulonephritis, and diabetic nephropathy.

IgA deficiency is a condition characterized by significantly reduced levels or absence of secretory immunoglobulin A (IgA), an important antibody that plays a crucial role in the immune function of mucous membranes lining the respiratory and gastrointestinal tracts. IgA helps to prevent the attachment and multiplication of pathogens, such as bacteria and viruses, on these surfaces.

In individuals with IgA deficiency, the lack of adequate IgA levels makes them more susceptible to recurrent infections, allergies, and autoimmune disorders. The condition can be asymptomatic or may present with various symptoms, such as respiratory tract infections, gastrointestinal issues, and chronic sinusitis. IgA deficiency is typically diagnosed through blood tests that measure the immunoglobulin levels. While there is no cure for IgA deficiency, treatment focuses on managing symptoms and preventing infections through medications, immunizations, and lifestyle modifications.

Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.

IgG has several important functions:

1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.

IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.

Nephrotic syndrome is a group of symptoms that indicate kidney damage, specifically damage to the glomeruli—the tiny blood vessel clusters in the kidneys that filter waste and excess fluids from the blood. The main features of nephrotic syndrome are:

1. Proteinuria (excess protein in urine): Large amounts of a protein called albumin leak into the urine due to damaged glomeruli, which can't properly filter proteins. This leads to low levels of albumin in the blood, causing fluid buildup and swelling.
2. Hypoalbuminemia (low blood albumin levels): As albumin leaks into the urine, the concentration of albumin in the blood decreases, leading to hypoalbuminemia. This can cause edema (swelling), particularly in the legs, ankles, and feet.
3. Edema (fluid retention and swelling): With low levels of albumin in the blood, fluids move into the surrounding tissues, causing swelling or puffiness. The swelling is most noticeable around the eyes, face, hands, feet, and abdomen.
4. Hyperlipidemia (high lipid/cholesterol levels): The kidneys play a role in regulating lipid metabolism. Damage to the glomeruli can lead to increased lipid production and high cholesterol levels in the blood.

Nephrotic syndrome can result from various underlying kidney diseases, such as minimal change disease, membranous nephropathy, or focal segmental glomerulosclerosis. Treatment depends on the underlying cause and may include medications to control inflammation, manage high blood pressure, and reduce proteinuria. In some cases, dietary modifications and lifestyle changes are also recommended.

An antigen-antibody complex is a type of immune complex that forms when an antibody binds to a specific antigen. An antigen is any substance that triggers an immune response, while an antibody is a protein produced by the immune system to neutralize or destroy foreign substances like antigens.

When an antibody binds to an antigen, it forms a complex that can be either soluble or insoluble. Soluble complexes are formed when the antigen is small and can move freely through the bloodstream. Insoluble complexes, on the other hand, are formed when the antigen is too large to move freely, such as when it is part of a bacterium or virus.

The formation of antigen-antibody complexes plays an important role in the immune response. Once formed, these complexes can be recognized and cleared by other components of the immune system, such as phagocytes, which help to prevent further damage to the body. However, in some cases, the formation of large numbers of antigen-antibody complexes can lead to inflammation and tissue damage, contributing to the development of certain autoimmune diseases.

Complement C3 is a protein that plays a central role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C3 can be activated through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Once activated, it breaks down into two fragments, C3a and C3b.

C3a is an anaphylatoxin that helps to recruit immune cells to the site of infection or injury, while C3b plays a role in opsonization, which is the process of coating pathogens or damaged cells with proteins to make them more recognizable to the immune system. Additionally, C3b can also activate the membrane attack complex (MAC), which forms a pore in the membrane of target cells leading to their lysis or destruction.

In summary, Complement C3 is an important protein in the complement system that helps to identify and eliminate pathogens and damaged cells from the body through various mechanisms.

The basement membrane is a thin, specialized layer of extracellular matrix that provides structural support and separates epithelial cells (which line the outer surfaces of organs and blood vessels) from connective tissue. It is composed of two main layers: the basal lamina, which is produced by the epithelial cells, and the reticular lamina, which is produced by the connective tissue. The basement membrane plays important roles in cell adhesion, migration, differentiation, and survival.

The basal lamina is composed mainly of type IV collagen, laminins, nidogens, and proteoglycans, while the reticular lamina contains type III collagen, fibronectin, and other matrix proteins. The basement membrane also contains a variety of growth factors and cytokines that can influence cell behavior.

Defects in the composition or organization of the basement membrane can lead to various diseases, including kidney disease, eye disease, and skin blistering disorders.

A biopsy is a medical procedure in which a small sample of tissue is taken from the body to be examined under a microscope for the presence of disease. This can help doctors diagnose and monitor various medical conditions, such as cancer, infections, or autoimmune disorders. The type of biopsy performed will depend on the location and nature of the suspected condition. Some common types of biopsies include:

1. Incisional biopsy: In this procedure, a surgeon removes a piece of tissue from an abnormal area using a scalpel or other surgical instrument. This type of biopsy is often used when the lesion is too large to be removed entirely during the initial biopsy.

2. Excisional biopsy: An excisional biopsy involves removing the entire abnormal area, along with a margin of healthy tissue surrounding it. This technique is typically employed for smaller lesions or when cancer is suspected.

3. Needle biopsy: A needle biopsy uses a thin, hollow needle to extract cells or fluid from the body. There are two main types of needle biopsies: fine-needle aspiration (FNA) and core needle biopsy. FNA extracts loose cells, while a core needle biopsy removes a small piece of tissue.

4. Punch biopsy: In a punch biopsy, a round, sharp tool is used to remove a small cylindrical sample of skin tissue. This type of biopsy is often used for evaluating rashes or other skin abnormalities.

5. Shave biopsy: During a shave biopsy, a thin slice of tissue is removed from the surface of the skin using a sharp razor-like instrument. This technique is typically used for superficial lesions or growths on the skin.

After the biopsy sample has been collected, it is sent to a laboratory where a pathologist will examine the tissue under a microscope and provide a diagnosis based on their findings. The results of the biopsy can help guide further treatment decisions and determine the best course of action for managing the patient's condition.

Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.

Vasculitis is a group of disorders characterized by inflammation of the blood vessels, which can cause changes in the vessel walls including thickening, narrowing, or weakening. These changes can restrict blood flow, leading to organ and tissue damage. The specific symptoms and severity of vasculitis depend on the size and location of the affected blood vessels and the extent of inflammation. Vasculitis can affect any organ system in the body, and its causes can vary, including infections, autoimmune disorders, or exposure to certain medications or chemicals.

Hematuria is a medical term that refers to the presence of blood in urine. It can be visible to the naked eye, which is called gross hematuria, or detected only under a microscope, known as microscopic hematuria. The blood in urine may come from any site along the urinary tract, including the kidneys, ureters, bladder, or urethra. Hematuria can be a symptom of various medical conditions, such as urinary tract infections, kidney stones, kidney disease, or cancer of the urinary tract. It is essential to consult a healthcare professional if you notice blood in your urine to determine the underlying cause and receive appropriate treatment.

Nephritis is a medical term that refers to inflammation of the kidneys, specifically affecting the glomeruli - the tiny filtering units inside the kidneys. The condition can cause damage to the glomeruli, leading to impaired kidney function and the leakage of protein and blood into the urine.

Nephritis can result from a variety of causes, including infections, autoimmune disorders, and exposure to certain medications or toxins. Depending on the severity and underlying cause, nephritis may be treated with medications, dietary modifications, or other therapies aimed at reducing inflammation and preserving kidney function. In severe cases, hospitalization and more intensive treatments may be necessary.

Focal segmental glomerulosclerosis (FSGS) is a pattern of kidney injury that involves scarring or sclerosis in some (segmental) areas of some (focal) glomeruli. Glomeruli are the tiny blood vessel clusters within the kidneys that filter waste and excess fluids from the blood.

In FSGS, the scarring occurs due to damage to the glomerular basement membrane, which can be caused by various factors such as genetic mutations, viral infections, or immune system disorders. The damage leads to the accumulation of extracellular matrix proteins and the formation of scar tissue, impairing the kidney's ability to filter blood effectively.

FSGS is characterized by proteinuria (protein in the urine), hematuria (blood in the urine), hypertension (high blood pressure), and declining kidney function, which can lead to end-stage renal disease if left untreated. The focal and segmental nature of the scarring means that not all glomeruli are affected, and only some areas of each affected glomerulus are damaged, making FSGS a highly variable condition with different clinical presentations and outcomes.

Serum sickness is an immune-mediated hypersensitivity reaction that typically occurs within 1 to 3 weeks after the administration of foreign proteins or drugs, such as certain types of antibiotics, antiserums, or monoclonal antibodies. It is characterized by symptoms such as fever, rash, joint pain, and lymphadenopathy (swollen lymph nodes). These symptoms are caused by the formation of immune complexes, which deposit in various tissues and activate the complement system, leading to inflammation. Serum sickness can be treated with antihistamines, corticosteroids, and other immunomodulatory agents. It is important to note that serum sickness is different from anaphylaxis, which is a more severe, life-threatening allergic reaction that occurs immediately after exposure to an allergen.

The Glomerular Basement Membrane (GBM) is a part of the filtration barrier in the nephron of the kidney. It is a thin, porous sheet of extracellular matrix that lies between the glomerular endothelial cells and the visceral epithelial cells (podocytes). The GBM plays a crucial role in the process of ultrafiltration, allowing the passage of water and small molecules while preventing the loss of larger proteins into the urine. It is composed mainly of type IV collagen, laminin, nidogen, and heparan sulfate proteoglycans. Certain kidney diseases, such as Goodpasture's disease and some forms of glomerulonephritis, can involve damage to the GBM.

Complement C3 Nephritic Factor (C3NeF) is a type of autoantibody that activates the complement system and plays a significant role in the development of certain types of kidney diseases. The complement system is a part of the immune system that helps to eliminate pathogens and damaged cells from the body.

C3NeF is specifically directed against the C3 convertase enzyme complex, which is a critical component of the complement system's activation pathway. By binding to this enzyme complex, C3NeF stabilizes it and enhances its activity, leading to excessive complement activation and subsequent tissue damage.

In the context of kidney diseases, C3NeF has been associated with several forms of glomerulonephritis, including membranoproliferative glomerulonephritis (MPGN) type II, also known as dense deposit disease (DDD). The persistent activation of the complement system by C3NeF can result in the accumulation of complement components and immune complexes in the glomeruli, causing inflammation, tissue injury, and ultimately leading to kidney function impairment.

It is essential to diagnose and monitor C3NeF levels in patients with kidney diseases, as it may help guide treatment decisions and assess disease prognosis. Therapeutic strategies targeting the complement system, such as eculizumab, have shown promising results in managing C3NeF-associated kidney diseases.

Mesangial cells are specialized cells that are found in the mesangium, which is the middle layer of the glomerulus in the kidney. The glomerulus is a network of capillaries where blood filtration occurs. Mesangial cells play an important role in maintaining the structure and function of the glomerulus. They help regulate the size of the filtration slits between the capillary endothelial cells and the podocytes (specialized epithelial cells) by contracting and relaxing, similar to smooth muscle cells. Additionally, mesangial cells can phagocytize immune complexes and other debris in the glomerulus, contributing to the body's immune response. They also produce extracellular matrix components that provide structural support for the glomerulus. Mesangial cell dysfunction or injury can contribute to kidney diseases such as glomerulonephritis and diabetic nephropathy.

The complement system is a group of proteins found in the blood and on the surface of cells that when activated, work together to help eliminate pathogens such as bacteria, viruses, and fungi from the body. The proteins are normally inactive in the bloodstream. When they encounter an invading microorganism or foreign substance, a series of reactions take place leading to the activation of the complement system. Activation results in the production of effector molecules that can punch holes in the cell membranes of pathogens, recruit and activate immune cells, and help remove debris and dead cells from the body.

There are three main pathways that can lead to complement activation: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteins that work together in a cascade-like manner to amplify the response and generate effector molecules. The three main effector molecules produced by the complement system are C3b, C4b, and C5b. These molecules can bind to the surface of pathogens, marking them for destruction by other immune cells.

Complement proteins also play a role in the regulation of the immune response. They help to prevent excessive activation of the complement system, which could damage host tissues. Dysregulation of the complement system has been implicated in a number of diseases, including autoimmune disorders and inflammatory conditions.

In summary, Complement System Proteins are a group of proteins that play a crucial role in the immune response by helping to eliminate pathogens and regulate the immune response. They can be activated through three different pathways, leading to the production of effector molecules that mark pathogens for destruction. Dysregulation of the complement system has been linked to various diseases.

The Fluorescent Antibody Technique (FAT) is a type of immunofluorescence assay used in laboratory medicine and pathology for the detection and localization of specific antigens or antibodies in tissues, cells, or microorganisms. In this technique, a fluorescein-labeled antibody is used to selectively bind to the target antigen or antibody, forming an immune complex. When excited by light of a specific wavelength, the fluorescein label emits light at a longer wavelength, typically visualized as green fluorescence under a fluorescence microscope.

The FAT is widely used in diagnostic microbiology for the identification and characterization of various bacteria, viruses, fungi, and parasites. It has also been applied in the diagnosis of autoimmune diseases and certain cancers by detecting specific antibodies or antigens in patient samples. The main advantage of FAT is its high sensitivity and specificity, allowing for accurate detection and differentiation of various pathogens and disease markers. However, it requires specialized equipment and trained personnel to perform and interpret the results.

Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease that can affect almost any organ or system in the body. In SLE, the immune system produces an exaggerated response, leading to the production of autoantibodies that attack the body's own cells and tissues, causing inflammation and damage. The symptoms and severity of SLE can vary widely from person to person, but common features include fatigue, joint pain, skin rashes (particularly a "butterfly" rash across the nose and cheeks), fever, hair loss, and sensitivity to sunlight.

Systemic lupus erythematosus can also affect the kidneys, heart, lungs, brain, blood vessels, and other organs, leading to a wide range of symptoms such as kidney dysfunction, chest pain, shortness of breath, seizures, and anemia. The exact cause of SLE is not fully understood, but it is believed to involve a combination of genetic, environmental, and hormonal factors. Treatment typically involves medications to suppress the immune system and manage symptoms, and may require long-term management by a team of healthcare professionals.

Cryoglobulinemia is a medical condition characterized by the presence of abnormal proteins called cryoglobulins in the blood. These proteins become insoluble at lower temperatures and can form immune complexes that can cause inflammation and damage to small blood vessels when they precipitate in cooler parts of the body.

Cryoglobulinemia is often associated with underlying conditions such as autoimmune diseases (such as rheumatoid arthritis or lupus), chronic infections (such as hepatitis C), and certain types of cancer (such as lymphoma). Symptoms can vary widely, but may include purpura (purple spots on the skin), joint pain, peripheral neuropathy (nerve damage causing numbness or weakness), fatigue, and kidney problems.

The diagnosis of cryoglobulinemia is typically made by detecting cryoglobulins in the blood through a special test that requires the blood sample to be kept at cold temperatures. Treatment for cryoglobulinemia depends on the underlying cause, but may include medications such as corticosteroids, immunosuppressants, or chemotherapy drugs.

Antinuclear antibodies (ANA) are a type of autoantibody that target structures found in the nucleus of a cell. These antibodies are produced by the immune system and attack the body's own cells and tissues, leading to inflammation and damage. The presence of ANA is often used as a marker for certain autoimmune diseases, such as systemic lupus erythematosus (SLE), Sjogren's syndrome, rheumatoid arthritis, scleroderma, and polymyositis.

ANA can be detected through a blood test called the antinuclear antibody test. A positive result indicates the presence of ANA in the blood, but it does not necessarily mean that a person has an autoimmune disease. Further testing is usually needed to confirm a diagnosis and determine the specific type of autoantibodies present.

It's important to note that ANA can also be found in healthy individuals, particularly as they age. Therefore, the test results should be interpreted in conjunction with other clinical findings and symptoms.

'Mice, Inbred MRL-lpr' refers to a specific strain of laboratory mice that are used in biomedical research. The 'MRL' part of the name stands for the breeding colony where they were originally developed, which is the Mouse Repository at the Jackson Laboratory in Bar Harbor, Maine. The 'lpr' designation indicates that these mice carry a mutation in the Fas gene, also known as lpr (lymphoproliferation) gene, which leads to an autoimmune disorder characterized by lymphadenopathy (enlarged lymph nodes), splenomegaly (enlarged spleen), and production of autoantibodies.

The MRL-lpr mice are known for their accelerated aging phenotype, which includes the development of a variety of age-related diseases such as atherosclerosis, osteoporosis, and cancer. They also develop a severe form of systemic lupus erythematosus (SLE), an autoimmune disease that affects many organs in the body. The MRL-lpr mice are widely used as a model to study the pathogenesis of SLE and other autoimmune diseases, as well as to test potential therapies for these conditions.

It is important to note that while inbred mouse strains like MRL-lpr provide valuable insights into human disease mechanisms, they do not perfectly replicate all aspects of human disease, and results obtained in mice may not always translate directly to humans. Therefore, findings from mouse studies should be interpreted with caution and validated in human studies before being applied in clinical practice.

Thy-1, also known as Thy-1 antigen or CD90, is a glycosylphosphatidylinositol (GPI)-anchored protein found on the surface of various cells in the body. It was first discovered as a cell surface antigen on thymocytes, hence the name Thy-1.

Thy-1 is a member of the immunoglobulin superfamily and is widely expressed in different tissues, including the brain, where it is found on the surface of neurons and glial cells. In the immune system, Thy-1 is expressed on the surface of T lymphocytes, natural killer (NK) cells, and some subsets of dendritic cells.

The function of Thy-1 is not fully understood, but it has been implicated in various biological processes, including cell adhesion, signal transduction, and regulation of immune responses. Thy-1 has also been shown to play a role in the development and maintenance of the nervous system, as well as in the pathogenesis of certain neurological disorders.

As an antigen, Thy-1 can be recognized by specific antibodies, which can be used in various research and clinical applications, such as immunohistochemistry, flow cytometry, and cell sorting.

Cryoglobulins are immunoglobulins (a type of antibody) that precipitate or become insoluble at reduced temperatures, typically below 37°C (98.6°F), and re-dissolve when rewarmed. They can be found in various clinical conditions such as infections, inflammatory diseases, and lymphoproliferative disorders.

The presence of cryoglobulins in the blood can lead to a variety of symptoms, including purpura (a type of skin rash), arthralgias (joint pain), neuropathy (nerve damage), and glomerulonephritis (kidney inflammation). The diagnosis of cryoglobulinemia is made by detecting the presence of cryoglobulins in the serum, which requires special handling and processing of the blood sample. Treatment of cryoglobulinemia depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive agents, or targeted therapies.

Interstitial nephritis is a condition characterized by inflammation in the interstitium (the tissue between the kidney tubules) of one or both kidneys. This inflammation can be caused by various factors, including infections, autoimmune disorders, medications, and exposure to certain toxins.

The inflammation may lead to symptoms such as hematuria (blood in the urine), proteinuria (protein in the urine), decreased urine output, and kidney dysfunction. In some cases, interstitial nephritis can progress to chronic kidney disease or even end-stage renal failure if left untreated.

The diagnosis of interstitial nephritis typically involves a combination of medical history, physical examination, laboratory tests (such as urinalysis and blood tests), and imaging studies (such as ultrasound or CT scan). A kidney biopsy may also be performed to confirm the diagnosis and assess the severity of the inflammation.

Treatment for interstitial nephritis depends on the underlying cause, but may include corticosteroids, immunosuppressive medications, or discontinuation of any offending medications. In some cases, supportive care such as dialysis may be necessary to manage kidney dysfunction until the inflammation resolves.

Streptococcal infections are a type of infection caused by group A Streptococcus bacteria (Streptococcus pyogenes). These bacteria can cause a variety of illnesses, ranging from mild skin infections to serious and potentially life-threatening conditions such as sepsis, pneumonia, and necrotizing fasciitis (flesh-eating disease).

Some common types of streptococcal infections include:

* Streptococcal pharyngitis (strep throat) - an infection of the throat and tonsils that can cause sore throat, fever, and swollen lymph nodes.
* Impetigo - a highly contagious skin infection that causes sores or blisters on the skin.
* Cellulitis - a bacterial infection of the deeper layers of the skin and underlying tissue that can cause redness, swelling, pain, and warmth in the affected area.
* Scarlet fever - a streptococcal infection that causes a bright red rash on the body, high fever, and sore throat.
* Necrotizing fasciitis - a rare but serious bacterial infection that can cause tissue death and destruction of the muscles and fascia (the tissue that covers the muscles).

Treatment for streptococcal infections typically involves antibiotics to kill the bacteria causing the infection. It is important to seek medical attention if you suspect a streptococcal infection, as prompt treatment can help prevent serious complications.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Autoimmune diseases are a group of disorders in which the immune system, which normally protects the body from foreign invaders like bacteria and viruses, mistakenly attacks the body's own cells and tissues. This results in inflammation and damage to various organs and tissues in the body.

In autoimmune diseases, the body produces autoantibodies that target its own proteins or cell receptors, leading to their destruction or malfunction. The exact cause of autoimmune diseases is not fully understood, but it is believed that a combination of genetic and environmental factors contribute to their development.

There are over 80 different types of autoimmune diseases, including rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, Hashimoto's thyroiditis, Graves' disease, psoriasis, and inflammatory bowel disease. Symptoms can vary widely depending on the specific autoimmune disease and the organs or tissues affected. Treatment typically involves managing symptoms and suppressing the immune system to prevent further damage.

Kidney disease, also known as nephropathy or renal disease, refers to any functional or structural damage to the kidneys that impairs their ability to filter blood, regulate electrolytes, produce hormones, and maintain fluid balance. This damage can result from a wide range of causes, including diabetes, hypertension, glomerulonephritis, polycystic kidney disease, lupus, infections, drugs, toxins, and congenital or inherited disorders.

Depending on the severity and progression of the kidney damage, kidney diseases can be classified into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI is a sudden and often reversible loss of kidney function that occurs over hours to days, while CKD is a progressive and irreversible decline in kidney function that develops over months or years.

Symptoms of kidney diseases may include edema, proteinuria, hematuria, hypertension, electrolyte imbalances, metabolic acidosis, anemia, and decreased urine output. Treatment options depend on the underlying cause and severity of the disease and may include medications, dietary modifications, dialysis, or kidney transplantation.

Lipoid nephrosis is a historical term for a kidney disorder now more commonly referred to as minimal change disease (MCD). It is a type of glomerulonephritis which is characterized by the loss of proteins in the urine (proteinuria) due to damage to the glomeruli, the tiny filtering units within the kidneys.

The term "lipoid" refers to the presence of lipids or fats in the glomeruli, which can be observed under a microscope. However, it's worth noting that not all cases of MCD involve lipid accumulation in the glomeruli.

MCD is typically idiopathic, meaning its cause is unknown, but it can also occur as a secondary condition related to other medical disorders such as allergies, infections, or medications. It primarily affects children, but can also occur in adults. Treatment usually involves corticosteroids and other immunosuppressive therapies to control proteinuria and prevent kidney damage.

Immunoglobulin A (IgA), Secretory is a type of antibody that plays a crucial role in the immune function of mucous membranes. These membranes line various body openings, such as the respiratory and gastrointestinal tracts, and serve to protect the body from potential pathogens by producing mucus.

Secretory IgA (SIgA) is the primary immunoglobulin found in secretions of the mucous membranes, and it is produced by a special type of immune cell called plasma cells located in the lamina propria, a layer of tissue beneath the epithelial cells that line the mucosal surfaces.

SIgA exists as a dimer, consisting of two IgA molecules linked together by a protein called the J chain. This complex is then transported across the epithelial cell layer to the luminal surface, where it becomes associated with another protein called the secretory component (SC). The SC protects the SIgA from degradation by enzymes and helps it maintain its function in the harsh environment of the mucosal surfaces.

SIgA functions by preventing the attachment and entry of pathogens into the body, thereby neutralizing their infectivity. It can also agglutinate (clump together) microorganisms, making them more susceptible to removal by mucociliary clearance or peristalsis. Furthermore, SIgA can modulate immune responses and contribute to the development of oral tolerance, which is important for maintaining immune homeostasis in the gut.

'NZB mice' is a term used to refer to an inbred strain of laboratory mice that are genetically identical to each other and have been used extensively in biomedical research. The 'NZB' designation stands for "New Zealand Black," which refers to the coat color of these mice.

NZB mice are known to spontaneously develop an autoimmune disease that is similar to human systemic lupus erythematosus (SLE), a chronic inflammatory disorder caused by an overactive immune system. This makes them a valuable model for studying the genetic and environmental factors that contribute to the development of SLE, as well as for testing new therapies and treatments.

It's important to note that while NZB mice are an inbred strain, they may still exhibit some variability in their disease phenotype due to genetic modifiers or environmental influences. Therefore, researchers often use large cohorts of mice and standardized experimental conditions to ensure the reproducibility and reliability of their findings.

Lupus vulgaris is not related to systemic lupus erythematosus, which is an autoimmune disease. Instead, it's a specific form of cutaneous tuberculosis, a bacterial infection that affects the skin. It's caused by the Mycobacterium tuberculosis bacteria, the same organism responsible for pulmonary tuberculosis and other forms of tuberculosis.

Lupus vulgaris typically occurs in people who have had prior tuberculous infection or those with a weakened immune system. The condition is characterized by slowly growing, reddish-brown or violaceous papules, nodules, and plaques that may ulcerate and form scars. Lesions often have an apple jelly appearance when a glass slide is pressed against them and examined under a dermatoscope.

Lupus vulgaris lesions usually occur on the face, especially the nose, cheeks, and ears, but they can appear on other parts of the body as well. The condition can lead to significant disfigurement if left untreated. Diagnosis typically involves skin biopsy and culture or PCR for Mycobacterium tuberculosis. Treatment usually consists of a combination of multiple antituberculous drugs, such as isoniazid, rifampin, ethambutol, and pyrazinamide, along with local therapies like surgical excision or laser treatment.

WKY (Wistar Kyoto) is not a term that refers to "rats, inbred" in a medical definition. Instead, it is a strain of laboratory rat that is widely used in biomedical research. WKY rats are an inbred strain, which means they are the result of many generations of brother-sister matings, resulting in a genetically uniform population.

WKY rats originated from the Wistar Institute in Philadelphia and were established as a normotensive control strain to contrast with other rat strains that exhibit hypertension. They have since been used in various research areas, including cardiovascular, neurological, and behavioral studies. Compared to other commonly used rat strains like the spontaneously hypertensive rat (SHR), WKY rats are known for their lower blood pressure, reduced stress response, and greater emotionality.

In summary, "WKY" is a designation for an inbred strain of laboratory rat that is often used as a control group in biomedical research due to its normotensive characteristics.

Kidney tubules are the structural and functional units of the kidney responsible for reabsorption, secretion, and excretion of various substances. They are part of the nephron, which is the basic unit of the kidney's filtration and reabsorption process.

There are three main types of kidney tubules:

1. Proximal tubule: This is the initial segment of the kidney tubule that receives the filtrate from the glomerulus. It is responsible for reabsorbing approximately 65% of the filtrate, including water, glucose, amino acids, and electrolytes.
2. Loop of Henle: This U-shaped segment of the tubule consists of a thin descending limb, a thin ascending limb, and a thick ascending limb. The loop of Henle helps to concentrate urine by creating an osmotic gradient that allows water to be reabsorbed in the collecting ducts.
3. Distal tubule: This is the final segment of the kidney tubule before it empties into the collecting duct. It is responsible for fine-tuning the concentration of electrolytes and pH balance in the urine by selectively reabsorbing or secreting substances such as sodium, potassium, chloride, and hydrogen ions.

Overall, kidney tubules play a critical role in maintaining fluid and electrolyte balance, regulating acid-base balance, and removing waste products from the body.

Immunoglobulin M (IgM) is a type of antibody that is primarily found in the blood and lymph fluid. It is the first antibody to be produced in response to an initial exposure to an antigen, making it an important part of the body's primary immune response. IgM antibodies are large molecules that are composed of five basic units, giving them a pentameric structure. They are primarily found on the surface of B cells as membrane-bound immunoglobulins (mlgM), where they function as receptors for antigens. Once an mlgM receptor binds to an antigen, it triggers the activation and differentiation of the B cell into a plasma cell that produces and secretes large amounts of soluble IgM antibodies.

IgM antibodies are particularly effective at agglutination (clumping) and complement activation, which makes them important in the early stages of an immune response to help clear pathogens from the bloodstream. However, they are not as stable or long-lived as other types of antibodies, such as IgG, and their levels tend to decline after the initial immune response has occurred.

In summary, Immunoglobulin M (IgM) is a type of antibody that plays a crucial role in the primary immune response to antigens by agglutination and complement activation. It is primarily found in the blood and lymph fluid, and it is produced by B cells after they are activated by an antigen.

Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by the immune system's B cells in response to the presence of foreign substances, such as bacteria, viruses, and toxins. These Y-shaped proteins play a crucial role in identifying and neutralizing pathogens and other antigens, thereby protecting the body against infection and disease.

Immunoglobulins are composed of four polypeptide chains: two identical heavy chains and two identical light chains, held together by disulfide bonds. The variable regions of these chains form the antigen-binding sites, which recognize and bind to specific epitopes on antigens. Based on their heavy chain type, immunoglobulins are classified into five main isotypes or classes: IgA, IgD, IgE, IgG, and IgM. Each class has distinct functions in the immune response, such as providing protection in different body fluids and tissues, mediating hypersensitivity reactions, and aiding in the development of immunological memory.

In medical settings, immunoglobulins can be administered therapeutically to provide passive immunity against certain diseases or to treat immune deficiencies, autoimmune disorders, and other conditions that may benefit from immunomodulation.

Wegener Granulomatosis is a rare, chronic granulomatous vasculitis that affects small and medium-sized blood vessels. It is also known as granulomatosis with polyangiitis (GPA). The disease primarily involves the respiratory tract (nose, sinuses, trachea, and lungs) and kidneys but can affect other organs as well.

The characteristic features of Wegener Granulomatosis include necrotizing granulomas, vasculitis, and inflammation of the blood vessel walls. These abnormalities can lead to various symptoms such as cough, shortness of breath, nosebleeds, sinus congestion, skin lesions, joint pain, and kidney problems.

The exact cause of Wegener Granulomatosis is unknown, but it is believed to be an autoimmune disorder where the body's immune system mistakenly attacks its own tissues and organs. The diagnosis of Wegener Granulomatosis typically involves a combination of clinical symptoms, laboratory tests, imaging studies, and biopsy findings. Treatment usually includes immunosuppressive therapy to control the inflammation and prevent further damage to the affected organs.

Henoch-Schönlein purpura (HSP) is a type of small vessel vasculitis, which is a condition characterized by inflammation of the blood vessels. HSP primarily affects children, but it can occur in adults as well. It is named after two German physicians, Eduard Heinrich Henoch and Johann Schönlein, who first described the condition in the mid-19th century.

The main feature of HSP is a purpuric rash, which is a type of rash that appears as small, red or purple spots on the skin. The rash is caused by leakage of blood from the small blood vessels (capillaries) beneath the skin. In HSP, this rash typically occurs on the legs and buttocks, but it can also affect other parts of the body, such as the arms, face, and trunk.

In addition to the purpuric rash, HSP is often accompanied by other symptoms, such as joint pain and swelling, abdominal pain, nausea, vomiting, and diarrhea. In severe cases, it can also affect the kidneys, leading to hematuria (blood in the urine) and proteinuria (protein in the urine).

The exact cause of HSP is not known, but it is thought to be related to an abnormal immune response to certain triggers, such as infections or medications. Treatment typically involves supportive care, such as pain relief and fluid replacement, as well as medications to reduce inflammation and suppress the immune system. In most cases, HSP resolves on its own within a few weeks or months, but it can lead to serious complications in some individuals.

Antibodies are proteins produced by the immune system in response to the presence of a foreign substance, such as a bacterium or virus. They are capable of identifying and binding to specific antigens (foreign substances) on the surface of these invaders, marking them for destruction by other immune cells. Antibodies are also known as immunoglobulins and come in several different types, including IgA, IgD, IgE, IgG, and IgM, each with a unique function in the immune response. They are composed of four polypeptide chains, two heavy chains and two light chains, that are held together by disulfide bonds. The variable regions of the heavy and light chains form the antigen-binding site, which is specific to a particular antigen.

Isoantibodies are antibodies produced by the immune system that recognize and react to antigens (markers) found on the cells or tissues of another individual of the same species. These antigens are typically proteins or carbohydrates present on the surface of red blood cells, but they can also be found on other cell types.

Isoantibodies are formed when an individual is exposed to foreign antigens, usually through blood transfusions, pregnancy, or tissue transplantation. The exposure triggers the immune system to produce specific antibodies against these antigens, which can cause a harmful immune response if the individual receives another transfusion or transplant from the same donor in the future.

There are two main types of isoantibodies:

1. Agglutinins: These are IgM antibodies that cause red blood cells to clump together (agglutinate) when mixed with the corresponding antigen. They develop rapidly after exposure and can cause immediate transfusion reactions or hemolytic disease of the newborn in pregnant women.
2. Hemolysins: These are IgG antibodies that destroy red blood cells by causing their membranes to become more permeable, leading to lysis (bursting) of the cells and release of hemoglobin into the plasma. They take longer to develop but can cause delayed transfusion reactions or hemolytic disease of the newborn in pregnant women.

Isoantibodies are detected through blood tests, such as the crossmatch test, which determines compatibility between a donor's and recipient's blood before transfusions or transplants.

Electron microscopy (EM) is a type of microscopy that uses a beam of electrons to create an image of the sample being examined, resulting in much higher magnification and resolution than light microscopy. There are several types of electron microscopy, including transmission electron microscopy (TEM), scanning electron microscopy (SEM), and reflection electron microscopy (REM).

In TEM, a beam of electrons is transmitted through a thin slice of the sample, and the electrons that pass through the sample are focused to form an image. This technique can provide detailed information about the internal structure of cells, viruses, and other biological specimens, as well as the composition and structure of materials at the atomic level.

In SEM, a beam of electrons is scanned across the surface of the sample, and the electrons that are scattered back from the surface are detected to create an image. This technique can provide information about the topography and composition of surfaces, as well as the structure of materials at the microscopic level.

REM is a variation of SEM in which the beam of electrons is reflected off the surface of the sample, rather than scattered back from it. This technique can provide information about the surface chemistry and composition of materials.

Electron microscopy has a wide range of applications in biology, medicine, and materials science, including the study of cellular structure and function, disease diagnosis, and the development of new materials and technologies.

Creatinine is a waste product that's produced by your muscles and removed from your body by your kidneys. Creatinine is a breakdown product of creatine, a compound found in meat and fish, as well as in the muscles of vertebrates, including humans.

In healthy individuals, the kidneys filter out most of the creatinine and eliminate it through urine. However, when the kidneys are not functioning properly, creatinine levels in the blood can rise. Therefore, measuring the amount of creatinine in the blood or urine is a common way to test how well the kidneys are working. High creatinine levels in the blood may indicate kidney damage or kidney disease.

Dysgammaglobulinemia is a medical term that refers to an abnormal gamma globulin or immunoglobulin (antibody) level in the blood. Gamma globulins are proteins that play a crucial role in the immune system and help fight off infections. Immunoglobulins are classified into five types (IgA, IgD, IgE, IgG, and IgM), each with a specific function in the immune response.

In dysgammaglobulinemia, there is an imbalance in the levels of these immunoglobulins, which can be either elevated or decreased. This condition can result from various underlying causes, including genetic disorders, autoimmune diseases, infections, and malignancies that affect the bone marrow or lymphatic system.

Depending on the specific pattern of immunoglobulin levels, dysgammaglobulinemia can be further classified into different types, such as:

1. Hypogammaglobulinemia - a decrease in one or more classes of immunoglobulins
2. Agammaglobulinemia - a severe deficiency or absence of all classes of immunoglobulins
3. Hypergammaglobulinemia - an elevation of one or more classes of immunoglobulins

Dysgammaglobulinemia can lead to increased susceptibility to infections, autoimmune disorders, and other health complications. Therefore, it is essential to identify the underlying cause and provide appropriate treatment to manage the condition and prevent further complications.

Collagen Type IV is a type of collagen that forms the structural basis of basement membranes, which are thin, sheet-like structures that separate and support cells in many types of tissues. It is a major component of the basement membrane's extracellular matrix and provides strength and flexibility to this structure. Collagen Type IV is composed of three chains that form a distinctive, mesh-like structure. Mutations in the genes encoding Collagen Type IV can lead to a variety of inherited disorders affecting the kidneys, eyes, and ears.

Peroxidase is a type of enzyme that catalyzes the chemical reaction in which hydrogen peroxide (H2O2) is broken down into water (H2O) and oxygen (O2). This enzymatic reaction also involves the oxidation of various organic and inorganic compounds, which can serve as electron donors.

Peroxidases are widely distributed in nature and can be found in various organisms, including bacteria, fungi, plants, and animals. They play important roles in various biological processes, such as defense against oxidative stress, breakdown of toxic substances, and participation in metabolic pathways.

The peroxidase-catalyzed reaction can be represented by the following chemical equation:

H2O2 + 2e- + 2H+ → 2H2O

In this reaction, hydrogen peroxide is reduced to water, and the electron donor is oxidized. The peroxidase enzyme facilitates the transfer of electrons between the substrate (hydrogen peroxide) and the electron donor, making the reaction more efficient and specific.

Peroxidases have various applications in medicine, industry, and research. For example, they can be used for diagnostic purposes, as biosensors, and in the treatment of wastewater and medical wastes. Additionally, peroxidases are involved in several pathological conditions, such as inflammation, cancer, and neurodegenerative diseases, making them potential targets for therapeutic interventions.

"Trimeresurus" is a genus of venomous pit vipers found primarily in Asia. Commonly known as "Asian pit vipers" or " temple pit vipers," these snakes are characterized by the presence of a heat-sensing pit organ between the eye and the nostril, which they use to detect the body heat of their prey. They are responsible for causing serious bites and occasionally fatal accidents in human beings.

It's important to note that "Trimeresurus" is a taxonomic term used in the field of biology, specifically in systematics and classification of organisms. It does not have a direct medical definition, but it refers to a group of snakes with medical significance due to their venomous nature.

Chronic kidney failure, also known as chronic kidney disease (CKD) stage 5 or end-stage renal disease (ESRD), is a permanent loss of kidney function that occurs gradually over a period of months to years. It is defined as a glomerular filtration rate (GFR) of less than 15 ml/min, which means the kidneys are filtering waste and excess fluids at less than 15% of their normal capacity.

CKD can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and recurrent kidney infections. Over time, the damage to the kidneys can lead to a buildup of waste products and fluids in the body, which can cause a range of symptoms including fatigue, weakness, shortness of breath, nausea, vomiting, and confusion.

Treatment for chronic kidney failure typically involves managing the underlying condition, making lifestyle changes such as following a healthy diet, and receiving supportive care such as dialysis or a kidney transplant to replace lost kidney function.

Kidney function tests (KFTs) are a group of diagnostic tests that evaluate how well your kidneys are functioning by measuring the levels of various substances in the blood and urine. The tests typically assess the glomerular filtration rate (GFR), which is an indicator of how efficiently the kidneys filter waste from the blood, as well as the levels of electrolytes, waste products, and proteins in the body.

Some common KFTs include:

1. Serum creatinine: A waste product that's produced by normal muscle breakdown and is excreted by the kidneys. Elevated levels may indicate reduced kidney function.
2. Blood urea nitrogen (BUN): Another waste product that's produced when protein is broken down and excreted by the kidneys. Increased BUN levels can suggest impaired kidney function.
3. Estimated glomerular filtration rate (eGFR): A calculation based on serum creatinine, age, sex, and race that estimates the GFR and provides a more precise assessment of kidney function than creatinine alone.
4. Urinalysis: An examination of a urine sample to detect abnormalities such as protein, blood, or bacteria that may indicate kidney disease.
5. Electrolyte levels: Measurement of sodium, potassium, chloride, and bicarbonate in the blood to ensure they're properly balanced, which is essential for normal kidney function.

KFTs are often ordered as part of a routine check-up or when kidney disease is suspected based on symptoms or other diagnostic tests. Regular monitoring of kidney function can help detect and manage kidney disease early, potentially preventing or slowing down its progression.

Immunosuppressive agents are medications that decrease the activity of the immune system. They are often used to prevent the rejection of transplanted organs and to treat autoimmune diseases, where the immune system mistakenly attacks the body's own tissues. These drugs work by interfering with the immune system's normal responses, which helps to reduce inflammation and damage to tissues. However, because they suppress the immune system, people who take immunosuppressive agents are at increased risk for infections and other complications. Examples of immunosuppressive agents include corticosteroids, azathioprine, cyclophosphamide, mycophenolate mofetil, tacrolimus, and sirolimus.

Blood Urea Nitrogen (BUN) is a laboratory value that measures the amount of urea nitrogen in the blood. Urea nitrogen is a waste product that is formed when proteins are broken down in the liver. The kidneys filter urea nitrogen from the blood and excrete it as urine.

A high BUN level may indicate impaired kidney function, as the kidneys are not effectively removing urea nitrogen from the blood. However, BUN levels can also be affected by other factors such as dehydration, heart failure, or gastrointestinal bleeding. Therefore, BUN should be interpreted in conjunction with other laboratory values and clinical findings.

The normal range for BUN is typically between 7-20 mg/dL (milligrams per deciliter) or 2.5-7.1 mmol/L (millimoles per liter), but the reference range may vary depending on the laboratory.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

Fibrin is defined as a protein that is formed from fibrinogen during the clotting of blood. It plays an essential role in the formation of blood clots, also known as a clotting or coagulation cascade. When an injury occurs and bleeding starts, fibrin threads form a net-like structure that entraps platelets and red blood cells to create a stable clot, preventing further loss of blood.

The process of forming fibrin from fibrinogen is initiated by thrombin, another protein involved in the coagulation cascade. Thrombin cleaves fibrinogen into fibrin monomers, which then polymerize to form long strands of fibrin. These strands cross-link with each other through a process catalyzed by factor XIIIa, forming a stable clot that protects the wound and promotes healing.

It is important to note that abnormalities in fibrin formation or breakdown can lead to bleeding disorders or thrombotic conditions, respectively. Proper regulation of fibrin production and degradation is crucial for maintaining healthy hemostasis and preventing excessive clotting or bleeding.

Prednisolone is a synthetic glucocorticoid drug, which is a class of steroid hormones. It is commonly used in the treatment of various inflammatory and autoimmune conditions due to its potent anti-inflammatory and immunosuppressive effects. Prednisolone works by binding to specific receptors in cells, leading to changes in gene expression that reduce the production of substances involved in inflammation, such as cytokines and prostaglandins.

Prednisolone is available in various forms, including tablets, syrups, and injectable solutions. It can be used to treat a wide range of medical conditions, including asthma, rheumatoid arthritis, inflammatory bowel disease, allergies, skin conditions, and certain types of cancer.

Like other steroid medications, prednisolone can have significant side effects if used in high doses or for long periods of time. These may include weight gain, mood changes, increased risk of infections, osteoporosis, diabetes, and adrenal suppression. As a result, the use of prednisolone should be closely monitored by a healthcare professional to ensure that its benefits outweigh its risks.

Rheumatic fever is a systemic inflammatory disease that may occur following an untreated Group A streptococcal infection, such as strep throat. It primarily affects children between the ages of 5 and 15, but it can occur at any age. The condition is characterized by inflammation in various parts of the body, including the heart (carditis), joints (arthritis), skin (erythema marginatum, subcutaneous nodules), and brain (Sydenham's chorea).

The onset of rheumatic fever usually occurs 2-4 weeks after a streptococcal infection. The exact cause of the immune system's overreaction leading to rheumatic fever is not fully understood, but it involves molecular mimicry between streptococcal antigens and host tissues.

The Jones Criteria are used to diagnose rheumatic fever, which include:

1. Evidence of a preceding streptococcal infection (e.g., positive throat culture or rapid strep test, elevated or rising anti-streptolysin O titer)
2. Carditis (heart inflammation), including new murmurs or changes in existing murmurs, electrocardiogram abnormalities, or evidence of heart failure
3. Polyarthritis (inflammation of multiple joints) – typically large joints like the knees and ankles, migratory, and may be associated with warmth, swelling, and pain
4. Erythema marginatum (a skin rash characterized by pink or red, irregularly shaped macules or rings that blanch in the center and spread outward)
5. Subcutaneous nodules (firm, round, mobile lumps under the skin, usually over bony prominences)
6. Sydenham's chorea (involuntary, rapid, irregular movements, often affecting the face, hands, and feet)

Treatment of rheumatic fever typically involves antibiotics to eliminate any residual streptococcal infection, anti-inflammatory medications like corticosteroids or nonsteroidal anti-inflammatory drugs (NSAIDs) to manage symptoms and prevent long-term heart complications, and secondary prophylaxis with regular antibiotic administration to prevent recurrent streptococcal infections.

Plasmapheresis is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies or toxins, is then removed and replaced with fresh plasma or a plasma substitute. The remaining blood cells are mixed with the new plasma and returned to the body. This process is also known as therapeutic plasma exchange (TPE). It's used to treat various medical conditions including certain autoimmune diseases, poisonings, and neurological disorders.

Macrophages are a type of white blood cell that are an essential part of the immune system. They are large, specialized cells that engulf and destroy foreign substances, such as bacteria, viruses, parasites, and fungi, as well as damaged or dead cells. Macrophages are found throughout the body, including in the bloodstream, lymph nodes, spleen, liver, lungs, and connective tissues. They play a critical role in inflammation, immune response, and tissue repair and remodeling.

Macrophages originate from monocytes, which are a type of white blood cell produced in the bone marrow. When monocytes enter the tissues, they differentiate into macrophages, which have a larger size and more specialized functions than monocytes. Macrophages can change their shape and move through tissues to reach sites of infection or injury. They also produce cytokines, chemokines, and other signaling molecules that help coordinate the immune response and recruit other immune cells to the site of infection or injury.

Macrophages have a variety of surface receptors that allow them to recognize and respond to different types of foreign substances and signals from other cells. They can engulf and digest foreign particles, bacteria, and viruses through a process called phagocytosis. Macrophages also play a role in presenting antigens to T cells, which are another type of immune cell that helps coordinate the immune response.

Overall, macrophages are crucial for maintaining tissue homeostasis, defending against infection, and promoting wound healing and tissue repair. Dysregulation of macrophage function has been implicated in a variety of diseases, including cancer, autoimmune disorders, and chronic inflammatory conditions.

Microscopic Polyangiitis (MPA) is a rare type of vasculitis, which is a group of disorders that cause inflammation in the blood vessels. In MPA, the small blood vessels in various organs become inflamed and damaged, leading to symptoms that can affect multiple organ systems.

The term "microscopic" refers to the fact that the diagnosis of this condition typically requires examination of tissue samples under a microscope to see the characteristic patterns of inflammation and damage in the small blood vessels.

MPA is an autoimmune disorder, which means that the body's immune system mistakenly attacks its own tissues and organs. In MPA, the immune system produces abnormal antibodies called ANCA (antineutrophil cytoplasmic antibodies) that target certain proteins in the white blood cells, leading to their activation and subsequent damage to the blood vessels.

The symptoms of MPA can vary widely depending on which organs are affected, but they may include fever, fatigue, weight loss, joint pain, skin rashes, cough, shortness of breath, and kidney problems such as proteinuria and hematuria. Treatment typically involves the use of immunosuppressive medications to suppress the overactive immune system and reduce inflammation in the blood vessels.

Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.

Disease progression is the worsening or advancement of a medical condition over time. It refers to the natural course of a disease, including its development, the severity of symptoms and complications, and the impact on the patient's overall health and quality of life. Understanding disease progression is important for developing appropriate treatment plans, monitoring response to therapy, and predicting outcomes.

The rate of disease progression can vary widely depending on the type of medical condition, individual patient factors, and the effectiveness of treatment. Some diseases may progress rapidly over a short period of time, while others may progress more slowly over many years. In some cases, disease progression may be slowed or even halted with appropriate medical interventions, while in other cases, the progression may be inevitable and irreversible.

In clinical practice, healthcare providers closely monitor disease progression through regular assessments, imaging studies, and laboratory tests. This information is used to guide treatment decisions and adjust care plans as needed to optimize patient outcomes and improve quality of life.

Autoantigens are substances that are typically found in an individual's own body, but can stimulate an immune response because they are recognized as foreign by the body's own immune system. In autoimmune diseases, the immune system mistakenly attacks and damages healthy tissues and organs because it recognizes some of their components as autoantigens. These autoantigens can be proteins, DNA, or other molecules that are normally present in the body but have become altered or exposed due to various factors such as infection, genetics, or environmental triggers. The immune system then produces antibodies and activates immune cells to attack these autoantigens, leading to tissue damage and inflammation.

An acute disease is a medical condition that has a rapid onset, develops quickly, and tends to be short in duration. Acute diseases can range from minor illnesses such as a common cold or flu, to more severe conditions such as pneumonia, meningitis, or a heart attack. These types of diseases often have clear symptoms that are easy to identify, and they may require immediate medical attention or treatment.

Acute diseases are typically caused by an external agent or factor, such as a bacterial or viral infection, a toxin, or an injury. They can also be the result of a sudden worsening of an existing chronic condition. In general, acute diseases are distinct from chronic diseases, which are long-term medical conditions that develop slowly over time and may require ongoing management and treatment.

Examples of acute diseases include:

* Acute bronchitis: a sudden inflammation of the airways in the lungs, often caused by a viral infection.
* Appendicitis: an inflammation of the appendix that can cause severe pain and requires surgical removal.
* Gastroenteritis: an inflammation of the stomach and intestines, often caused by a viral or bacterial infection.
* Migraine headaches: intense headaches that can last for hours or days, and are often accompanied by nausea, vomiting, and sensitivity to light and sound.
* Myocardial infarction (heart attack): a sudden blockage of blood flow to the heart muscle, often caused by a buildup of plaque in the coronary arteries.
* Pneumonia: an infection of the lungs that can cause coughing, chest pain, and difficulty breathing.
* Sinusitis: an inflammation of the sinuses, often caused by a viral or bacterial infection.

It's important to note that while some acute diseases may resolve on their own with rest and supportive care, others may require medical intervention or treatment to prevent complications and promote recovery. If you are experiencing symptoms of an acute disease, it is always best to seek medical attention to ensure proper diagnosis and treatment.

The Secretory Component (SC) is the receptor protein for the Fc region of IgA immunoglobulins. It is also known as the transporter protein, which helps in the transport of polymeric IgA and pentameric IgM across the epithelial cells and into various secretions such as saliva, tears, and milk. The SC plays a crucial role in mucosal immunity by facilitating the local immune defense against pathogens. It is produced by the epithelial cells and can be cleaved from the polymeric IgA to become the free SC, which has been shown to have anti-inflammatory properties.

An Enzyme-Linked Immunosorbent Assay (ELISA) is a type of analytical biochemistry assay used to detect and quantify the presence of a substance, typically a protein or peptide, in a liquid sample. It takes its name from the enzyme-linked antibodies used in the assay.

In an ELISA, the sample is added to a well containing a surface that has been treated to capture the target substance. If the target substance is present in the sample, it will bind to the surface. Next, an enzyme-linked antibody specific to the target substance is added. This antibody will bind to the captured target substance if it is present. After washing away any unbound material, a substrate for the enzyme is added. If the enzyme is present due to its linkage to the antibody, it will catalyze a reaction that produces a detectable signal, such as a color change or fluorescence. The intensity of this signal is proportional to the amount of target substance present in the sample, allowing for quantification.

ELISAs are widely used in research and clinical settings to detect and measure various substances, including hormones, viruses, and bacteria. They offer high sensitivity, specificity, and reproducibility, making them a reliable choice for many applications.

Complement activation is the process by which the complement system, a part of the immune system, is activated to help eliminate pathogens and damaged cells from the body. The complement system consists of a group of proteins that work together to recognize and destroy foreign substances.

Activation of the complement system can occur through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteolytic reactions that ultimately result in the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis and removal.

The classical pathway is typically activated by the binding of antibodies to antigens on the surface of a pathogen or damaged cell. The lectin pathway is activated by the recognition of specific carbohydrate structures on the surface of microorganisms. The alternative pathway can be spontaneously activated and serves as an amplification loop for both the classical and lectin pathways.

Complement activation plays a crucial role in the immune response, but uncontrolled or excessive activation can also lead to tissue damage and inflammation. Dysregulation of complement activation has been implicated in various diseases, including autoimmune disorders, inflammatory conditions, and neurodegenerative diseases.

Apoferritins are the protein shells or apoproteins of ferritin molecules that are devoid of iron. Ferritin is a protein in cells that stores iron and releases it in a form that can be used by the body. Apoferritin can bind with iron ions to form ferritin. It has a hollow, spherical structure and is often used as a model for studying protein folding and assembly.

An antigen-antibody reaction is a specific immune response that occurs when an antigen (a foreign substance, such as a protein or polysaccharide on the surface of a bacterium or virus) comes into contact with a corresponding antibody (a protective protein produced by the immune system in response to the antigen). The antigen and antibody bind together, forming an antigen-antibody complex. This interaction can neutralize the harmful effects of the antigen, mark it for destruction by other immune cells, or activate complement proteins to help eliminate the antigen from the body. Antigen-antibody reactions are a crucial part of the adaptive immune response and play a key role in the body's defense against infection and disease.

The Complement Membrane Attack Complex (MAC), also known as the Terminal Complement Complex (TCC), is a protein structure that forms in the final stages of the complement system's immune response. The complement system is a part of the innate immune system that helps to eliminate pathogens and damaged cells from the body.

The MAC is composed of several proteins, including C5b, C6, C7, C8, and multiple subunits of C9, which assemble on the surface of target cells. The formation of the MAC creates a pore-like structure in the cell membrane, leading to disruption of the membrane's integrity and ultimately causing cell lysis or damage.

The MAC plays an important role in the immune response by helping to eliminate pathogens that have evaded other immune defenses. However, uncontrolled activation of the complement system and formation of the MAC can also contribute to tissue damage and inflammation in various diseases, such as autoimmune disorders, age-related macular degeneration, and ischemia-reperfusion injury.

Podocytes are specialized cells that make up the visceral epithelial layer of the glomerular basement membrane in the kidney. They have long, interdigitating foot processes that wrap around the capillaries of the glomerulus and play a crucial role in maintaining the filtration barrier of the kidney. The slit diaphragms between the foot processes allow for the passage of small molecules while retaining larger proteins in the bloodstream. Podocytes also contribute to the maintenance and regulation of the glomerular filtration rate, making them essential for normal renal function. Damage or loss of podocytes can lead to proteinuria and kidney disease.

Beta-globulins are a group of proteins found in the beta region of a serum protein electrophoresis, which is a laboratory test used to separate and identify different types of proteins in the blood. This group includes several important proteins such as:

1. Beta-lipoproteins: These are responsible for transporting fat molecules, including cholesterol, throughout the body.
2. Transferrin: A protein that binds and transports iron in the blood.
3. Complement components: These proteins play a crucial role in the immune system's response to infection and inflammation.
4. Beta-2 microglobulin: A protein involved in the functioning of the immune system, elevated levels of which can be found in various conditions such as kidney disease and autoimmune disorders.
5. Hemopexin: A protein that binds and transports heme (a component of hemoglobin) in the blood.

It is important to note that any significant increase or decrease in beta-globulins can indicate an underlying medical condition, such as liver disease, kidney disease, or an autoimmune disorder. Therefore, abnormal results should be further evaluated by a healthcare professional for proper diagnosis and treatment.

Properdin is defined as a positive regulatory protein in the complement system, which is a part of the immune system. It plays a crucial role in the alternative pathway of complement activation. Properdin stabilizes the C3 convertase (C3bBb), preventing its decay and increasing the efficiency of the alternative pathway. This results in the production of the membrane attack complex, which leads to the lysis of foreign cells or pathogens. Deficiencies in properdin can lead to an increased susceptibility to bacterial infections.

Azathioprine is an immunosuppressive medication that is used to prevent the rejection of transplanted organs and to treat autoimmune diseases such as rheumatoid arthritis, lupus, and inflammatory bowel disease. It works by suppressing the activity of the immune system, which helps to reduce inflammation and prevent the body from attacking its own tissues.

Azathioprine is a prodrug that is converted into its active form, 6-mercaptopurine, in the body. This medication can have significant side effects, including decreased white blood cell count, increased risk of infection, and liver damage. It may also increase the risk of certain types of cancer, particularly skin cancer and lymphoma.

Healthcare professionals must carefully monitor patients taking azathioprine for these potential side effects. They may need to adjust the dosage or stop the medication altogether if serious side effects occur. Patients should also take steps to reduce their risk of infection and skin cancer, such as practicing good hygiene, avoiding sun exposure, and using sunscreen.

Kidney transplantation is a surgical procedure where a healthy kidney from a deceased or living donor is implanted into a patient with end-stage renal disease (ESRD) or permanent kidney failure. The new kidney takes over the functions of filtering waste and excess fluids from the blood, producing urine, and maintaining the body's electrolyte balance.

The transplanted kidney is typically placed in the lower abdomen, with its blood vessels connected to the recipient's iliac artery and vein. The ureter of the new kidney is then attached to the recipient's bladder to ensure proper urine flow. Following the surgery, the patient will require lifelong immunosuppressive therapy to prevent rejection of the transplanted organ by their immune system.

I'm happy to help! "Rats, Inbred Lew" is a specific strain of laboratory rats that have been inbred for research purposes. The "Lew" part of the name refers to the location where they were first developed, the Lewis Institute in Lake Bluff, Illinois, USA.

Inbreeding is a process of mating closely related individuals over many generations to create a genetically homogeneous population. This results in a high degree of genetic similarity among members of the strain, making them ideal for use as experimental models because any differences observed between individuals are more likely to be due to the experimental manipulation rather than genetic variation.

Inbred Lew rats have been widely used in biomedical research, particularly in studies related to hypertension and cardiovascular disease. They exhibit a number of unique characteristics that make them useful for these types of studies, including their susceptibility to developing high blood pressure when fed a high-salt diet or given certain drugs.

It's important to note that while inbred strains like Lew rats can be very useful tools for researchers, they are not perfect models for human disease. Because they have been bred in a controlled environment and selected for specific traits, they may not respond to experimental manipulations in the same way that humans or other animals would. Therefore, it's important to interpret findings from these studies with caution and consider multiple lines of evidence before drawing any firm conclusions.

Complement C4 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C4 is involved in the early stages of the complement activation cascade, where it helps to identify and tag foreign or abnormal cells for destruction by other components of the immune system.

Specifically, Complement C4 can be cleaved into two smaller proteins, C4a and C4b, during the complement activation process. C4b then binds to the surface of the target cell and helps to initiate the formation of the membrane attack complex (MAC), which creates a pore in the cell membrane and leads to lysis or destruction of the target cell.

Deficiencies or mutations in the Complement C4 gene can lead to various immune disorders, including certain forms of autoimmune diseases and susceptibility to certain infections.

Anti-idiotypic antibodies are a type of immune protein that recognizes and binds to the unique identifying region (idiotype) of another antibody. These antibodies are produced by the immune system as part of a regulatory feedback mechanism, where they can modulate or inhibit the activity of the original antibody. They have been studied for their potential use in immunotherapy and vaccine development.

Polyarteritis nodosa (PAN) is a rare, systemic necrotizing vasculitis that affects medium-sized and small muscular arteries. It is characterized by inflammation and damage to the walls of the arteries, leading to the formation of microaneurysms (small bulges in the artery wall) and subsequent narrowing or complete occlusion of the affected vessels. This can result in tissue ischemia (reduced blood flow) and infarction (tissue death), causing a wide range of clinical manifestations that vary depending on the organs involved.

The exact cause of PAN remains unclear, but it is believed to involve an autoimmune response triggered by various factors such as infections or exposure to certain drugs. The diagnosis of PAN typically requires a combination of clinical findings, laboratory tests, and imaging studies, often supported by histopathological examination of affected tissues. Treatment usually involves the use of immunosuppressive medications to control inflammation and prevent further damage to the arteries and organs.

Complement Factor H is a protein involved in the regulation of the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Specifically, Complement Factor H helps to regulate the activation and deactivation of the complement component C3b, preventing excessive or unwanted activation of the complement system and protecting host tissues from damage.

Complement Factor H is a crucial protein in maintaining the balance between the protective effects of the complement system and the potential for harm to the body's own cells and tissues. Deficiencies or mutations in Complement Factor H have been associated with several diseases, including age-related macular degeneration (AMD), atypical hemolytic uremic syndrome (aHUS), and C3 glomerulopathy.

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

Anti-Neutrophil Cytoplasmic Antibody (ANCA)-Associated Vasculitis (AAV) is a group of autoimmune diseases characterized by inflammation and damage to small blood vessels, particularly capillaries, venules, and arterioles. The condition is named after the presence of ANCAs in the patient's serum, which are autoantibodies that target specific proteins in the neutrophil cytoplasm.

AAV includes several subtypes, including:

1. Granulomatosis with Polyangiitis (GPA, formerly known as Wegener's granulomatosis) - a form of AAV that typically affects the respiratory tract and kidneys, characterized by the presence of granulomas (clusters of inflammatory cells).
2. Microscopic Polyangiitis (MPA) - a form of AAV that primarily affects small vessels in various organs, such as the kidneys, lungs, and skin.
3. Eosinophilic Granulomatosis with Polyangiitis (EGPA, formerly known as Churg-Strauss syndrome) - a form of AAV that involves asthma, allergies, and eosinophilia (an increased number of eosinophils in the blood), along with vasculitis affecting various organs.

The exact cause of ANCA-Associated Vasculitis is not fully understood, but it is believed to involve an interplay between genetic factors, environmental triggers, and dysregulation of the immune system. The condition can lead to a wide range of symptoms depending on which organs are affected, including fever, fatigue, weight loss, joint pain, skin rashes, cough, shortness of breath, nosebleeds, and kidney problems. Treatment typically involves immunosuppressive medications to control inflammation and prevent further damage to the affected organs.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Plasma exchange, also known as plasmapheresis, is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies, clotting factors, or toxins, is then removed and replaced with fresh plasma or a plasma substitute. This process helps to remove the harmful substances from the blood and allows the body to replenish its own plasma with normal components. Plasma exchange is used in the treatment of various medical conditions including autoimmune diseases, poisonings, and certain types of kidney diseases.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

Streptococcus pyogenes is a Gram-positive, beta-hemolytic streptococcus bacterium that causes various suppurative (pus-forming) and nonsuppurative infections in humans. It is also known as group A Streptococcus (GAS) due to its ability to produce the M protein, which confers type-specific antigenicity and allows for serological classification into more than 200 distinct Lancefield groups.

S. pyogenes is responsible for a wide range of clinical manifestations, including pharyngitis (strep throat), impetigo, cellulitis, erysipelas, scarlet fever, rheumatic fever, and acute poststreptococcal glomerulonephritis. In rare cases, it can lead to invasive diseases such as necrotizing fasciitis (flesh-eating disease) and streptococcal toxic shock syndrome (STSS).

The bacterium is typically transmitted through respiratory droplets or direct contact with infected skin lesions. Effective prevention strategies include good hygiene practices, such as frequent handwashing and avoiding sharing personal items, as well as prompt recognition and treatment of infections to prevent spread.

An antigen is a substance (usually a protein) that is recognized as foreign by the immune system and stimulates an immune response, leading to the production of antibodies or activation of T-cells. Antigens can be derived from various sources, including bacteria, viruses, fungi, parasites, and tumor cells. They can also come from non-living substances such as pollen, dust mites, or chemicals.

Antigens contain epitopes, which are specific regions on the antigen molecule that are recognized by the immune system. The immune system's response to an antigen depends on several factors, including the type of antigen, its size, and its location in the body.

In general, antigens can be classified into two main categories:

1. T-dependent antigens: These require the help of T-cells to stimulate an immune response. They are typically larger, more complex molecules that contain multiple epitopes capable of binding to both MHC class II molecules on antigen-presenting cells and T-cell receptors on CD4+ T-cells.
2. T-independent antigens: These do not require the help of T-cells to stimulate an immune response. They are usually smaller, simpler molecules that contain repetitive epitopes capable of cross-linking B-cell receptors and activating them directly.

Understanding antigens and their properties is crucial for developing vaccines, diagnostic tests, and immunotherapies.

Complement C1q is a protein that is part of the complement system, which is a group of proteins in the blood that help to eliminate pathogens and damaged cells from the body. C1q is the first component of the classical complement pathway, which is activated by the binding of C1q to antibodies that are attached to the surface of a pathogen or damaged cell.

C1q is composed of six identical polypeptide chains, each containing a collagen-like region and a globular head region. The globular heads can bind to various structures, including the Fc regions of certain antibodies, immune complexes, and some types of cells. When C1q binds to an activating surface, it triggers a series of proteolytic reactions that lead to the activation of other complement components and the formation of the membrane attack complex (MAC), which can punch holes in the membranes of pathogens or damaged cells, leading to their destruction.

In addition to its role in the immune system, C1q has also been found to have roles in various physiological processes, including tissue remodeling, angiogenesis, and the clearance of apoptotic cells. Dysregulation of the complement system, including abnormalities in C1q function, has been implicated in a variety of diseases, including autoimmune disorders, inflammatory diseases, and neurodegenerative conditions.

Globulins are a type of protein found in blood plasma, which is the clear, yellowish fluid that circulates throughout the body inside blood vessels. They are one of the three main types of proteins in blood plasma, along with albumin and fibrinogen. Globulins play important roles in the immune system, helping to defend the body against infection and disease.

Globulins can be further divided into several subcategories based on their size, electrical charge, and other properties. Some of the major types of globulins include:

* Alpha-1 globulins
* Alpha-2 globulins
* Beta globulins
* Gamma globulins

Gamma globulins are also known as immunoglobulins or antibodies, which are proteins produced by the immune system to help fight off infections and diseases. There are five main classes of immunoglobulins: IgA, IgD, IgE, IgG, and IgM. Each class of immunoglobulin has a different function in the body's defense mechanisms.

Abnormal levels of globulins can be indicative of various medical conditions, such as liver disease, kidney disease, or autoimmune disorders. Therefore, measuring the levels of different types of globulins in the blood is often used as a diagnostic tool to help identify and monitor these conditions.

Complement C3c is a protein component of the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C3c is formed when the third component of the complement system (C3) is cleaved into two smaller proteins, C3a and C3b, during the complement activation process.

C3b can then be further cleaved into C3c and C3dg. C3c is a stable fragment that remains in the circulation and can be measured in blood tests as a marker of complement activation. It plays a role in the opsonization of pathogens, which means it coats them to make them more recognizable to immune cells, and helps to initiate the membrane attack complex (MAC), which forms a pore in the cell membrane of pathogens leading to their lysis or destruction.

Abnormal levels of C3c may indicate an underlying inflammatory or immune-mediated condition, such as infection, autoimmune disease, or cancer.

Leukocytoclastic vasculitis, cutaneous is a type of vasculitis that is limited to the skin. Vasculitis refers to inflammation of the blood vessels, which can cause damage to the vessel walls and impair blood flow to various tissues in the body. In leukocytoclastic vasculitis, the small blood vessels (capillaries and venules) in the skin become inflamed, leading to damage and destruction of the vessel walls.

The term "leukocytoclastic" refers to the presence of nuclear debris from white blood cells (leukocytes) that have been destroyed within the affected blood vessels. This type of vasculitis is often associated with the deposition of immune complexes (formed by the interaction between antibodies and antigens) in the walls of the blood vessels, which triggers an inflammatory response.

Cutaneous leukocytoclastic vasculitis typically presents as palpable purpura (small to large, raised, purple or red spots on the skin), usually located on the lower extremities, but can also affect other areas of the body. Other symptoms may include burning or itching sensations in the affected area, and in some cases, ulcers or necrosis (tissue death) may occur.

The diagnosis of cutaneous leukocytoclastic vasculitis is typically made based on clinical presentation, laboratory tests, and histopathological examination of a skin biopsy specimen. Treatment usually involves addressing any underlying causes or triggers, as well as managing symptoms with medications such as corticosteroids or immunosuppressive agents.

The Bowman capsule is the initial component of the nephron, which is the functional unit of the kidney. It is a structural and functional part of the renal corpuscle, along with the glomerulus. The Bowman capsule surrounds the glomerulus and serves as a site for filtration, helping to separate small molecules from blood cells and large proteins in the process known as urine formation.

The Bowman capsule is composed of a single layer of epithelial cells called podocytes, which have foot-like processes that interdigitate with each other and form filtration slits. These slits are covered by a thin diaphragm, allowing for the passage of small molecules while retaining larger ones. The space within the Bowman capsule is called the urinary space or Bowman's space, where the filtrate from the blood collects before moving into the tubular system for further processing and eventual excretion as urine.

The alternative complement pathway is one of the three initiating pathways of the complement system, which is a part of the innate immune system that helps to clear pathogens and damaged cells from the body. The other two pathways are the classical and lectin pathways.

The alternative pathway is continuously activated at a low level, even in the absence of infection or injury, through the spontaneous cleavage of complement component C3 into C3a and C3b by the protease factor D in the presence of magnesium ions. The generated C3b can then bind covalently to nearby surfaces, including pathogens and host cells.

On self-surfaces, regulatory proteins like decay-accelerating factor (DAF) or complement receptor 1 (CR1) help to prevent the formation of the alternative pathway convertase and thus further activation of the complement system. However, on foreign surfaces, the C3b can recruit more complement components, forming a complex called the alternative pathway convertase (C3bBb), which cleaves additional C3 molecules into C3a and C3b.

The generated C3b can then bind to the surface and participate in the formation of the membrane attack complex (MAC), leading to the lysis of the target cell. The alternative pathway plays a crucial role in the defense against gram-negative bacteria, fungi, and parasites, as well as in the clearance of immune complexes and apoptotic cells. Dysregulation of the alternative complement pathway has been implicated in several diseases, including autoimmune disorders and atypical hemolytic uremic syndrome (aHUS).

Gamma-globulins are a type of protein found in the blood serum, specifically a class of immunoglobulins (antibodies) known as IgG. They are the most abundant type of antibody and provide long-term defense against bacterial and viral infections. Gamma-globulins can also be referred to as "gamma globulin" or "gamma immune globulins."

These proteins are produced by B cells, a type of white blood cell, in response to an antigen (a foreign substance that triggers an immune response). IgG gamma-globulins have the ability to cross the placenta and provide passive immunity to the fetus. They can be measured through various medical tests such as serum protein electrophoresis (SPEP) or immunoelectrophoresis, which are used to diagnose and monitor conditions related to immune system disorders, such as multiple myeloma or primary immunodeficiency diseases.

In addition, gamma-globulins can be administered therapeutically in the form of intravenous immunoglobulin (IVIG) to provide passive immunity for patients with immunodeficiencies, autoimmune disorders, or infectious diseases.

Monoclonal antibodies are a type of antibody that are identical because they are produced by a single clone of cells. They are laboratory-produced molecules that act like human antibodies in the immune system. They can be designed to attach to specific proteins found on the surface of cancer cells, making them useful for targeting and treating cancer. Monoclonal antibodies can also be used as a therapy for other diseases, such as autoimmune disorders and inflammatory conditions.

Monoclonal antibodies are produced by fusing a single type of immune cell, called a B cell, with a tumor cell to create a hybrid cell, or hybridoma. This hybrid cell is then able to replicate indefinitely, producing a large number of identical copies of the original antibody. These antibodies can be further modified and engineered to enhance their ability to bind to specific targets, increase their stability, and improve their effectiveness as therapeutic agents.

Monoclonal antibodies have several mechanisms of action in cancer therapy. They can directly kill cancer cells by binding to them and triggering an immune response. They can also block the signals that promote cancer growth and survival. Additionally, monoclonal antibodies can be used to deliver drugs or radiation directly to cancer cells, increasing the effectiveness of these treatments while minimizing their side effects on healthy tissues.

Monoclonal antibodies have become an important tool in modern medicine, with several approved for use in cancer therapy and other diseases. They are continuing to be studied and developed as a promising approach to treating a wide range of medical conditions.

Phospholipase A2 (PLA2) receptors are a group of proteins that are involved in the signaling pathways related to inflammation and immune response. PLA2 is an enzyme that cleaves phospholipids in cell membranes to produce arachidonic acid, which is a precursor for various eicosanoids, such as prostaglandins, leukotrienes, and thromboxanes, that play crucial roles in the inflammatory response.

There are two main types of PLA2 receptors: secreted PLA2 (sPLA2) receptors and intracellular PLA2 (iPLA2) receptors. The sPLA2 receptors are found on the cell surface and mediate the binding and internalization of sPLA2 enzymes, which are released from activated immune cells during inflammation. The iPLA2 receptors, on the other hand, are located inside the cell and regulate the intracellular levels of arachidonic acid and other lipid mediators.

Abnormal activation or regulation of PLA2 receptors has been implicated in various pathological conditions, including inflammatory diseases, neurodegenerative disorders, and cancer. Therefore, understanding the structure, function, and regulation of these receptors is important for developing new therapeutic strategies to target these diseases.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Chemokine (C-C motif) ligand 2, also known as monocyte chemoattractant protein-1 (MCP-1), is a small signaling protein that belongs to the chemokine family. Chemokines are a group of cytokines, or regulatory proteins, that play important roles in immune responses and inflammation by recruiting various immune cells to sites of infection or injury.

CCL2 specifically acts as a chemoattractant for monocytes, memory T cells, and dendritic cells, guiding them to migrate towards the source of infection or tissue damage. It does this by binding to its receptor, CCR2, which is expressed on the surface of these immune cells.

CCL2 has been implicated in several pathological conditions, including atherosclerosis, rheumatoid arthritis, and various cancers, where it contributes to the recruitment of immune cells that can exacerbate tissue damage or promote tumor growth and metastasis. Therefore, targeting CCL2 or its signaling pathways has emerged as a potential therapeutic strategy for these diseases.

Rheumatoid factor (RF) is an autoantibody, specifically an immunoglobulin M (IgM) antibody, that can be detected in the blood serum of some people with rheumatoid arthritis (RA), other inflammatory conditions, and infectious diseases. RF targets the Fc portion of IgG, leading to immune complex formation and subsequent inflammation, which contributes to the pathogenesis of RA. However, not all patients with RA test positive for RF, and its presence does not necessarily confirm a diagnosis of RA. Other conditions can also lead to elevated RF levels, such as infections, liver diseases, and certain malignancies. Therefore, the interpretation of RF results should be considered alongside other clinical, laboratory, and imaging findings for an accurate diagnosis and appropriate management.

A chronic disease is a long-term medical condition that often progresses slowly over a period of years and requires ongoing management and care. These diseases are typically not fully curable, but symptoms can be managed to improve quality of life. Common chronic diseases include heart disease, stroke, cancer, diabetes, arthritis, and COPD (chronic obstructive pulmonary disease). They are often associated with advanced age, although they can also affect children and younger adults. Chronic diseases can have significant impacts on individuals' physical, emotional, and social well-being, as well as on healthcare systems and society at large.

Antibody formation, also known as humoral immune response, is the process by which the immune system produces proteins called antibodies in response to the presence of a foreign substance (antigen) in the body. This process involves several steps:

1. Recognition: The antigen is recognized and bound by a type of white blood cell called a B lymphocyte or B cell, which then becomes activated.
2. Differentiation: The activated B cell undergoes differentiation to become a plasma cell, which is a type of cell that produces and secretes large amounts of antibodies.
3. Antibody production: The plasma cells produce and release antibodies, which are proteins made up of four polypeptide chains (two heavy chains and two light chains) arranged in a Y-shape. Each antibody has two binding sites that can recognize and bind to specific regions on the antigen called epitopes.
4. Neutralization or elimination: The antibodies bind to the antigens, neutralizing them or marking them for destruction by other immune cells. This helps to prevent the spread of infection and protect the body from harmful substances.

Antibody formation is an important part of the adaptive immune response, which allows the body to specifically recognize and respond to a wide variety of pathogens and foreign substances.

Methylprednisolone is a synthetic glucocorticoid drug, which is a class of hormones that naturally occur in the body and are produced by the adrenal gland. It is often used to treat various medical conditions such as inflammation, allergies, and autoimmune disorders. Methylprednisolone works by reducing the activity of the immune system, which helps to reduce symptoms such as swelling, pain, and redness.

Methylprednisolone is available in several forms, including tablets, oral suspension, and injectable solutions. It may be used for short-term or long-term treatment, depending on the condition being treated. Common side effects of methylprednisolone include increased appetite, weight gain, insomnia, mood changes, and increased susceptibility to infections. Long-term use of methylprednisolone can lead to more serious side effects such as osteoporosis, cataracts, and adrenal suppression.

It is important to note that methylprednisolone should be used under the close supervision of a healthcare provider, as it can cause serious side effects if not used properly. The dosage and duration of treatment will depend on various factors such as the patient's age, weight, medical history, and the condition being treated.

Blood protein disorders refer to a group of medical conditions that affect the production or function of proteins in the blood. These proteins are crucial for maintaining the proper functioning of the body's immune system, transporting nutrients, and preventing excessive bleeding. Some examples of blood protein disorders include:

1. Hemophilia: A genetic disorder caused by a deficiency or absence of clotting factors in the blood, leading to prolonged bleeding and poor clot formation.
2. Von Willebrand disease: A genetic disorder characterized by abnormal or deficient von Willebrand factor, which is necessary for platelet function and proper clotting.
3. Dysproteinemias: Abnormal levels of certain proteins in the blood, such as immunoglobulins (antibodies) or paraproteins, which can indicate underlying conditions like multiple myeloma or macroglobulinemia.
4. Hypoproteinemia: Low levels of total protein in the blood, often caused by liver disease, malnutrition, or kidney disease.
5. Hyperproteinemia: Elevated levels of total protein in the blood, which can be caused by dehydration, inflammation, or certain types of cancer.
6. Hemoglobinopathies: Genetic disorders affecting the structure and function of hemoglobin, a protein found in red blood cells that carries oxygen throughout the body. Examples include sickle cell anemia and thalassemia.
7. Disorders of complement proteins: Abnormalities in the complement system, which is a group of proteins involved in the immune response, can lead to conditions like autoimmune disorders or recurrent infections.

Treatment for blood protein disorders varies depending on the specific condition and its severity but may include medications, transfusions, or other medical interventions.

Renal insufficiency, also known as kidney failure, is a medical condition in which the kidneys are unable to properly filter waste products and excess fluids from the blood. This results in a buildup of these substances in the body, which can cause a variety of symptoms such as weakness, shortness of breath, and fluid retention. Renal insufficiency can be acute, meaning it comes on suddenly, or chronic, meaning it develops over time. It is typically diagnosed through blood tests, urine tests, and imaging studies. Treatment may include medications to control symptoms, dietary changes, and in severe cases, dialysis or a kidney transplant.

Immunoelectrophoresis (IEP) is a laboratory technique used in the field of clinical pathology and immunology. It is a method for separating and identifying proteins, particularly immunoglobulins or antibodies, in a sample. This technique combines the principles of electrophoresis, which separates proteins based on their electric charge and size, with immunological reactions, which detect specific proteins using antigen-antibody interactions.

In IEP, a protein sample is first separated by electrophoresis in an agarose or agar gel matrix on a glass slide or in a test tube. After separation, an antibody specific to the protein of interest is layered on top of the gel and allowed to diffuse towards the separated proteins. This creates a reaction between the antigen (protein) and the antibody, forming a visible precipitate at the point where they meet. The precipitate line's position and intensity can then be analyzed to identify and quantify the protein of interest.

Immunoelectrophoresis is particularly useful in diagnosing various medical conditions, such as immunodeficiency disorders, monoclonal gammopathies (like multiple myeloma), and other plasma cell dyscrasias. It can help detect abnormal protein patterns, quantify specific immunoglobulins, and identify the presence of M-proteins or Bence Jones proteins, which are indicative of monoclonal gammopathies.

Albuminuria is a medical condition that refers to the presence of albumin in the urine. Albumin is a type of protein normally found in the blood, but not in the urine. When the kidneys are functioning properly, they prevent large proteins like albumin from passing through into the urine. However, when the kidneys are damaged or not working correctly, such as in nephrotic syndrome or other kidney diseases, small amounts of albumin can leak into the urine.

The amount of albumin in the urine is often measured in milligrams per liter (mg/L) or in a spot urine sample, as the albumin-to-creatinine ratio (ACR). A small amount of albumin in the urine is called microalbuminuria, while a larger amount is called macroalbuminuria or proteinuria. The presence of albuminuria can indicate kidney damage and may be a sign of underlying medical conditions such as diabetes or high blood pressure. It is important to monitor and manage albuminuria to prevent further kidney damage and potential complications.

'Immune sera' refers to the serum fraction of blood that contains antibodies produced in response to an antigenic stimulus, such as a vaccine or an infection. These antibodies are proteins known as immunoglobulins, which are secreted by B cells (a type of white blood cell) and can recognize and bind to specific antigens. Immune sera can be collected from an immunized individual and used as a source of passive immunity to protect against infection or disease. It is often used in research and diagnostic settings to identify or measure the presence of specific antigens or antibodies.

The spleen is an organ in the upper left side of the abdomen, next to the stomach and behind the ribs. It plays multiple supporting roles in the body:

1. It fights infection by acting as a filter for the blood. Old red blood cells are recycled in the spleen, and platelets and white blood cells are stored there.
2. The spleen also helps to control the amount of blood in the body by removing excess red blood cells and storing platelets.
3. It has an important role in immune function, producing antibodies and removing microorganisms and damaged red blood cells from the bloodstream.

The spleen can be removed without causing any significant problems, as other organs take over its functions. This is known as a splenectomy and may be necessary if the spleen is damaged or diseased.

Acute kidney injury (AKI), also known as acute renal failure, is a rapid loss of kidney function that occurs over a few hours or days. It is defined as an increase in the serum creatinine level by 0.3 mg/dL within 48 hours or an increase in the creatinine level to more than 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days, or a urine volume of less than 0.5 mL/kg per hour for six hours.

AKI can be caused by a variety of conditions, including decreased blood flow to the kidneys, obstruction of the urinary tract, exposure to toxic substances, and certain medications. Symptoms of AKI may include decreased urine output, fluid retention, electrolyte imbalances, and metabolic acidosis. Treatment typically involves addressing the underlying cause of the injury and providing supportive care, such as dialysis, to help maintain kidney function until the injury resolves.

Cyclophosphamide is an alkylating agent, which is a type of chemotherapy medication. It works by interfering with the DNA of cancer cells, preventing them from dividing and growing. This helps to stop the spread of cancer in the body. Cyclophosphamide is used to treat various types of cancer, including lymphoma, leukemia, multiple myeloma, and breast cancer. It can be given orally as a tablet or intravenously as an injection.

Cyclophosphamide can also have immunosuppressive effects, which means it can suppress the activity of the immune system. This makes it useful in treating certain autoimmune diseases, such as rheumatoid arthritis and lupus. However, this immunosuppression can also increase the risk of infections and other side effects.

Like all chemotherapy medications, cyclophosphamide can cause a range of side effects, including nausea, vomiting, hair loss, fatigue, and increased susceptibility to infections. It is important for patients receiving cyclophosphamide to be closely monitored by their healthcare team to manage these side effects and ensure the medication is working effectively.

Myeloblastin is not typically used as a medical term in current literature. However, in the field of hematology, "myeloblast" refers to an immature cell that develops into a white blood cell called a granulocyte. These myeloblasts are normally found in the bone marrow and are part of the body's immune system.

If you meant 'Myeloperoxidase,' I can provide a definition for it:

Myeloperoxidase (MPO) is a peroxidase enzyme that is abundant in neutrophil granulocytes, a type of white blood cell involved in the immune response. MPO plays an essential role in the microbicidal activity of these cells by generating hypochlorous acid and other reactive oxygen species to kill invading pathogens.

Nephrosis is an older term that was used to describe a group of kidney diseases, primarily characterized by the damage and loss of function in the glomeruli - the tiny filtering units within the kidneys. This results in the leakage of large amounts of protein (primarily albumin) into the urine, a condition known as proteinuria.

The term "nephrosis" was often used interchangeably with "minimal change nephropathy," which is a specific type of kidney disorder that demonstrates little to no changes in the glomeruli under a microscope, despite significant protein leakage. However, current medical terminology and classifications prefer the use of more precise terms to describe various kidney diseases, such as minimal change disease, focal segmental glomerulosclerosis, or membranous nephropathy, among others.

It is important to consult with a healthcare professional or refer to updated medical resources for accurate and current information regarding kidney diseases and their specific diagnoses.

Immunoglobulins, also known as antibodies, are proteins produced by the immune system to recognize and neutralize foreign substances like pathogens or antigens. The term "immunoglobulin isotypes" refers to the different classes of immunoglobulins that share a similar structure but have distinct functions and properties.

There are five main isotypes of immunoglobulins in humans, namely IgA, IgD, IgE, IgG, and IgM. Each isotype has a unique heavy chain constant region (CH) that determines its effector functions, such as binding to Fc receptors, complement activation, or protection against pathogens.

IgA is primarily found in external secretions like tears, saliva, and breast milk, providing localized immunity at mucosal surfaces. IgD is expressed on the surface of B cells and plays a role in their activation and differentiation. IgE is associated with allergic responses and binds to mast cells and basophils, triggering the release of histamine and other mediators of inflammation.

IgG is the most abundant isotype in serum and has several subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their effector functions. IgG can cross the placenta, providing passive immunity to the fetus. IgM is the first antibody produced during an immune response and is primarily found in the bloodstream, where it forms large pentameric complexes that are effective at agglutination and complement activation.

Overall, immunoglobulin isotypes play a crucial role in the adaptive immune response, providing specific and diverse mechanisms for recognizing and neutralizing foreign substances.

Neutrophils are a type of white blood cell that are part of the immune system's response to infection. They are produced in the bone marrow and released into the bloodstream where they circulate and are able to move quickly to sites of infection or inflammation in the body. Neutrophils are capable of engulfing and destroying bacteria, viruses, and other foreign substances through a process called phagocytosis. They are also involved in the release of inflammatory mediators, which can contribute to tissue damage in some cases. Neutrophils are characterized by the presence of granules in their cytoplasm, which contain enzymes and other proteins that help them carry out their immune functions.

... is the most common glomerulonephritis worldwide; the global incidence is 2.5/100,000 per year amongst adults. ... IgA nephropathy (IgAN), also known as Berger's disease (/bɛərˈʒeɪ/) (and variations), or synpharyngitic glomerulonephritis, is ... D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy". Q J Med. 64 (245): 709-27. PMID 3329736. C ... Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus. There are other diseases ...
IgA nephropathy is the most common glomerulonephritis throughout the world Primary IgA nephropathy is characterized by ... D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy". Q J Med. 64 (245): 709-727. PMID 3329736. ... All of these infections have in common the activation of mucosal defenses and hence IgA antibody production. Kidney disease ... as opposed to post-streptococcal glomerulonephritis which occurs some time (weeks) after initial infection. Less commonly ...
Glomerular diseases include diabetic nephropathy, glomerulonephritis and IgA nephropathy; renal tubular diseases include acute ... Glomerular diseases include diabetic nephropathy, glomerulonephritis and IgA nephropathy; renal tubular diseases include acute ...
Idiopathic mesangial proliferative glomerulonephritis does not involve the deposition of either IgA or IgG immune complexes, ... IgA nephropathy is the most common cause of MesPGN. It is thought abnormally glycosylated IgA form polymers and deposit in the ... Subsequently, IgA immune complexes bind to IgA receptors on mesangial cells and induce injury to mesangial cells through ... Most glomerulonephritis' classification and prognosis are aided by histological evaluation by renal biopsy. The renal biopsy is ...
June 2009). "Pauci-immune crescentic glomerulonephritis associated with ANCA of IgA class". Am. J. Kidney Dis. 53 (6): 1063-7. ... Systemic vasculitis#Pauci-immune Goodpasture Syndrome and Poststrep Glomerulonephritis Microscopic polyangiitis, Eosinophilic ... post-streptococcal glomerulonephritis (granular), and diffuse proliferative nephritis (granular). The negative ...
The other commonly associated disease is Immunoglobulin A (IgA) nephropathy. Post-infectious glomerulonephritis can also be ... Diffuse proliferative glomerulonephritis (DPGN) is a type of glomerulonephritis that is the most serious form of renal lesions ... "Glomerulonephritis - Symptoms and causes". Mayo Clinic. Retrieved 2020-12-16. "Diffuse Proliferative Glomerulonephritis: ... If a patient has DPGN, that means they have an active form of glomerulonephritis. Treatment of DPGN depends on the severity of ...
Nephritic syndrome: IgA nephropathy, Post-streptococcal glomerulonephritis, Benign familial hematuria, Alport syndrome. Sickle ... Glomerular causes include: IgA nephropathy Thin glomerular basement membrane disease Hereditary nephritis (Alport's disease) ... Membranoproliferative glomerulonephritis Lupus nephritis Henoch-Shonlein purpura Nephritic syndrome Nephrotic syndrome ... can cause a person to get a very specific manifestation known as post-streptococcal glomerulonephritis. This manifestation ...
"The long pentraxin PTX3 is synthesized in IgA glomerulonephritis and activates mesangial cells". Journal of Immunology. 170 (3 ...
Glomerular diseases include diabetic kidney disease, glomerulonephritis (inflammation), glomerulosclerosis (hardening of the ... glomeruli), and IgA nephropathy. Due to the connection between the glomerulus and the glomerular filtration rate, the ...
Other abnormalities that are found include glomerulosclerosis, IgA nephropathy and interstitial nephritis. Immunofluorescence ... that is followed by focal and segmental necrotizing glomerulonephritis with crescents. ...
Membranoproliferative glomerulonephritis (MPGN) - Another type of glomerulonephritis that is caused primarily by immune complex ... Davin, J. C.; Ten Berge, I. J.; Weening, J. J. (March 2001). "What is the difference between IgA nephropathy and Henoch- ... It often occurs in the glomerulus, where it is called glomerulonephritis. Glomerulonephritis is characterized by inflammation ... "Acute Poststreptococcal Glomerulonephritis: Background, Pathophysiology, Epidemiology". 2018-12-05. {{cite journal}}: Cite ...
... post-infective glomerulonephritis, IgA nephropathy, and IgA vasculitis.: 558 Type 3 rapidly progressive glomerulonephritis, ... Nephritic syndrome Nephritis Lupus nephritis Rapidly progressive glomerulonephritis "glomerulonephritis" at Dorland's Medical ... This form of glomerulonephritis may be associated with conditions such as HIV and heroin abuse, or inherited as Alport syndrome ... Glomerulonephritis (GN) is a term used to refer to several kidney diseases (usually affecting both kidneys). Many of the ...
... poststreptococcal glomerulonephritis, rheumatoid arthritis, and systemic sclerosis. Less common causes also include IgA ... glomerulonephritis) occur. PRS is associated with a high rate of morbidity and death. The term was first used by Goodpasture in ...
... and IgA nephropathy-that involves the glomerulus may progress to RPGN if severe enough. Also known as pauci-immune RPGN, type ... Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of kidney ... "Orphanet: Rapidly progressive glomerulonephritis". www.orpha.net. Retrieved 31 July 2019. Cotran, Ramzi S.; Kumar, Vinay; ... "Rapidly Progressive Glomerulonephritis: Background, Pathophysiology, Epidemiology". 2018-04-05. Morita T, Suzuki Y, Churg J ( ...
Coeliac disease is associated with immune complex glomerulonephritis. Anti-gliadin IgA antibodies are found also more commonly ... "Increased Prevalence of Anti-Gliadin IgA-Antibodies with Aberrant Duodenal Histopathological Findings in Patients with IgA- ... In GSE, it appears to be associated with the IgA-less phenotype. Unlike other forms of megaloblastic anemia, GSEA MA is not a ... While GI disease is one of the major symptoms of GSE that are characterized by increased levels of IgA/IgG to food proteins, ...
... glomerulonephritis, iga MeSH C12.777.419.570.363.615 - glomerulonephritis, membranoproliferative MeSH C12.777.419.570.363.625 ... glomerulonephritis MeSH C12.777.419.570.363.304 - anti-glomerular basement membrane disease MeSH C12.777.419.570.363.304.300 - ... glomerulonephritis, membranous MeSH C12.777.419.570.363.640 - glomerulosclerosis, focal MeSH C12.777.419.570.363.680 - lupus ...
1985 State Science and Technology Progress Award (Third Class) for the study on diagnosis and treatment of glomerulonephritis ... for the study on immunopathogenesis of IgA nephritis 1991 State Science and Technology Progress Award (Second Class) for the ...
IgA nephropathy (i.e. Berger's disease) IgM nephropathy Membranoproliferative glomerulonephritis Membranous nephropathy Minimal ... such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease (lipoid nephrosis) Strenuous ... Sjögren syndrome Post-infectious glomerulonephritis Living kidney donor Polycystic kidney disease Amyloidosis Pre-malignant ...
Causes of acute glomerulonephritis: IgA nephropathy Lupus nephritis Type 1 membranoproliferative glomerulonephritis Bacterial ... Acute proliferative glomerulonephritis (post-streptococcal glomerulonephritis) is caused by an infection with streptococcus ... for which it is also known as postinfectious glomerulonephritis (PIGN) or poststreptococcal glomerulonephritis (PSGN). It can ... and the terms infection-related glomerulonephritis or bacterial infection-related glomerulonephritis are also used. Acute ...
Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the ... Berthoux FC, Mohey H, Afiani A (January 2008). "Natural history of primary IgA nephropathy". Seminars in Nephrology. 28 (1): 4- ... "Hereditary and acquired complement dysregulation in membranoproliferative glomerulonephritis". Thrombosis and Haemostasis. 101 ...
While the glomerulonephritis occurring in mixed disease appears to be due to inflammatory vasculitis, the glomerulonephritis ... Monoclonal IgG or, rarely, IgA, κ light chain, or λ light chain cryoglobulins occur in cases of multiple myeloma and the pre- ... Mixtures of monoclonal or polyclonal IgM, IgG, and/or IgA along with blood complement proteins such as C4 are the cryoglobulins ... IgA antibodies, monoclonal κ, or λ free light chain portions of these antibodies, and proteins of the blood complement system, ...
IgA, IgE, IgE, or IgM; b) intact IgG, IgA, IgE, IgD, or IgM plus high concentrations of a free (i.e. not bound to a heavy chain ... selectively in the kidneys glomeruli to cause various forms of organized deposit and non-organized deposit glomerulonephritis ... For example, the IgA form of MGUS, while once considered to have a poorer prognosis than IgG MGUS, was found to have a ... Antibodies are classified as IgG, IgA, IgE, IgD, and IgM based on their being made up of γ, α, ε, δ, or μ heavy chains, ...
Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. Risk ... Primary glomerular disease such as focal segmental glomerulosclerosis and IgA nephropathy (or nephritis) Secondary glomerular ... and glomerulonephritis. About one of five adults with hypertension and one of three adults with diabetes have CKD. If the cause ... and glomerulonephritis at 238,000. CKD is initially without symptoms, and is usually detected on routine screening blood work ...
It is considered a form of hypersensitivity vasculitis but is distinguished by prominent deposits of IgA. This is the most ... Produces granulomatous inflammation of the respiratory tracts and necrotizing, pauci-immune glomerulonephritis. Most common ... Systemic vasculitis due to tissue deposition of IgA-containing immune complexes. Biopsy of lesions shows inflammation of small ... triggering drug in relation to symptoms Palpable purpura Maculopapular rash Skin biopsy showing neutrophils around vessel IgA ...
"Multiparametric Quantitative MRI for the Detection of IgA Nephropathy Using Tomoelastography, DWI, and BOLD Imaging". ... "Evaluation of renal fibrosis in various causes of glomerulonephritis by MR elastography: a clinicopathologic comparative ...
Post-streptococcal glomerulonephritis (PSGN) is an uncommon complication of either a strep throat or a streptococcal skin ... Despite the emergence of antibiotics as a treatment for group A streptococcus, cases of iGAS are an increasing problem, ... Post-streptococcal glomerulonephritis Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections ... iGAS). Infection of GAS may spread through direct contact with mucus or sores on the skin. GAS infections can cause over ...
"An investigation into asymmetrical cortical regulation of salivary S-IgA in conscious man using transcranial magnetic ... "Autonomic Renal Denervation Ameliorates Experimental Glomerulonephritis". Journal of the American Society of Nephrology. 19 (7 ...
Poststreptococcal glomerulonephritis: This is inflammation of the kidney, which presents 1-2 weeks after a group A ... The World Health Organization has reported an increase in scarlet fever (and iGAS - invasive GAS cases) in England, and other ... Antibiotic therapy has not been shown to prevent the development of post-streptococcal glomerulonephritis. Another important ... fever that are complicated by the immune-mediated sequelae of acute rheumatic fever and post-streptococcal glomerulonephritis. ...
IgA) IgA1 IgA2 Immunoglobulin D (IgD) Immunoglobulin E (IgE) Immunoglobulin G (IgG) IgG1 IgG2 IgG3 IgG4 Immunoglobulin M (IgM) ... Henoch-Schönlein purpura Hypersensitivity vasculitis Reactive arthritis Farmer's lung Post-streptococcal glomerulonephritis ...
In a similar manner, Sirolimus prevents B cell differentiation into plasma cells, reducing production of IgM, IgG, and IgA ... Later during the treatment, some patients develop serum sickness or immune complex glomerulonephritis. Serum sickness arises ...
The SOP previously called mesangial IgA glomerulonephritis has been renamed.See the SOP information page for IgA nephropathy ...
Compared to patients with non-IgA-dominant PIGN, increased serum IgA was more commonly present in IgA-dominant group (p = 0.007 ... BACKGROUND: IgA-dominant postinfectious glomerulonephritis (PIGN) is a unique form of PIGN. It has been linked to ... IgA-dominant postinfectious glomerulonephritis: not peculiar to staphylococcal infection and diabetic patients.. Yao-Ko Wen, ... CONCLUSIONS: IgA-dominant PIGN resembles poststreptococcal glomerulonephritis in its histological spectrum and ultrastructural ...
... is a term used to describe a distinct histologic form of glomerulonephritis common to various types of systemic inflammatory ... Renal survival is best with IgA nephropathy, which has an indolent course with a favorable outcome. Death due to DPGN in IgA ... Diffuse proliferative glomerulonephritis (DPGN) is a term used to describe a distinct histologic form of glomerulonephritis ... encoded search term (Diffuse Proliferative Glomerulonephritis) and Diffuse Proliferative Glomerulonephritis What to Read Next ...
Membranous Glomerulonephritis * Fast Five Quiz: IgA Nephropathy Presentation and Diagnosis * HIV-Associated Nephropathy and ... mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis, membranous glomerulonephritis) is ... KDIGO Clinical Practice Guideline for Glomerulonephritis (GN). Kidney Int. June 2012. 2 suppl 2:[Full Text]. ... Although hematuria is the most common presentation in Whites with IgA nephropathy, nephrotic syndrome and renal insufficiency ...
Abbreviations: Gal-3, Galectin-3; CKD, chronic kidney disease; MCD, minimal change disease; MGN, membranous glomerulonephritis ... IgA, immunoglobulin A; DM, diabetes mellitus. ... glomerulonephritis or other pathological findings in kidney ... Abbreviations: Gal-3, Galectin-3; CKD, chronic kidney disease; MCD, minimal change disease; MGN, membranous glomerulonephritis ...
IgA nephropathy is the most common glomerulonephritis worldwide; the global incidence is 2.5/100,000 per year amongst adults. ... IgA nephropathy (IgAN), also known as Bergers disease (/bɛərˈʒeɪ/) (and variations), or synpharyngitic glomerulonephritis, is ... DAmico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy". Q J Med. 64 (245): 709-27. PMID 3329736. C ... Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus. There are other diseases ...
Glomerulonephritis. *Granulomatosis with polyangiitis (GPA). *IgA nephropathy, Hennoch Schoenlein purpura. *Lupus. *Lupus ... Mass General Vasculitis & Glomerulonephritis Center. 101 Merrimac St.. 1st Floor. Boston, MA 02114 Phone: 617-726-4132. ... Vasculitis and glomerulonephritis. Dr. Niles was the first to identify the C-ANCA protein, has developed assays for ANCA and ...
The same was true for the incidence of IgA nephropathy, lupus nephritis and pauci-immune glomerulonephritis. In contrast, we ... The most common primary glomerulonephritis was IgA nephropathy at 32.7% of cases, followed by lupus nephritis (29.8%) and pauci ... the mean incidence of glomerulonephritis was 1.3/100,000/year. Between 2007 and 2016, the incidence of all glomerulonephritis ... Incidence of glomerulonephritis in the western part of Switzerland over the last decade *Giliane Nanchen+− ...
A Rare Case of Proliferative Glomerulonephritis with Monoclonal IgA Lambda Deposits with Crescents. 10:00 AM - 12:00 PM. ... A Rare Case of Proliferative Glomerulonephritis with Monoclonal IgA Lambda Deposits with Crescents. November 04, 2023 , 10:00 ... Proliferative Glomerulonephritis with Monoclonal IgG Deposits: A Mysterious Renal Disorder. 10:00 AM - 12:00 PM. ... Cryoglobulinemic Glomerulonephritis in the Setting of Chronic Lymphocytic Leukemia. 10:00 AM - 12:00 PM. ...
DAmico G. The commonest glomerulonephritis in the world: IgA nephropathy. Q J Med. 1987 Sep. 64(245):709-27. [QxMD MEDLINE ... IgA nephropathy: perspectives on pathogenesis and classification. Clin Nephrol. 1985 Oct. 24(4):161-79. [QxMD MEDLINE Link]. ... Mittal A, Dijoo M, Sabhikhi A, Gulati S. Henoch Schönlein purpura nephritis developing in a child with known IgA nephropathy. ... Mesangiocapillary glomerulonephritis. Glomerular lobulations, thickening of the mesangial matrix and glomerular basement ...
IgA glomerulonephritis disease_progression. ISO. RGD:736732. 7207366. DNA:SNPs:3 utr:2093C>T, 2180C>T (human). RGD. ... IgA glomerulonephritis ISO. RGD:736732. 7207380. DNA:SNP:5 utr, exon:267G>A (human). RGD. ... IgA glomerulonephritis disease_progression. ISO. RGD:736732. 7207372. DNA:SNP: :23167A>G (human). RGD. ... Human ortholog(s) of this gene implicated in IgA glomerulonephritis and familial encephalopathy with neuroserpin inclusion ...
Glomerulonephritis is a type of kidney disease in which the part of your kidneys that helps filter waste and fluids from the ... Glomerulonephritis is a type of kidney disease in which the part of your kidneys that helps filter waste and fluids from the ... IgA nephropathy (disorder in which antibodies called IgA build up in kidney tissue) ... Glomerulonephritis - chronic; Chronic nephritis; Glomerular disease; Necrotizing glomerulonephritis; Glomerulonephritis - ...
IgA glomerulonephritis; Tetrahydrofuran; THF; Solvents; Occupational kidney disease; Plumbing hazards ... A case was described of a 28 year old plumber who suffered from gross hematuria and segmental proliferative glomerulonephritis ...
Acute poststreptococcal glomerulonephritis (PSGN) is the archetype of acute GN. ... Acute glomerulonephritis (GN) comprises a specific set of renal diseases in which an immunologic mechanism triggers ... Immune complex-mediated glomerulonephritis (eg, lupus nephritis, IgA nephropathy, PSGN, fibrillary glomerulonephritis) ... encoded search term (Acute Glomerulonephritis) and Acute Glomerulonephritis What to Read Next on Medscape ...
Glomerulonephritis(2). * Iga Nephropathy (bergers Disease) (2) * Renal Failure(2). * Acute Renal Failure (arf) (acute Kidney ...
About IgA nephropathy (IgAN). IgAN is a progressive, rare kidney disease that mostly affects young adults5. It is estimated ... The incidence of primary glomerulonephritis worldwide: a systematic review of the literature. Nephrol Dial Transplant. 2011;26( ... Predicting Progression of IgA Nephropathy: New Clinical Progression Risk Score. Moura IC, ed. PLoS ONE. 2012;7(6):e38904. doi: ... In IgAN, autoimmune reaction to an abnormal form of IgA results in formation of immune complexes that deposit in the kidney5,7, ...
Glomerulonephritis.. *IgA Nephropathy.. *Lupus Nephritis.. *Polycystic Kidney Disease.. *Rare diseases.. Autoimmune diseases:. ...
Interleukin-33 Exacerbates IgA Glomerulonephritis in Transgenic Mice Overexpressing B Cell Activating Factor ... including IgA. BAFF-transgenic mice overexpress BAFF and... ...
Evaluation of the Modified Oxford Score in Recurrent IgA Nephropathy in North American Kidney Transplant Recipients: The Banff ... Recurrent Glomerulonephritis Working Group Report. Alachkar, Nada; Delsante, Marco; Greenberg, Ross S.; More ... Evaluation of the Modified Oxford Score in Recurrent IgA Nephropathy in North American Kidney Transplant Recipients: The Banff ... Recurrent Glomerulonephritis Working Group Report. *Surgical Treatment of Hepatocellular Carcinoma: Multicenter Competing-risk ...
Yuenting Diana Kwong, MD, is a nephrologist practicing at UCSF Health. Learn more about Dr. Kwongs specialties and training.
Development of IgA vasculitis with severe glomerulonephritis after COVID-19 vaccination: a case report and literature review. ...
... and management of IgA nephropathy. Looking for the latest on clinical trials and approved treatments? Tune in! ... For crescentic disease, if you have clinical evidence of rapidly progressive glomerulonephritis (RPGN), for example, youre ... Rizk: We think that IgA vasculitis is on the same spectrum as IgA nephropathy. It is a disease that presents, typically, again ... This is referred to as galactose-deficient IgA, and its essentially an IgA molecule thats lacking the right number of ...
GlycosylationIgA glomerulonephritisKidneys--DiseasesMolecular biologyBiochemistryMedicine 2. Genetic Variants Within The ...
Glomerulonephritis. Glomerulosclerosis. Goodpasture Syndrome. Hemolytic Uremic Syndrome. Immunoglobulin A (IgA) Syndrome. ...
The Committee on IgA nephropathy in Japan has published new clinical guidelines(2nd edition) for the diagnosis and treatment of ... This disorder, considered to be an immune-complex-mediated glomerulonephritis, is characterized by granular deposition of IgA ( ... IgA Nephropathy with Poorly Developed Lymphoepithelial Symbiosis of the Palatine Tonsils Cohort Study of Advanced IgA ... International IgA Nephropathy Network Clinico-Pathological Classification of IgA Nephropathy Clinical Manifestations and ...
IgA Nephropathy and focal segmental glomerulosclerosis. ... as well as within the Glomerulonephritis and Vasculitis Clinic. ... Glomerulonephritis Fellowship The University of North Carolina (UNC) Division of Nephrology and the UNC Kidney Center offer a ... The GN Fellow may participate ongoing clinical studies in vasculitis and glomerulonephritis at the UNC Kidney Center. The UNC ... Koyal Jain, Program Director, Glomerulonephritis and Vasculitis Fellowship ([email protected]). Please copy Ms. Rochelle ...
... biopsy was performed and the presence of IgA deposits and cellular crescents indicated rapidly progressive glomerulonephritis ...
... but not to IgA. Staining for immunoglobulins was not observed in kidney sections of an age-matched control that died due to ... Glomerulonephritis and Cardiovascular Disease in the Pygmy Marmoset (Callithrix pygmaea) American Association of Zoo ... This study characterizes a specific type of glomerulonephritis in the pygmy marmoset (Callithrix pygmaea), which can progress ... Although specific antigenic causes initiating glomerulonephritis were not determined in these pygmy marmosets, MPGN in humans ...
Many patients have increased IgE and IgA, with low IgM. T cell numbers and function decline with age. There is an increased ... incidence of autoimmune manifestations (vasculitis, hemolytic anemia, glomerulonephritis) and tumors (leukemia, lymphoma, EBV- ...
  • Although hematuria is the most common presentation in Whites with IgA nephropathy, nephrotic syndrome and renal insufficiency may also be present. (medscape.com)
  • Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus. (wikipedia.org)
  • There are other diseases associated with glomerular IgA deposits, the most common being IgA vasculitis (formerly known as Henoch-Schönlein purpura [HSP]), which is considered by many to be a systemic form of IgA nephropathy. (wikipedia.org)
  • HSP is associated with a more benign prognosis than IgA nephropathy. (wikipedia.org)
  • In non-aggressive IgA nephropathy there is traditionally a slow progression to chronic kidney failure in 25-30% of cases during a period of 20 years. (wikipedia.org)
  • citation needed] Histologically, IgA nephropathy may show mesangial widening and focal and segmental inflammation. (wikipedia.org)
  • In terms of the renal manifestation of Henoch-Schönlein purpura, it has been found that although it shares the same histological spectrum as IgA nephropathy, a greater frequency of severe lesions such as glomerular necrosis and crescents were observed. (wikipedia.org)
  • The same was true for the incidence of IgA nephropathy, lupus nephritis and pauci-immune glomerulonephritis. (smw.ch)
  • In addition, normal complement levels suggest kidney diseases such as immune complex disease, idiopathic rapidly progressive glomerulonephritis, and immunoglobulin G (IgG) or immunoglobulin A (IgA) nephropathy. (medscape.com)
  • Basel, October 30, 2023 - Novartis today announced positive topline results from the interim analysis of the ongoing pivotal Phase III ALIGN study (NCT04573478) of atrasentan, an oral endothelin A receptor antagonist (ERA), in patients with IgA nephropathy (IgAN) 1 . (novartis.com)
  • S2 Episode 3: Does Your Patient Have IgA Nephropathy? (medscape.com)
  • Today, we'll be discussing immunoglobulin A (IgA) nephropathy with my guest, Dr Dana Rizk. (medscape.com)
  • The first thing I want to know is how does someone become interested in studying IgA nephropathy? (medscape.com)
  • And when I moved to the UAB, I had the fortune of meeting Dr Bruce Julian, who was a colleague of mine and a world authority in IgA nephropathy. (medscape.com)
  • IgA nephropathy to me is very fascinating, and I would like to know what is the pathogenesis? (medscape.com)
  • Why do people get IgA nephropathy? (medscape.com)
  • We have come a long way understanding how IgA nephropathy develops. (medscape.com)
  • Not everybody, of course, is going to develop IgA nephropathy. (medscape.com)
  • Primary IgA nephropathy has first been described as a new disease entity almost 40 years ago. (karger.com)
  • This disorder, considered to be an immune-complex-mediated glomerulonephritis, is characterized by granular deposition of IgA (mainly IgA1) and C3 in the glomerular mesangial areas and is defined as nephropathy showing proliferative changes in the glomerular mesangial cells and increases in the mesangial matrices. (karger.com)
  • In this publication, international nephrologists and basic scientists report the most recent data on IgA nephropathy. (karger.com)
  • The UNC Kidney Center is currently participating in several clinical studies in ANCA-associated vasculitis, lupus nephritis, IgA Nephropathy and focal segmental glomerulosclerosis. (unc.edu)
  • In contrast, no significant association was demonstrated for either IgA nephropathy or membranous nephropathy. (newswise.com)
  • Anthera Pharmaceuticals is a biopharmaceutical company focused on developing and commercializing products to treat serious and life-threatening diseases, including lupus, lupus with glomerulonephritis, IgA nephropathy, and exocrine pancreatic insufficiency due to cystic fibrosis. (globenewswire.com)
  • ABSTRACTImmunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. (journaltocs.ac.uk)
  • IgA nephropathy: IgA is an antibody produced to fight infections. (nkfs.org)
  • Histopathological diagnoses were focal segmental glomerulosclerosis (8), mesangial proliferative glomerulonephritis (4), IgM nephropathy (3), and minimal change disease (1). (nephcure.org)
  • Dr. Jennette's clinical and clinicopathologic studies of kidney disease have focused on a wide variety of glomerular diseases including minimal change disease, focal segmental glomerulosclerosis, C1q nephropathy, membranous nephropathy, diabetic glomerulosclerosis, IgA nephropathy, lupus nephritis, anti-GBM glomerulonephritis, and ANCA-glomerulonephritis. (unc.edu)
  • Immunoglobulin A Nephropathy Immunoglobulin A (IgA) nephropathy is deposition of IgA immune complexes in glomeruli, manifesting as slowly progressive hematuria, proteinuria, and, often, renal insufficiency. (msdmanuals.com)
  • MZB is being used to treat renal transplantation patients, IgA nephropathy, lupus erythematosus, and childhood nephrotic syndrome (NS), and some recent studies have assessed the efficacy of oral MZB pulse therapy for severe lupus nephritis, steroid-resistant NS, and frequently relapsing-steroid-dependent NS. (hindawi.com)
  • This review summarizes the published findings on the efficacy of MZB for renal disease including IgA nephropathy, lupus nephritis, and NS, as well as of oral MZB pulse therapy for severe lupus nephritis and NS, and also the mechanism of the effect of oral MZB pulse therapy on the lymphocyte cell cycle. (hindawi.com)
  • Differentiating Staphylococcus infection-associated glomerulonephritis and primary IgA nephropathy: a mass spectrometry-based exploratory study. (louisville.edu)
  • Young adults and children, often associated with HIV, heroin use, igA nephropathy and maladaption of nephron loss damage to podocyte initiates to global sclerosis. (freezingblue.com)
  • Background: IgA nephropathy (IgAN) is one of the most frequently occurring types of chronic glomerulonephritis. (elsevierpure.com)
  • Glomerulonephritis, IgA nephropathy, and hemolytic uremic syndrome have been described in some patients. (lu.se)
  • In patients presenting with nephrotic syndrome , distinguishing focal segmental glomerulosclerosis (FSGS) from other glomerular diseases (eg, minimal-change disease, mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis, membranous glomerulonephritis) is clinically difficult. (medscape.com)
  • Fakhouri F. Approche clinique des glomérulonéphrites membranoprolifératives primitives [Clinical approach to primary membranoproliferative glomerulonephritis]. (smw.ch)
  • Low serum complement levels are seen in postinfectious glomerulonephritis, systemic lupus erythematosus nephritis, bacterial endocarditis, and membranoproliferative glomerulonephritis. (medscape.com)
  • Under the same conditions, kidney diseases characteristic of membranoproliferative glomerulonephritis (MPGN) or poststreptococcal glomerulonephritis (PSGN) also may be considered. (medscape.com)
  • Histopathology, electron microscopy and immunohistochemistry were consistent with an immune-mediated membranoproliferative glomerulonephritis (MPGN). (vin.com)
  • Renal biopsy revealed membranoproliferative glomerulonephritis, with lobulated glomerular tufts, endocapillary proliferation, thickened basement membrane, and glomerular hyaline thrombi suggestive of cryoglobulin deposits. (who.int)
  • Diffuse proliferative glomerulonephritis (DPGN) is a term used to describe a distinct histologic form of glomerulonephritis common to various types of systemic inflammatory diseases, including autoimmune disorders (eg, systemic lupus erythematosus [SLE]), vasculitis syndromes (eg, granulomatosis with polyangiitis), and infectious processes. (medscape.com)
  • specifically it is a form of glomerulonephritis or an inflammation of the glomeruli of the kidney. (wikipedia.org)
  • is the most common form of glomerulonephritis. (msdmanuals.com)
  • The diagnosis of glomerular diseases: acute glomerulonephritis and the nephrotic syndrome. (smw.ch)
  • Diffuse endocapillary-proliferative glomerulonephritis was found in all cases, and three patients also had crescentic glomerulonephritis. (qxmd.com)
  • Binding of these autoantibodies to the GBM induces rapidly progressive glomerulonephritis (RPGN) and crescentic glomerulonephritis. (medscape.com)
  • The typical morphologic pattern seen on light microscopy is DPGN, with focal necrotizing lesions and crescents in more than 50% of glomeruli (ie, crescentic glomerulonephritis). (medscape.com)
  • Diffuse mesangial proliferation or crescentic glomerulonephritis may also be present. (wikipedia.org)
  • Syed R, Rehman A, Valecha G, El-Sayegh S. Pauci-Immune Crescentic Glomerulonephritis: An ANCA-Associated Vasculitis. (smw.ch)
  • The classic presentation for the non-aggressive form (in 40-50% of the cases) is episodic hematuria, which usually starts within a day or two of a non-specific upper respiratory tract infection (hence synpharyngitic), as opposed to post-streptococcal glomerulonephritis, which occurs some time (weeks) after initial infection. (wikipedia.org)
  • In DPGN, more than 50% of the glomeruli (diffuse) show an increase in mesangial, epithelial, endothelial (proliferative), and inflammatory cells (ie, glomerulonephritis). (medscape.com)
  • In contrast, when fewer than 50% of the glomeruli are involved, the condition is termed focal proliferative glomerulonephritis. (medscape.com)
  • Glomerulonephritis is a condition in which the glomeruli, the tiny filters in the kidney, become inflamed. (nkfs.org)
  • However, the significance of glomerular IgA-dominant deposition in PIGN remains unclear. (qxmd.com)
  • Immunofluorescence shows mesangial deposition of IgA often with C3 and properdin and smaller amounts of other immunoglobulins (IgG or IgM). (wikipedia.org)
  • Immunofluorescence showed diffuse deposition of glomerular basement membrane immunoglobulin (Ig)M and complement component C3, with mesangial IgG, but negative for C4, fibrin and IgA. (who.int)
  • 2. IgAN secondary to another condition (e.g., liver cirrhosis), or other causes of mesangial IgA deposition including IgA vasculitis (i.e. (who.int)
  • Untreated strep throat or skin infections caused by Streptococcus bacteria may trigger a sudden bout of acute glomerulonephritis. (nkfs.org)
  • These findings are characteristic of diffuse proliferative glomerulonephritis. (medscape.com)
  • A case was described of a 28 year old plumber who suffered from gross hematuria and segmental proliferative glomerulonephritis with immunoglobulin-A deposits who requested a health hazard evaluation from NIOSH. (cdc.gov)
  • Apart from being one of the most common types of chronic glomerulonephritis, it is also the most frequent case of end-stage renal disease. (karger.com)
  • The University of North Carolina (UNC) Division of Nephrology and the UNC Kidney Center offer a postdoctoral fellowship, the UNC Glomerulonephritis (GN) fellowship, focused on glomerular diseases and vasculitis. (unc.edu)
  • Some people with chronic glomerulonephritis have no history of kidney disease. (medlineplus.gov)
  • Although specific antigenic causes initiating glomerulonephritis were not determined in these pygmy marmosets, MPGN in humans can be triggered by chronic infections or parasitism. (vin.com)
  • IgAN is the most common form of primary glomerulonephritis and is associated with a significant reduction in life expectancy," said Brian J. G. Pereira, M.D., CEO of Visterra, Inc., and the senior author of the New England Journal of Medicine paper. (otsuka-us.com)
  • IgA-dominant postinfectious glomerulonephritis: not peculiar to staphylococcal infection and diabetic patients. (qxmd.com)
  • IgA-dominant postinfectious glomerulonephritis (PIGN) is a unique form of PIGN. (qxmd.com)
  • Berger's disease) is the most common form of primary glomerulonephritis worldwide and is the most common cause of kidney failure in young adults. (otsuka-us.com)
  • IgA-dominant PIGN resembles poststreptococcal glomerulonephritis in its histological spectrum and ultrastructural appearance. (qxmd.com)
  • Glomerulonephritis is a type of kidney disease in which the part of your kidneys that helps filter waste and fluids from the blood is damaged. (medlineplus.gov)
  • If too much IgA proteins are deposited in the kidneys, it can inflame the kidney filters and impair their function. (nkfs.org)
  • The GN Fellow may participate ongoing clinical studies in vasculitis and glomerulonephritis at the UNC Kidney Center. (unc.edu)
  • The pathogenesis of antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis is unknown, although microvasculitis is the predominant feature without immune complex formation. (medscape.com)
  • Activation of the complement system through the classic pathway by immune complexes or direct cell-mediated injury in ANCA-associated glomerulonephritis results in the recruitment of inflammatory cellular infiltrates (eg, lymphocytes, macrophages, neutrophils), proliferation of the mesangial and endothelial cells, and necrosis. (medscape.com)
  • Glomerulonephritis may be caused by problems with the body's immune system. (medlineplus.gov)
  • A procedure called plasmapheresis may sometimes be used for glomerulonephritis caused by immune system problems. (medlineplus.gov)
  • Starting with clinical reviews on topics such as the clinico-pathological classification, new treatment approaches, and the role of renal biopsies, the focus then shifts towards basic reviews on, for example, candidate genes, the pathogenic role of IgA receptors or immune complex formation. (karger.com)
  • Membranous glomerulonephritis is characterized by a diffuse thickening of the wall of glomerular capillaries and by subepithelial deposits of immune complexes (Nash AS- 1969). (vin.com)
  • The disease is due to immune complex deposits of IgG and C3, sometimes but less often they are deposits of IgA and IgM. (vin.com)
  • citation needed] The disease derives its name from deposits of immunoglobulin A (IgA) in a granular pattern in the mesangium (by immunofluorescence), a region of the renal glomerulus. (wikipedia.org)
  • Children and young adults, Abnormal amounts of IgA deposits post viral infections of upper respiratory tract. (freezingblue.com)
  • Immunohistochemistry studies performed on kidney sections of selected animals showed focal mesangial staining to IgG and IgM, but not to IgA. (vin.com)
  • Increasing serum IgA may be involved in the pathogenesis of this form of PIGN. (qxmd.com)
  • What does that have to do with the pathogenesis where IgA is typically acting? (medscape.com)
  • Dr. Jennette's more basic research (funded by NIH NIDDK) focuses on the pathogenesis of glomerulonephritis, vasculitis and granulomatosis caused by anti-neutrophil cytoplasmic autoantibodies (ANCA) using in vitro assays, animal models, and human specimens. (unc.edu)
  • Glomerulonephritis is a rare yet serious group of diseases with a high risk of progression to end-stage renal disease. (smw.ch)
  • IgA is the predominant immunoglobulin that is produced at the mucosal surface. (medscape.com)
  • Their demographic, clinical, and renal biopsy findings were summarized and compared with the data of 32 patients with non-IgA-dominant PIGN. (qxmd.com)
  • Clinical studies are typically conducted through the UNC Clinical and Translational Research Center, as well as within the Glomerulonephritis and Vasculitis Clinic. (unc.edu)
  • The objective of this study was to assess the incidence of the different forms of glomerulonephritis in the western part of Switzerland and its changes over the last 10 years, compared with international data. (smw.ch)
  • The incidence was calculated as the number of patients newly diagnosed with glomerulonephritis divided by the number of inhabitants of all the above-mentioned cantons during the year under review, as retrieved from the federal statistical office of Switzerland. (smw.ch)
  • Overall, the mean incidence of glomerulonephritis was 1.3/100,000/year. (smw.ch)
  • Between 2007 and 2016, the incidence of all glomerulonephritis taken together remained stable. (smw.ch)
  • The incidence of glomerulonephritis in the western part of Switzerland was low and remained stable over time, in line with European data. (smw.ch)
  • The incidence of primary glomerulonephritis worldwide: a systematic review of the literature. (smw.ch)
  • There is an increased incidence of autoimmune manifestations (vasculitis, hemolytic anemia, glomerulonephritis) and tumors (leukemia, lymphoma, EBV-related brain tumor). (esid.org)
  • Researchers observed incremental increases in the incidence of 2 types of kidney disease-lupus nephritis and ANCA-related glomerulonephritis-with increasingly lower income. (newswise.com)
  • Therefore, urinalysis during active inflammation (or glomerulonephritis) characteristically shows an active urinary sediment, with RBCs or casts, WBCs or casts, and variable degrees of proteinuria (ie, nephritic pattern). (medscape.com)
  • When those levels go up, that is recognized by the body as being an abnormal finding against which we start forming autoantibodies, the IgA or IgG subtype. (medscape.com)
  • Our data suggested that IgA-dominant PIGN was not peculiar to staphylococcal infection and diabetic patients. (qxmd.com)
  • If methicillin-resistant Staphylococcus aureus (MRSA) is the inciting agent, then hypocomplementemia is usually not present, but plasma immunoglobulins, especially IgA, are markedly elevated. (medscape.com)
  • We reported 10 patients with IgA-dominant PIGN encountered at a single center, each characterized by subepithelial humps. (qxmd.com)
  • Compared to patients with non-IgA-dominant PIGN, increased serum IgA was more commonly present in IgA-dominant group (p = 0.007). (qxmd.com)
  • The GN Fellow actively participates in a busy weekly Glomerulonephritis and Vasculitis Clinic, in which fifty to seventy patients are seen weekly. (unc.edu)
  • Many patients have increased IgE and IgA, with low IgM. (esid.org)
  • BACKGROUND: Kidney transplant patients with glomerulonephritis (GN) as their native disease may receive significant amounts of pre-transplant immunosuppression (PTI), which could increase the risk for development of malignancy post-transplant. (bvsalud.org)
  • When these get deposited in the kidney filters, they can cause inflammation leading to glomerulonephritis. (nkfs.org)
  • IgA vasculitis presents with a characteristic purpuric skin rash, arthritis, and abdominal pain, and occurs more commonly in children. (wikipedia.org)