Kidney
Kidney Tubules
Pancreatic Neoplasms
Kidney Cortex
Neoplasms
Acute Kidney Injury
Neoplasms, Cystic, Mucinous, and Serous
Kidney Failure, Chronic
Decreased expression of the pro-apoptotic protein Par-4 in renal cell carcinoma. (1/5944)
Par-4 is a widely expressed leucine zipper protein that confers sensitization to apoptosis induced by exogenous insults. Because the expression of genes that promote apoptosis may be down-regulated during tumorigenesis, we sought to examine the expression of Par-4 in human tumors. We present here evidence that Par-4 protein levels were severely decreased in human renal cell carcinoma specimens relative to normal tubular cells. Replenishment of Par-4 protein levels in renal cell carcinoma cell lines conferred sensitivity to apoptosis. Because apoptosis may serve as a defense mechanism against malignant transformation or progression, decreased expression of Par-4 may contribute to the pathophysiology of renal cell carcinoma. (+info)Surgery-related factors and local recurrence of Wilms tumor in National Wilms Tumor Study 4. (2/5944)
OBJECTIVE: To assess the prognostic factors for local recurrence in Wilms tumor. SUMMARY BACKGROUND DATA: Current therapy for Wilms tumor has evolved through four studies of the National Wilms Tumor Study Group. As adverse prognostic factors were identified, treatment of children with Wilms tumor has been tailored based on these factors. Two-year relapse-free survival of children in the fourth study (NWTS-4) exceeded 91%. Factors once of prognostic import for local recurrence may lose their significance as more effective therapeutic regimens are devised. METHODS: Children evaluated were drawn from the records of NWTS-4. A total of 2482 randomized or followed patients were identified. Local recurrence, defined as recurrence in the original tumor bed, retroperitoneum, or within the abdominal cavity or pelvis, occurred in 100 children. Using a nested case-control study design, 182 matched controls were selected. Factors were analyzed for their association with local failure. Relative risks and 95% confidence intervals were calculated, taking into account the matching. RESULTS: The largest relative risks for local recurrence were observed in patients with stage III disease, those with unfavorable histology (especially diffuse anaplasia), and those reported to have tumor spillage during surgery. Multiple regression analysis adjusting for the combined effects of histology, lymph node involvement, and age revealed that tumor spillage remained significant. The relative risk of local recurrence from spill was largest in children with stage II disease. The absence of lymph node biopsy was also associated with an increased relative risk of recurrence, which was largest in children with stage I disease. The survival of children after local recurrence is poor, with an average survival rate at 2 years after relapse of 43%. Survival was dependent on initial stage: those who received more therapy before relapse had a worse prognosis. CONCLUSIONS: This study has demonstrated that surgical rupture of the tumor must be prevented by the surgeon, because spills produce an increased risk of local relapse. Both local and diffuse spills produce this risk. Stage II children with local spill appear to require more aggressive therapy than that used in NWTS-4. The continued critical importance of lymph node sampling in conjunction with nephrectomy for Wilms tumor is also established. Absence of lymph node biopsy may result in understaging and inadequate treatment of the child and may produce an increased risk of local recurrence. (+info)Profound variation in dihydropyrimidine dehydrogenase activity in human blood cells: major implications for the detection of partly deficient patients. (3/5944)
Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. To identify patients suffering from a complete or partial DPD deficiency, the activity of DPD is usually determined in peripheral blood mononuclear cells (PBM cells). In this study, we demonstrated that the highest activity of DPD was found in monocytes followed by that of lymphocytes, granulocytes and platelets, whereas no significant activity of DPD could be detected in erythrocytes. The activity of DPD in PBM cells proved to be intermediate compared with the DPD activity observed in monocytes and lymphocytes. The mean percentage of monocytes in the PBM cells obtained from cancer patients proved to be significantly higher than that observed in PBM cells obtained from healthy volunteers. Moreover, a profound positive correlation was observed between the DPD activity of PBM cells and the percentage of monocytes, thus introducing a large inter- and intrapatient variability in the activity of DPD and hindering the detection of patients with a partial DPD deficiency. (+info)Methylation-associated silencing of the tissue inhibitor of metalloproteinase-3 gene suggest a suppressor role in kidney, brain, and other human cancers. (4/5944)
Tissue inhibitor of metalloproteinase-3 (TIMP-3) antagonizes matrix metalloproteinase activity and can suppress tumor growth, angiogenesis, invasion, and metastasis. Loss of TIMP-3 has been related to the acquisition of tumorigenesis. Herein, we show that TIMP-3 is silenced in association with aberrant promoter-region methylation in cell lines derived from human cancers. TIMP-3 expression was restored after 5-aza-2'deoxycytidine-mediated demethylation of the TIMP-3 proximal promoter region. Genomic bisulfite sequencing revealed that TIMP-3 silencing was related to the overall density of methylation and that discrete regions within the TIMP-3 CpG island may be important for the silencing of this gene. Aberrant methylation of TIMP-3 occurred in primary cancers of the kidney, brain, colon, breast, and lung, but not in any of 41 normal tissue samples. The most frequent TIMP-3 methylation was found in renal cancers, which originate in the tissue that normally expresses the highest TIMP-3 levels. This methylation correlated with a lack of detectable TIMP-3 protein in these tumors. Together, these data show that methylation-associated inactivation of TIMP-3 is frequent in many human tumors. (+info)Isolation and characterization of a rat homologue of the human tuberous sclerosis 1 gene (Tsc1) and analysis of its mutations in rat renal carcinomas. (5/5944)
In the Eker rat, a germ-line mutation in the homologue of the human tuberous sclerosis gene (Tsc2) causes renal cell carcinomas (RCs) with a complete penetrance in all heterozygotes. Tsc2 mutations have also been found in a subset of chemically induced non-Eker rat RCs. Because tuberous sclerosis patients with alteration of either of the two predisposing genes (TSC1 and TSC2) show identical symptoms, the products of these two genes are thought to be involved in a common biological pathway. In this study, to analyze the possible overlap between the functions of Tsc2 and Tscl gene products, we isolated and characterized a rat homologue of the TSC1 gene (Tsc1). The rat Tsc1 gene, which has an identical exon-intron structure to that of human TSC1 and is localized on rat chromosome 3, has been shown to encode a protein (hamartin) that is highly homologous to the human counterpart with an approximately 86% amino acid sequence identity. Using PCR-single-strand conformational polymorphism analysis, we identified two splicing donor site mutations in one chemically induced rat RC (1 of 15). This suggests that alterations of the Tsc1 gene may be involved in the development of a subset of rat RCs. (+info)Presentation of renal tumor antigens by human dendritic cells activates tumor-infiltrating lymphocytes against autologous tumor: implications for live kidney cancer vaccines. (6/5944)
The clinical impact of dendritic cells (DCs) in the treatment of human cancer depends on their unique role as the most potent antigen-presenting cells that are capable of priming an antitumor T-cell response. Here, we demonstrate that functional DCs can be generated from peripheral blood of patients with metastatic renal cell carcinoma (RCC) by culture of monocytes/macrophages (CD14+) in autologous serum containing medium (RPMI) in the presence of granulocyte macrophage colony-stimulating factor and interleukin (IL) 4. For testing the capability of RCC-antigen uptake and processing, we loaded these DCs with autologous tumor lysate (TuLy) using liposomes, after which cytometric analysis of the DCs revealed a markedly increased expression of HLA class I antigen and a persistent high expression of class II. The immunogenicity of DC-TuLy was further tested in cultures of renal tumor infiltrating lymphocytes (TILs) cultured in low-dose IL-2 (20 Biologic Response Modifier Program units/ml). A synergistic effect of DC-TuLy and IL-2 in stimulating a T cell-dependent immune response was demonstrated by: (a) the increase of growth expansion of TILs (9.4-14.3-fold; day 21); (b) the up-regulation of the CD3+ CD56- TcR+ (both CD4+ and CD8+) cell population; (c) the augmentation of T cell-restricted autologous tumor lysis; and (d) the enhancement of IFN-gamma, tumor necrosis factor-alpha, granulocyte macrophage colony-stimulating factor, and IL-6 mRNA expression by TILs. Taken together, these data implicate that DC-TuLy can activate immunosuppressed TIL via an induction of enhanced antitumor CTL responses associated with production of Thl cells. This indicates a potential role of DC-TuLy vaccines for induction of active immunity in patients with advanced RCC. (+info)A possible contributory role of BK virus infection in neuroblastoma development. (7/5944)
The tumor suppressor protein p53 is aberrantly localized to the cytoplasm of neuroblastoma cells, compromising the suppressor function of this protein. Such tumors are experimentally induced in transgenic mice expressing the large tumor (T) antigen of polyomaviruses. The oncogenic mechanisms of T antigen include complex formation with, and inactivation of, the tumor suppressor protein p53. Samples from 18 human neuroblastomas and five normal human adrenal glands were examined. BK virus DNA was detected in all neuroblastomas and none of five normal adrenal glands by PCR. Using DNA in situ hybridization, polyomaviral DNA was found in the tumor cells of 17 of 18 neuroblastomas, but in none of five adrenal medullas. Expression of the large T antigen was detected in the tumor cells of 16 of 18 neuroblastomas, but in none of the five adrenal medullas. By double immunostaining BK virus T antigen and p53 was colocalized to the cytoplasm of the tumor cells. Immunoprecipitation revealed binding between the two proteins. The presence and expression of BK virus in neuroblastomas, but not in normal adrenal medulla, and colocalization and binding to p53, suggest that this virus may play a contributory role in the development of this neoplasm. (+info)Immunohistochemical detection of JC virus in nontumorous renal tissue of a patient with renal cancer but without progressive multifocal leukoencephalopathy. (8/5944)
We performed immunohistochemical staining on the nontumorous renal tissue of 45 patients with renal cancer but without progressive multifocal encephalopathy using JCV-specific antibody. For one patient we found positive staining of the nuclei of the renal collecting ducts. Immunoelectron microscopic examination of the positive cell nuclei revealed electron-dense polyomavirus-like particles. (+info)Kidney neoplasms refer to abnormal growths or tumors in the kidney tissues that can be benign (non-cancerous) or malignant (cancerous). These growths can originate from various types of kidney cells, including the renal tubules, glomeruli, and the renal pelvis.
Malignant kidney neoplasms are also known as kidney cancers, with renal cell carcinoma being the most common type. Benign kidney neoplasms include renal adenomas, oncocytomas, and angiomyolipomas. While benign neoplasms are generally not life-threatening, they can still cause problems if they grow large enough to compromise kidney function or if they undergo malignant transformation.
Early detection and appropriate management of kidney neoplasms are crucial for improving patient outcomes and overall prognosis. Regular medical check-ups, imaging studies, and urinalysis can help in the early identification of these growths, allowing for timely intervention and treatment.
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.
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.
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.
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.
Pancreatic neoplasms refer to abnormal growths in the pancreas that can be benign or malignant. The pancreas is a gland located behind the stomach that produces hormones and digestive enzymes. Pancreatic neoplasms can interfere with the normal functioning of the pancreas, leading to various health complications.
Benign pancreatic neoplasms are non-cancerous growths that do not spread to other parts of the body. They are usually removed through surgery to prevent any potential complications, such as blocking the bile duct or causing pain.
Malignant pancreatic neoplasms, also known as pancreatic cancer, are cancerous growths that can invade and destroy surrounding tissues and organs. They can also spread (metastasize) to other parts of the body, such as the liver, lungs, or bones. Pancreatic cancer is often aggressive and difficult to treat, with a poor prognosis.
There are several types of pancreatic neoplasms, including adenocarcinomas, neuroendocrine tumors, solid pseudopapillary neoplasms, and cystic neoplasms. The specific type of neoplasm is determined through various diagnostic tests, such as imaging studies, biopsies, and blood tests. Treatment options depend on the type, stage, and location of the neoplasm, as well as the patient's overall health and preferences.
The kidney cortex is the outer region of the kidney where most of the functional units called nephrons are located. It plays a crucial role in filtering blood and regulating water, electrolyte, and acid-base balance in the body. The kidney cortex contains the glomeruli, proximal tubules, loop of Henle, and distal tubules, which work together to reabsorb necessary substances and excrete waste products into the urine.
Neoplasms are abnormal growths of cells or tissues in the body that serve no physiological function. They can be benign (non-cancerous) or malignant (cancerous). Benign neoplasms are typically slow growing and do not spread to other parts of the body, while malignant neoplasms are aggressive, invasive, and can metastasize to distant sites.
Neoplasms occur when there is a dysregulation in the normal process of cell division and differentiation, leading to uncontrolled growth and accumulation of cells. This can result from genetic mutations or other factors such as viral infections, environmental exposures, or hormonal imbalances.
Neoplasms can develop in any organ or tissue of the body and can cause various symptoms depending on their size, location, and type. Treatment options for neoplasms include surgery, radiation therapy, chemotherapy, immunotherapy, and targeted therapy, among others.
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.
Neoplasms: Neoplasms refer to abnormal growths of tissue that can be benign (non-cancerous) or malignant (cancerous). They occur when the normal control mechanisms that regulate cell growth and division are disrupted, leading to uncontrolled cell proliferation.
Cystic Neoplasms: Cystic neoplasms are tumors that contain fluid-filled sacs or cysts. These tumors can be benign or malignant and can occur in various organs of the body, including the pancreas, ovary, and liver.
Mucinous Neoplasms: Mucinous neoplasms are a type of cystic neoplasm that is characterized by the production of mucin, a gel-like substance produced by certain types of cells. These tumors can occur in various organs, including the ovary, pancreas, and colon. Mucinous neoplasms can be benign or malignant, and malignant forms are often aggressive and have a poor prognosis.
Serous Neoplasms: Serous neoplasms are another type of cystic neoplasm that is characterized by the production of serous fluid, which is a thin, watery fluid. These tumors commonly occur in the ovary and can be benign or malignant. Malignant serous neoplasms are often aggressive and have a poor prognosis.
In summary, neoplasms refer to abnormal tissue growths that can be benign or malignant. Cystic neoplasms contain fluid-filled sacs and can occur in various organs of the body. Mucinous neoplasms produce a gel-like substance called mucin and can also occur in various organs, while serous neoplasms produce thin, watery fluid and commonly occur in the ovary. Both mucinous and serous neoplasms can be benign or malignant, with malignant forms often being aggressive and having a poor prognosis.
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.
Cystic kidney disease
Malignant rhabdoid tumour
Membranoproliferative glomerulonephritis
Renal oncocytoma
Yu Baofa
Papillary renal cell carcinoma
Eye neoplasm
Oncocytoma
Pseudocyst
Pelvic lipomatosis
Metanephric adenoma
C2orf81
Mesoblastic nephroma
Hydronephrosis
Analgesic nephropathy
Granular cell tumor
Oncocyte
Adrenal tumor
Hamartoma
Laboratory rat
Timeline of tuberous sclerosis
Bernice Eddy
Mammalian kidney
Adenosarcoma
Corticosteroid
Renal anaplastic sarcoma
List of ICD-9 codes 140-239: neoplasms
Cathepsin H
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CSNK1D
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Prostatic Neoplasms1
- Prognosis --Several studies have demonstrated that a large proportion of neuroendocrine differentiated prostatic neoplasms are positive for neuron-specific enolase and chromogranin A [4,6]. (cancernetwork.com)
Carcinoma1
- Argani, P. Intraductal spread by metastatic islet cell tumor (well-differentiated pancreatic endocrine neoplasm) involving the breast of a child, mimicking a primary mammary carcinoma. (hopkinsmedicine.org)
Myeloproliferative neoplasm1
- I'm joined today by Dr. Ruben Mesa, the director of the UT Health San Antonio MD Anderson Cancer Center and world-renowned MPN (myeloproliferative neoplasm) expert, and a dear colleague. (curetoday.com)
Chronic1
- Kidney - Nephropathy, Obstructive in a female F344/N rat from a chronic study. (nih.gov)
Neuroendocrine neoplasms4
- Primary neuroendocrine neoplasms of the kidney: a case report and literature review. (bvsalud.org)
- However, detecting and monitoring neuroendocrine neoplasms remains challenging because of their nonspecific nature . (bvsalud.org)
- Pancreatic neuroendocrine neoplasms (pNENs) are an increasingly common group of malignancies that arise within the endocrine tissue of the pancreas. (rarediseases.org)
- Nonfunctioning neuroendocrine neoplasms can still cause symptoms relating to tumor size and location such as obstruction or internal bleeding. (rarediseases.org)
Malignant Neoplasm1
- The following conditions each represent 1 percent or more of diagnostic radiology claims: subarachnoid hemorrhage, malignant neoplasm of colon, malignant neoplasm of pancreas, cerebral thrombosis with infarction, acute cerebrovascular accident (CVA), cerebral aneurysm, pelvis fracture, ankle fracture, and intracranial abscess. (thedoctors.com)
Epithelial2
- The most frequently encountered neoplastic pancreatic cysts include intraductal papillary mucinous neoplasm (IPMN), serous cystadenoma (SCA), mucinous cystic neoplasm with ovarian stroma (MCN), and solid pseudopapillary epithelial neoplasm. (medscape.com)
- [ 5 ] Other, rarer cystic lesions, such as solid pseudopapillary epithelial neoplasm and cystic pancreatic neuroendocrine tumor (cPNET), tend to harbor features that suggest a specific diagnosis, usually leading to surgical removal. (medscape.com)
Cystic12
- Pancreatic cystic neoplasms represent a small yet increasingly detected entity of pancreatic abnormalities. (medscape.com)
- Approximately 70% of pancreatic cystic neoplasms are discovered incidentally. (medscape.com)
- Note the smooth external contour typical of a mucinous cystic neoplasm. (medscape.com)
- Cystic kidney disease refers to a wide range of hereditary, developmental, and acquired conditions and with the inclusion of neoplasms with cystic changes, over 40 classifications and subtypes have been identified. (wikipedia.org)
- Cystic disease may involve one or both kidneys and may, or may not, occur in the presence of other anomalies. (wikipedia.org)
- Of the cystic kidney diseases, the most common is polycystic kidney disease with two sub-types: the less prevalent autosomal recessive and more prevalent autosomal dominant. (wikipedia.org)
- Another example of cystic kidney disease is Medullary sponge kidney. (wikipedia.org)
- Cystic kidney disease includes various conditions related to the formation of cysts in one or both kidneys. (wikipedia.org)
- Examples of acquired cystic kidney disease include simple cysts and medullary sponge kidney (MSK). (wikipedia.org)
- Other types of genetic cystic kidney disease include juvenile nephronophthisis (JNPHP), medullary cystic kidney disease (MCKD), and glomerulocystic kidney disease (GCKD). (wikipedia.org)
- Those genes encode for polycystic proteins and mutations regarding those genes are inherited and responsible for the disorder of autosomal dominant cystic kidney disease. (wikipedia.org)
- citation needed] Many forms of cystic kidney disease can be detected in children prior to birth. (wikipedia.org)
Lung1
- Abnormalities which affect both kidneys can have an effect on the baby's amniotic fluid volume, which can in turn lead to problems with lung development. (wikipedia.org)
Abnormalities2
- Abnormalities, which only affect one kidney, are unlikely to cause a problem with the healthy arrival of a baby. (wikipedia.org)
- Histologically, L2hgdh knockout kidneys have no demonstrable histologic abnormalities. (duke.edu)
Benign1
- However, the proportion of neuroendocrine differentiation was found to be much higher in follow-up studies and it is now thought that 50% to 100% of all prostate neoplasms (including benign prostatic tissue) contain at least some neuroendocrine cells [3,5]. (cancernetwork.com)
Prostate1
- Neuroendocrine differentiation has been foundin 50% to 100% of prostate neoplasms of all stages. (cancernetwork.com)
Failure2
- In the United States, more than half a million people have PKD, making it the fourth leading cause of kidney failure. (wikipedia.org)
- The disease is usually manifested before age 30, and 45% develop kidney failure by age 60. (wikipedia.org)
Cysts4
- citation needed] PKD causes numerous cysts to grow in the kidneys. (wikipedia.org)
- These cysts are filled with fluid and if they grow excessively, changing the shape of them and making them larger, leading to kidney damage. (wikipedia.org)
- MRI can be used to monitor the development of cysts and growth of kidneys. (wikipedia.org)
- Several sub centimeter simple cortical cysts are seen at kidneys. (radiopaedia.org)
Renal Cell C1
- Renal cell cancer is the most frequently encountered malignant tumor in the kidney. (diagnosticimaging.com)
Metabolism1
- Despite L2HGDH being highly expressed in the kidney, its role in renal metabolism has not been explored. (duke.edu)
Acute1
- Vancomycin-associated acute kidney injury (AKI) continues to pose a major challenge to both patients and healthcare providers. (frontiersin.org)
Histologic1
- Wilms tumour (WT), the most common embryonal neoplasm of the childhood kidney, has long intrigued investigators by its histologic similarity to the developing kidney 1 . (nature.com)
Left kidney2
- Computed tomography urography revealed a small (approximately 19- × 16-mm) nodular shadow in the left kidney . (bvsalud.org)
- A 50×45mm mass is seen in the left kidney. (radiopaedia.org)
Childhood kidney1
- The only variant culture was derived from mesoblastic nephroma, a distinct childhood kidney neoplasm. (uni-wuerzburg.de)
Tumour1
- Wilms tumour is an embryonal tumour of childhood that closely resembles the developing kidney. (nature.com)
Alterations1
- RR CC was named for its morphologic resemblance to pediatric malignant rhabdoid tumor (MRT) of the kidney, which is a highly aggressive tumor characterized by cells that resemble rhabdomyoblasts and by genetic alterations involving chromosome 22, particularly the hSNF5/INI1 gene on 22q11.2. (medscape.com)
Tumors2
- Primary kidney neuroendocrine tumors (NETs) are rare renal malignancies . (bvsalud.org)
- In most cases, there will be a solitary tumor in one kidney, but 5-13% of children have bilateral tumors and 10% have multifocal tumors in a single kidney. (medscape.com)
Workup1
- Patients with impaired renal function and documented allergic reaction to iodinated contrast agents can undergo a complete diagnostic kidney workup on MRI. (diagnosticimaging.com)
Obstructive2
Bone1
- Well, as we think about the myeloproliferative neoplasms, they are a group of illnesses of the bone marrow. (curetoday.com)
Systemic1
- nonfunctioning neoplasms may produce hormones, but no systemic symptoms. (rarediseases.org)
Transplantation6
- To compare the incidence of cancer in patients receiving immune suppression after kidney transplantation with incidence in the same population in 2 periods before receipt of immune suppression: during dialysis and during end-stage kidney disease before renal replacement therapy (RRT). (nih.gov)
- Kidney transplantation is associated with a marked increase in cancer risk at a wide variety of sites. (nih.gov)
- Treatment of post-transplantation lymphoproliferative disorders after kidney transplant with rituximab and conversion to m-TOR inhibitor. (univalle.edu.co)
- To describe the clinical response, overall and graft survival of patients in our center with this complication after kidney transplantation, which received rituximab as part of their treatment as well as conversion to m-TOR. (univalle.edu.co)
- Retrospective study, which included patients, diagnosed with post-transplant lymphoproliferative disorders after kidney transplantation from January 2011 to July 2014. (univalle.edu.co)
- There are no standardized treatment regimens for lymphoproliferative disorders after kidney transplantation, but these patients can be managed successfully with reduction of immunosuppression, conversion to m-TOR and rituximab-based schemes. (univalle.edu.co)
Stones3
- I ended up seeing Dr Cahoon through an ER visit because of kidney stones. (vitals.com)
- I had a surgery to remove those stones and ended up with stones in my other kidney as well. (vitals.com)
- In addition, a few small stones less than 3mm are present at both kidneys. (radiopaedia.org)
Polycythemia1
- One group of those are the myeloproliferative neoplasms, which includes essential thrombocythemia, a disease named for having too many platelets, polycythemia vera, a disease named for having too many red blood cells, and myelofibrosis. (curetoday.com)