Hardening of the KIDNEY due to infiltration by fibrous connective tissue (FIBROSIS), usually caused by renovascular diseases or chronic HYPERTENSION. Nephrosclerosis leads to renal ISCHEMIA.
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
A condition of markedly elevated BLOOD PRESSURE with DIASTOLIC PRESSURE usually greater than 120 mm Hg. Malignant hypertension is characterized by widespread vascular damage, PAPILLEDEMA, retinopathy, HYPERTENSIVE ENCEPHALOPATHY, and renal dysfunction.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
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.
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
Pathological processes of the KIDNEY or its component tissues.
Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.

Vascular endothelin-1 gene expression and synthesis and effect on renal type I collagen synthesis and nephroangiosclerosis during nitric oxide synthase inhibition in rats. (1/143)

BACKGROUND: The progression of hypertension during NO deficiency is associated with renal vascular fibrosis due to increased extracellular matrix (mainly collagen I) formation. The purpose of the present study was to investigate whether endothelin-1 (ET-1) is involved in this pathophysiological process. METHODS AND RESULTS: Treatment of rats for 4 weeks with the NO synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) 50 mg. kg-1. d-1 increased systolic blood pressure to 159+/-12 mm Hg. In animals treated with L-NAME, histological evaluation of renal sections revealed an increased formation of extracellular matrix (Masson's trichrome), and specifically of collagens (Sirius red). A part of this fibrosis was attributed to abnormal collagen I presence, because mRNA expression of the collagen I alpha1 chain (reverse transcription-polymerase chain reaction) and procollagen I formation (radioimmunoassay) were increased 3- and 2.5-fold, respectively, in the renal resistance vessels of hypertensive animals. In subsequent experiments, we examined whether ET-1 was involved in activation of collagen I formation. mRNA expression (RNase protection assay) of preproET-1 and ET-1 content (radioimmunoassay) were 10-fold and 3-fold increased, respectively, in renal microvessels of rats treated with L-NAME. Interestingly, in these vessels, ET-1 (immunostaining) was colocalized with sudanophilic lesions. Bosentan, an ET receptor antagonist (20 mg. kg-1. d-1), coadministered with L-NAME canceled the increased mRNA expression and synthesis of collagen I and attenuated the severity of renal vascular lesions without affecting L-NAME-induced high blood pressure. CONCLUSIONS: These data demonstrate that ET-1 synthesis is increased in renal microvessels when NO production is suppressed. In this model of hypertension, ET-1 is a major activator of collagen I formation in renal resistance vessels and participates in the development of renal fibrosis without affecting systolic blood pressure.  (+info)

Heavy metal nephropathy of rodents. (2/143)

Heavy metal nephropathy is a pathologic entity of the renal tubular epithelium of rats, evoked by lead, gold, and other heavy metals. It is characterized acutely by coagulative necrosis, subacutely by cortical fibrosis, and chronically by cytomegaly and karyomegaly. Finally, adenomas develop, some of which become malignant.  (+info)

Strain differences of hypertension induced by dietary NG-nitro-L-arginine in normotensive rats. (3/143)

When the potent inhibitor of nitric oxide (NO) synthesis NG-nitro-L-arginine (L-NNA) was incorporated into the diet, hypertension was induced and sustained due to the effects of the long-term inhibition of endothelium-dependent relaxing factor (EDRF)/NO. The effects of L-NNA on normotensive rats of four strains (Donryu, Sprague-Dawley (SD), Wistar, and Wistar-Kyoto (WKY)) were compared relative to control rats. L-NNA administration caused a sharp initial increase in systolic blood pressure (SBP) at 2 weeks in all animals, and this was followed by a gradual and steady increase until 4 weeks. At the end of the experiments (5 weeks), the mean SBP of Donryu and SD rats was decreased. The maximum blood pressure of Donryu and Wistar rats during the experiments exceeded 200 mmHg, but that of SD and WKY rats was below 200 mmHg. Body weight loss and death were observed only in L-NNA-fed Donryu rats. Pathological changes in the kidneys and the morbidity rates for the lesions were determined, and indicated that the Donryu L-NNA group was 100% positive. These results suggest that the Donryu strain is more sensitive to L-NNA than the other strains. That dietary L-NNA-induced hypertension in normotensive rats of the four strains provides a new artificially-induced hypertensive model in which vasoconstriction occurs mainly due to EDRF deficiency.  (+info)

Disposition of [G-(3)H]paclitaxel and cremophor EL in a patient with severely impaired renal function. (4/143)

In the present work, we studied the pharmacokinetics and metabolic disposition of [G-(3)H]paclitaxel in a female patient with recurrent ovarian cancer and severe renal impairment (creatinine clearance: approximately 20 ml/min) due to chronic hypertension and prior cisplatin treatment. During six 3-weekly courses of paclitaxel at a dose level of 157.5 mg/m(2) (viz. a 10% dose reduction), the renal function remained stable. Pharmacokinetic evaluation revealed a reproducible and surprisingly high paclitaxel area under the plasma concentration-time curve of 26.0 +/- 1.11 microM.h (mean +/- S.D.; n = 6; c.v. = 4.29%), and a terminal disposition half-life of approximately 29 h. Both parameters are substantially increased ( approximately 1.5-fold) when compared with kinetic data obtained from patients with normal renal function. The cumulative urinary excretion of the parent drug was consistently low and averaged 1.58 +/- 0.417% (+/- S.D.) of the dose. Total fecal excretion (measured in one course) was 52.9% of the delivered radioactivity, and mainly comprised known mono- and dihydroxylated metabolites, with unchanged paclitaxel accounting for only 6.18%. The plasma area under the plasma concentration-time curve of the paclitaxel vehicle Cremophor EL, which can profoundly alter the kinetics of paclitaxel, was 114.9 +/- 5.39 microl.h/ml, and not different from historic data in patients with normal or mild renal dysfunction. Urinary excretion of Cremophor EL was less than 0.1% of the total amount administered. These data indicate that the substantial increase in systemic exposure of the patient to paclitaxel relates to decreased renal metabolism and/or urinary elimination of polar radioactive species, most likely lacking an intact taxane ring fragment.  (+info)

Effects of angiotensin inhibitors on renal injury and angiotensin receptor expression in early hypertensive nephrosclerosis. (5/143)

Angiotensin converting enzyme inhibitors (ACEI) are known to inhibit the progression of established renal failure. The aim of this study was to compare the efficacy of an ACEI and an AT1 receptor antagonist (AT1R-Ant) in preventing the development of renal disease, at an early stage of hypertensive nephrosclerosis. SHRSP/Izm rats (n = 61) were treated from 10 wk until 22 wk with the ACEI delapril (40 mg/kg/d) or the AT1R-Ant candesartan cilexetil (1 mg/kg/d). Proteinuria, and structural/ultrastructural changes were assessed at 14 and 22 wk. Treatment with either agent resulted in reductions in blood pressure and cardiovascular hypertrophy. Neither proteinuria nor major renal histological changes were evident at 14 wk. At 22 wk, however, proteinuria accompanied by nephrosclerotic changes was seen in the untreated SHRSP/Izm. Treatment with either ACEI or AT1R-Ant resulted in similar reductions in proteinuria (untreated, 32.2 +/- 7.4; delapril-treated, 5.5 +/- 1.2; candesartan-treated, 3.9 +/- 0.3 mg/100 g/d). Prominent sclerosis of small-to-medium sized renal arteries was seen in the untreated SHRSP/Izm at 22 wk, but was similarly attenuated by the ACEI and AT1R-Ant. The glomerular ultrastructure was comparable between the two groups. No significant changes in renal AT1a or AT1b receptor subtype mRNA expression were seen throughout the course of the study. In contrast, a decrease in AT2 receptor mRNA was seen in the drug-treated groups at 14 wk but not at 22 wk. These results suggest that both ACEI and AT1R-Ant have similar efficacy in attenuating the onset of renal injury in early hypertensive nephrosclerosis, and that treatment with either agent is associated with a transient decrease in AT2 receptor mRNA expression.  (+info)

Expression of decorin, biglycan, and collagen type I in human renal fibrosing disease. (6/143)

BACKGROUND: The extracellular matrix proteoglycans decorin and biglycan may have a pathogenic role in renal fibrosing disease via regulation of the activity of growth factors, such as transforming growth factor-beta, and effects on collagen type I fibrillogenesis. The expression of decorin and biglycan in human glomerular diseases characterized by mesangial sclerosis is unknown. METHODS: Decorin, biglycan, and collagen type I were localized immunohistochemically in human renal biopsy cases of amyloidosis (N = 18), diabetic nephropathy (N = 11), fibrillary glomerulonephritis (N = 5), immunotactoid glomerulopathy (N = 5), light-chain deposition disease (N = 4), idiopathic mesangial sclerosis (N = 4), and nephrosclerosis (N = 6), and in morphologically normal tissues obtained from tumor nephrectomies (N = 8). Decorin and biglycan mRNA synthesis was evaluated by in situ hybridization. RESULTS: Decorin and biglycan protein were not identified in normal glomeruli. Decorin accumulated in amyloid deposits, but not in deposits of fibrillary glomerulonephritis or immunotactoid glomerulopathy. Biglycan weakly accumulated in amyloid deposits, and both decorin and biglycan weakly stained mesangial nodules in cases of morphologically advanced light-chain deposition disease and diabetic nephropathy. In all analyzed cases, irrespective of the underlying disease, decorin and biglycan accumulated in glomeruli in areas of fibrous organization of the urinary space and in areas of tubulointerstitial fibrosis. Biglycan, but not decorin, accumulated in the neointima of arteriosclerotic blood vessels. Decorin and biglycan mRNA synthesis was detected at sites of proteoglycan accumulation in glomeruli, interstitium, and neointima. Collagen type I colocalized with decorin and biglycan deposits. CONCLUSIONS: Differences in extracellular matrix proteoglycan composition may be diagnostically useful in distinguishing morphologically similar diseases. Distinct patterns of proteoglycan expression may be related to modulation of specific growth factor activity in different glomerular diseases.  (+info)

What is 'nephrosclerosis'? lessons from the US, Japan, and Mexico. (7/143)

BACKGROUND: Selected features of 'nephrosclerosis' can be quantitated morphometrically in renal histology at autopsy. Specimens are available from Japan, Mexico, and the US (blacks and whites). METHODS: Autopsies of men and women aged 15-79 years provided renal samples for paraffin sectioning. These were assembled in New Orleans for objective evaluation after standardized staining with PAS-Alcian blue and interspersion with each other. Obsolescence of glomeruli, interstitial fibrosis, fibroplastic intimal thickenings of arteries, and arteriolar hyalinization, as operationally defined, were measured by objective morphometry. RESULTS: Obsolescence of glomeruli and interstitial fibrosis displayed the expected correlation with arterial intimal fibroplasia, but failed to confirm any direct association with arteriolar hyalinization. Some of the variation of 'nephrosclerosis', within and between populations, cannot be fully explained by microvascular defects. CONCLUSIONS: Arterial intimal fibroplasia appeared to promote 'nephrosclerosis', in the sense of fibrous replacement of atrophied nephrons, but arteriolar hyalinization did not. Hyaline deposits in arterioles may offer little or no threat to the integrity of the affected nephrons. 'Nephrosclerosis' appears to be multifactorial; it may be, in part, a consequence of fibroplasia in microscopic arteries causing ischaemic injury to scattered nephrons, but may also be a confluence of basically separate conditions, only some of which are known.  (+info)

Induction of apoptosis during development of hypertensive nephrosclerosis. (8/143)

BACKGROUND: As the biology of programmed cell death, or apoptosis, is clarified, a role for this process in the pathophysiology of organ dysfunction and fibrosis has been hypothesized. Hypertensive nephrosclerosis represents an important cause of end-stage renal disease. One model of the progressive, noninflammatory, sclerotic renal lesion of hypertension is the Dahl/Rapp salt-sensitive rat, which was examined in this study. METHODS: Male, Dahl/Rapp salt-sensitive (SS) and Sprague-Dawley rats were placed on either 0.3 or 8.0% NaCl diets for three weeks. Blood pressure was determined, and the kidneys were harvested for histochemical analysis and to obtain total RNA for RNase protection assays and total protein for Western blotting. RESULTS: An increase in apoptosis in the glomerular and tubular compartments was observed only in kidneys of SS rats on the high-salt diet. These findings occurred at a time when renal function was markedly impaired and irreversible changes in renal morphology developed. Temporally associated with this increase in apoptosis was augmented expression of pro-apoptotic molecules that included Fas, Bax, and Bcl-XS. CONCLUSIONS: The inappropriate shift in expression of proteins that facilitate apoptosis in the nephron, along with ongoing cell death that manifested at a time when renal function was deteriorating, supported an important role for this process in development of hypertensive nephrosclerosis.  (+info)

Nephrosclerosis is a medical term that refers to the thickening and scarring (fibrosis) of the small arteries and arterioles in the kidneys, resulting in reduced blood flow and damage to the kidney tissue. This process can lead to decreased kidney function and ultimately result in chronic kidney disease or end-stage renal failure.

The two main types of nephrosclerosis are:

1. Hypertensive nephrosclerosis: This type is caused by long-term high blood pressure (hypertension), which damages the small blood vessels in the kidneys over time, leading to scarring and thickening of the arterial walls.
2. Ischemic nephrosclerosis: This type results from reduced blood flow to the kidneys due to atherosclerosis or other vascular diseases that cause narrowing or blockage of the renal arteries.

Nephrosclerosis is often asymptomatic in its early stages, but as the condition progresses, it may lead to symptoms such as proteinuria (protein in the urine), hematuria (blood in the urine), edema (swelling), and hypertension. Diagnosis typically involves a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment focuses on managing underlying conditions such as high blood pressure and diabetes, which can help slow or prevent further kidney damage.

Renal hypertension, also known as renovascular hypertension, is a type of secondary hypertension (high blood pressure) that is caused by narrowing or obstruction of the renal arteries or veins, which supply blood to the kidneys. This can lead to decreased blood flow and oxygen delivery to the kidney tissue, activating the renin-angiotensin-aldosterone system (RAAS) and resulting in increased peripheral vascular resistance, sodium retention, and extracellular fluid volume, ultimately causing hypertension.

Renal hypertension can be classified into two types:

1. Renin-dependent renal hypertension: This is caused by a decrease in blood flow to the kidneys, leading to increased renin release from the juxtaglomerular cells of the kidney. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that causes an increase in peripheral vascular resistance and blood pressure.
2. Renin-independent renal hypertension: This is caused by increased sodium retention and extracellular fluid volume, leading to an increase in blood pressure. This can be due to various factors such as obstructive sleep apnea, primary aldosteronism, or pheochromocytoma.

Renal hypertension is often asymptomatic but can lead to serious complications such as kidney damage, heart failure, and stroke if left untreated. Diagnosis of renal hypertension involves imaging studies such as renal artery duplex ultrasound, CT angiography, or magnetic resonance angiography (MRA) to identify any narrowing or obstruction in the renal arteries or veins. Treatment options include medications such as ACE inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers, and diuretics, as well as interventions such as angioplasty and stenting to improve blood flow to the kidneys.

Malignant hypertension is a severe form of hypertension (high blood pressure) that is characterized by extremely high blood pressure readings, typically greater than 180/120 mmHg, along with evidence of damage to one or more organ systems. This condition is considered a medical emergency and requires immediate treatment.

Malignant hypertension can cause rapid and severe damage to various organs in the body, including the brain, heart, kidneys, and eyes. Symptoms may include severe headache, visual disturbances, confusion, shortness of breath, chest pain, nausea, vomiting, seizures, and even coma.

The exact cause of malignant hypertension is not always known, but it can be associated with certain underlying medical conditions such as kidney disease, autoimmune disorders, pregnancy-related complications, or the use of certain medications. Treatment typically involves aggressive blood pressure control using intravenous medications in a hospital setting, along with management of any underlying conditions and prevention of further organ damage.

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.

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.

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.

Hypertension is a medical term used to describe abnormally high blood pressure in the arteries, often defined as consistently having systolic blood pressure (the top number in a blood pressure reading) over 130 mmHg and/or diastolic blood pressure (the bottom number) over 80 mmHg. It is also commonly referred to as high blood pressure.

Hypertension can be classified into two types: primary or essential hypertension, which has no identifiable cause and accounts for about 95% of cases, and secondary hypertension, which is caused by underlying medical conditions such as kidney disease, hormonal disorders, or use of certain medications.

If left untreated, hypertension can lead to serious health complications such as heart attack, stroke, heart failure, and chronic kidney disease. Therefore, it is important for individuals with hypertension to manage their condition through lifestyle modifications (such as healthy diet, regular exercise, stress management) and medication if necessary, under the guidance of a healthcare professional.

SHR (Spontaneously Hypertensive Rats) are an inbred strain of rats that were originally developed through selective breeding for high blood pressure. They are widely used as a model to study hypertension and related cardiovascular diseases, as well as neurological disorders such as stroke and dementia.

Inbred strains of animals are created by mating genetically identical individuals (siblings or offspring) for many generations, resulting in a population that is highly homozygous at all genetic loci. This means that the animals within an inbred strain are essentially genetically identical to one another, which makes them useful for studying the effects of specific genes or environmental factors on disease processes.

SHR rats develop high blood pressure spontaneously, without any experimental manipulation, and show many features of human hypertension, such as increased vascular resistance, left ventricular hypertrophy, and renal dysfunction. They also exhibit a number of behavioral abnormalities, including hyperactivity, impulsivity, and cognitive deficits, which make them useful for studying the neurological consequences of hypertension and other cardiovascular diseases.

Overall, inbred SHR rats are an important tool in biomedical research, providing a valuable model for understanding the genetic and environmental factors that contribute to hypertension and related disorders.

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.

Angiotensin-Converting Enzyme (ACE) inhibitors are a class of medications that are commonly used to treat various cardiovascular conditions, such as hypertension (high blood pressure), heart failure, and diabetic nephropathy (kidney damage in people with diabetes).

ACE inhibitors work by blocking the action of angiotensin-converting enzyme, an enzyme that converts the hormone angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor, meaning it narrows blood vessels and increases blood pressure. By inhibiting the conversion of angiotensin I to angiotensin II, ACE inhibitors cause blood vessels to relax and widen, which lowers blood pressure and reduces the workload on the heart.

Some examples of ACE inhibitors include captopril, enalapril, lisinopril, ramipril, and fosinopril. These medications are generally well-tolerated, but they can cause side effects such as cough, dizziness, headache, and elevated potassium levels in the blood. It is important for patients to follow their healthcare provider's instructions carefully when taking ACE inhibitors and to report any unusual symptoms or side effects promptly.

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.

Renal dialysis is a medical procedure that is used to artificially remove waste products, toxins, and excess fluids from the blood when the kidneys are no longer able to perform these functions effectively. This process is also known as hemodialysis.

During renal dialysis, the patient's blood is circulated through a special machine called a dialyzer or an artificial kidney, which contains a semi-permeable membrane that filters out waste products and excess fluids from the blood. The cleaned blood is then returned to the patient's body.

Renal dialysis is typically recommended for patients with advanced kidney disease or kidney failure, such as those with end-stage renal disease (ESRD). It is a life-sustaining treatment that helps to maintain the balance of fluids and electrolytes in the body, prevent the buildup of waste products and toxins, and control blood pressure.

There are two main types of renal dialysis: hemodialysis and peritoneal dialysis. Hemodialysis is the most common type and involves using a dialyzer to filter the blood outside the body. Peritoneal dialysis, on the other hand, involves placing a catheter in the abdomen and using the lining of the abdomen (peritoneum) as a natural filter to remove waste products and excess fluids from the body.

Overall, renal dialysis is an essential treatment option for patients with kidney failure, helping them to maintain their quality of life and prolong their survival.

... alone hardly ever causes severe damage to the kidney, except in susceptible populations, such as African ... Benign nephrosclerosis refers to the renal changes most commonly occurring in association with long-standing hypertension. It ... In advanced cases of benign nephrosclerosis the glomerular tufts may become globally sclerosed. Diffuse tubular atrophy and ...
Malignant nephrosclerosis is where hypertensive nephrosclerosis occurs in presence of malignant hypertension (when DBP > ... The majority of patients with benign nephrosclerosis have proteinuria in the range from 0.5 to 1 g/ 24hr. In the case of ... The tissue hardens and thickens which is known as nephrosclerosis. The narrowing of the blood vessels means less blood is going ... "Benign Hypertensive Arteriolar Nephrosclerosis". MSD Manual Consumer Version. Retrieved 2016-11-12. Guenevere Rae, Ph.D., ...
Ono H, Ono Y (November 1997). "Nephrosclerosis and hypertension". The Medical Clinics of North America. 81 (6): 1273-88. doi: ... the dilemma of nephrosclerosis". Kidney International Supplements. 68 (99): S52-6. doi:10.1111/j.1523-1755.2005.09910.x. PMID ...
O'Brien died on November 17, 1955 due to nephrosclerosis. "Tommy O'Brien NBL stats". basketball-reference.com. Sports Reference ...
with Paul Kimmelstiel: Kimmelstiel, P.; Wilson, C. (January 1936). "Benign and Malignant Hypertension and Nephrosclerosis: A ...
... hypertensive nephrosclerosis, heart failure, polycystic kidney disease, chronic kidney disease, interstitial fibrosis, focal ... "Reversible renal insufficiency due to angiotensin converting enzyme inhibitors in hypertensive nephrosclerosis". Annals of ...
He was also found to have chronic nephrosclerosis, or degeneration of the kidneys. Opera singer Birgit Nilsson painfully passed ...
Malformations of the urinary tract and nephrosclerosis are absent and vesicoureteral reflux is insignificant. Unlike segmental ...
The official cause on his death certificate is "nephrosclerosis and hypertension," contributed by "Chronic myocarditis". His ...
The strain on Bulgakov leads to an intensification of his inherited disease, nephrosclerosis, and his eventual death. The play ...
... nephrosclerosis and veno-occlusive disease. High density of cheetahs in a place, closeness to other large carnivores in ...
... basis and natural history of essential hypertension and pointed out that this disease could terminate with nephrosclerosis and ...
... nephrosclerosis, residual hypertension and diabetes, worsened by chronic kidney deficiency. A four-day period of mourning ...
Hyaline arteriolosclerosis is a major morphologic characteristic of benign nephrosclerosis, in which the arteriolar narrowing ...
... familial with gout Nephrosclerosis Nephrosis deafness urinary tract digital malformation Nephrosis neuronal dysmigration ...
... nephrosclerosis MeSH C12.777.419.630 - nephrosis MeSH C12.777.419.630.477 - nephrosis, lipoid MeSH C12.777.419.630.643 - ...
Hypertensive nephrosclerosis HIV Obesity Kidney loss Minimal change disease (MCD) Drugs, especially NSAIDs in the elderly ...
Aminoaciduria Fanconi syndrome in association with Wilson disease Hypertensive nephrosclerosis Interstitial nephritis Sickle ...
Benign nephrosclerosis alone hardly ever causes severe damage to the kidney, except in susceptible populations, such as African ... Benign nephrosclerosis refers to the renal changes most commonly occurring in association with long-standing hypertension. It ... In advanced cases of benign nephrosclerosis the glomerular tufts may become globally sclerosed. Diffuse tubular atrophy and ...
... hypertensive nephrosclerosis (HN) accounted for 28% of patients reaching end-stage renal disease (ESRD). The rate of ESRD ... encoded search term (Nephrosclerosis) and Nephrosclerosis What to Read Next on Medscape ... part of the confusion in the classification of hypertensive nephrosclerosis stems from the use of the word nephrosclerosis. [2 ... the terms hypertensive nephrosclerosis, benign nephrosclerosis, and nephroangiosclerosis are commonly used to describe the same ...
mild benign nephrosclerosis is present at autopsy in many persons > 60 years of age. Slideshow 1936470 by reia ... Benign Nephrosclerosis. Definition: renal changes in benign hypertension It is always associated with hyaline ... Benign Nephrosclerosis. An Image/Link below is provided (as is) to download presentation Download Policy: Content on the ... mild benign nephrosclerosis is present at autopsy in many persons , 60 years of age. • The frequency and severity of the ...
Blood pressure is the force of the blood as it flows through the blood vessels and the heart. Hypertension or high blood pressure is defined as blood pressure consistently exceeding 140/90mmHg when the person is at rest. Factors that can cause high blood pressure are having extra fluid in the blood and blood vessels that are narrow, stiff, or clogged.. High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. They may then be unable to remove waste and extra fluid from the body. Extra fluid in the blood vessels may further increase blood pressure even more, creating a vicious cycle that could damage the kidneys.. Over 1 in 3* Singaporean adults have hypertension. Hypertension can be broadly divided into two types: In essential Hypertension (95% of all cases of Hypertension), strong genetic and environmental factors lead to Hypertension. In secondary Hypertension (5% of all cases of HBP), an identifiable cause exists such as kidney disease, endocrine ...
Hypertensive Arteriolar Nephrosclerosis - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the MSD ... However, because chronic hypertension and hypertensive nephrosclerosis are common, hypertensive arteriolar nephrosclerosis is ... Symptoms and Signs of Hypertensive Arteriolar Nephrosclerosis Symptoms and signs of chronic kidney disease Symptoms and Signs ... Hypertensive arteriolar nephrosclerosis results when chronic hypertension Hypertension Hypertension is sustained elevation of ...
A 78-year-old man with renal insufficiency, who had been diagnosed with diabetic nephrosclerosis by renal biopsy 9 months ... A 78-year-old man with renal insufficiency, who had been diagnosed with diabetic nephrosclerosis by renal biopsy 9 months ... A 78-year-old man with renal insufficiency, who had been diagnosed with diabetic nephrosclerosis by renal biopsy 9 months ... A 78-year-old man with renal insufficiency, who had been diagnosed with diabetic nephrosclerosis by renal biopsy 9 months ...
Nephrosclerosis, arteriolar. 7507 Neuralgia: Cranial Nerves Fifth (trigeminal). 8405 Seventh (facial). 8407 ...
malignant hypertension (arteriolar nephrosclerosis). *poisoning due to black widow spider venom (black widow spider bites) ...
Toto RD: Hypertensive nephrosclerosis in African Americans. Kidney Int 2003, 64:2331-2341. ... Black Americans are at higher risk for developing hypertensive nephrosclerosis than whites. Hypertension is a major risk factor ...
Nephrosclerosis * Nephrotic Syndrome * Nephrotoxicity * Obesity Related Glomerulopathy * Pauci Immune Glopmerulonephritis * ...
The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries ... The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries ... benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were ... benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were ...
Porphyria syndrome associated with diabetic nephrosclerosis and erythropoietin. Compr Ther. 2006. 32(3):163-71. [QxMD MEDLINE ...
Hypertensive nephrosclerosis: A condition where chronic high blood pressure damages the kidneys tissue ...
Malignant Nephrosclerosis *- Patients with malignant hypertension ( BP gt 160/100 mm Hg) ...
Benign Hypertensive Arteriolar Nephrosclerosis. Blockage of the Renal Arteries. Cortical Necrosis of the Kidneys ...
nephrosclerosis. nephrosclerosis, hardening of the walls of the small arteries and arterioles (small arteries that convey blood ...
Nephrosclerosis;, etc. It are those images which Is the t response of their Cookies with its few dementia alcoholism. HTTP 500 ...
Partnership Arising From Mentorship Program Generates Investigation Into Hypertensive Nephrosclerosis Using Digital Spatial ...
Hypertensive Nephrosclerosis in African- Americans (AASK Study). History of Nephrology. BK Nephropathy in Post-Transplant ...
They can have kidney problems that include hardening of the kidneys (nephrosclerosis) and urine accumulation in the kidneys ( ...
Larger nephron size and nephrosclerosis predict progressive CKD and mortality after radical nephrectomy for tumor and ...
It can be labelled as primary malignant nephrosclerosis (NScl) or atypical HUS, based on primary thrombotic angiopathy. This, ...
A.D.A.M. content is best viewed in IE9 or above, Firefox and Google Chrome browser ...
Small kidneys usually indicate chronic, irreversible damage from diseases such as hypertensive nephrosclerosis, ischemic ...
Accelerated hypertension; Arteriolar nephrosclerosis; Nephrosclerosis - arteriolar; Hypertension - malignant; High blood ...
A. D. Rule, H. Amer, L. D. Cornell et al., "The association between age and nephrosclerosis on renal biopsy among healthy ...
However, nephrosclerosis was less common as the causative condition in Wakayama than in all Japan. The proportions of the ... Need for Education on the Differential Diagnosis between Chronic Glomerulonephritis and Nephrosclerosis, and Treatment of both ... Accordingly, some patients diagnosed with chronic glomerulonephritis might actually have nephrosclerosis, or treatment may be ... it is important to accurately differentiate between chronic glomerulonephritis and nephrosclerosis, and also to treat patients ...
  • The term hypertensive nephrosclerosis has traditionally been used to describe a clinical syndrome characterized by long-term essential hypertension , hypertensive retinopathy, left ventricular hypertrophy, minimal proteinuria , and progressive kidney failure. (medscape.com)
  • In fact, most of the literature dedicated to hypertensive nephrosclerosis is based on the assumption that progressive kidney failure in a patient with long-standing hypertension, moderate proteinuria, and no evidence suggesting an alternative diagnosis characterizes hypertensive nephrosclerosis. (medscape.com)
  • The lack of firm criteria on which to base a histologic diagnosis and the lack of a clear demonstration that hypertension initiates the development of kidney failure likely indicate that the true prevalence of hypertensive nephrosclerosis has been overestimated. (medscape.com)
  • Indeed, Carriazo et al suggest that hypertensive nephrosclerosis as a cause of end-stage renal disease (ESRD) may not exist at all. (medscape.com)
  • As reported by Zuccalà and Zucchelli (1996), part of the confusion in the classification of hypertensive nephrosclerosis stems from the use of the word nephrosclerosis. (medscape.com)
  • In the United States and Europe, the terms hypertensive nephrosclerosis, benign nephrosclerosis, and nephroangiosclerosis are commonly used to describe the same clinical condition. (medscape.com)
  • Hypertensive arteriolar nephrosclerosis is progressive renal impairment caused by chronic, poorly controlled hypertension. (msdmanuals.com)
  • Hypertensive arteriolar nephrosclerosis progresses to end-stage renal disease in only a small percentage of patients. (msdmanuals.com)
  • However, because chronic hypertension and hypertensive nephrosclerosis are common, hypertensive arteriolar nephrosclerosis is one of the most common diagnoses in patients with end-stage renal disease. (msdmanuals.com)
  • Black Americans are at higher risk for developing hypertensive nephrosclerosis than whites. (springer.com)
  • Small kidneys usually indicate chronic, irreversible damage from diseases such as hypertensive nephrosclerosis, ischemic nephropathy, or any other long-standing kidney disease. (medscape.com)
  • A 73-year-old male with a history of hypertensive nephrosclerosis leading to terminal chronic renal insufficiency and renal allograft underwent his annual skin checkup in our clinic. (karger.com)
  • After more than 30 girls were full and washed, Mr. called which bp medicine also has hctz the five carriages prepared by the village head and began hypertensive nephrosclerosis treatment to transport people to the county, including the pile of human traffickers tied into rice dumplings. (therug.ru)
  • hypertensive nephrosclerosis treatment kept asking why, but why, that was the secret that Sir hid in the coldest corner of his heart, it can drug abuse cause pulmonary hypertension was his wife, he would not tell it, so he had no choice but to say With a stubborn mouth, he dared to say no, and dealt with Mrs. Xu But who would. (therug.ru)
  • As soon as I was mentioned, Madam's raised eyebrows fell again For Mr. if Mr was worth fearing, then my was definitely a level of fear hypertensive nephrosclerosis treatment After working together for these years, Madam really knows the temper of Old Yandai. (therug.ru)
  • Recently, we have shown that treatment of stroke-prone spontaneously hypertensive rats with angiotensin inhibitors for a limited time-window before puberty results in an attenuation of hypertensive nephrosclerosis in later life. (elsevierpure.com)
  • A review of comorbid atherosclerotic disease in 7,200 end-stage renal disease patients indicated that occlusive disease of the renal arteries may contribute to progressive renal failure in 1.34% of the US dialysis population or in 14% of the Caucasian patients with hypertensive nephrosclerosis. (elsevierpure.com)
  • These changes are related to benign nephrosclerosis in hypertensive patients. (rahulgladwin.com)
  • Benign nephrosclerosis refers to the renal changes most commonly occurring in association with long-standing hypertension. (wikipedia.org)
  • In advanced cases of benign nephrosclerosis the glomerular tufts may become globally sclerosed. (wikipedia.org)
  • Benign nephrosclerosis alone hardly ever causes severe damage to the kidney, except in susceptible populations, such as African Americans, where it may lead to uremia and death. (wikipedia.org)
  • many renal diseases cause hypertension which in turn is associated with benign nephrosclerosis. (slideserve.com)
  • He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. (unboundmedicine.com)
  • The kidney showed benign nephrosclerosis due to arteriolosclerosis. (unboundmedicine.com)
  • Nephrectomy is also performed to treat malignant or benign tumors of the kidney, renovascular hypertention due to uncorrectable renal artery disease, or severe unilateral parenchymal damage from nephrosclerosis, pyelonephritis, reflux, or congenital dysplasia. (urotoday.com)
  • He argues that the use of the term nephrosclerosis to classify a patient with kidney failure leads to the possibility of an overlooked nephropathy complicated by hypertension and to the mistaken belief that drastic blood pressure control may retard progression to ESRD. (medscape.com)
  • A review of the literature showed several cases of necrotizing glomerulonephritis superimposed on diabetic nephropathy but only a few reported cases of MPO-ANCA glomerulonephritis associated with diabetic nephrosclerosis. (elsevierpure.com)
  • [ 2 ] Coined almost a century ago by Theodor Fahr, nephrosclerosis literally means "hardening of the kidney. (medscape.com)
  • They can have kidney problems that include hardening of the kidneys (nephrosclerosis) and urine accumulation in the kidneys (hydronephrosis), which can impair kidney function. (medlineplus.gov)
  • Myeloperoxidase-antineutrophil cytoplasmic antibody-associated glomerulonephritis superimposed on biopsy-proven diabetic nephrosclerosis. (elsevierpure.com)
  • We present a case of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-associated glomerulonephritis with diabetic nephrosclerosis, diagnosed by serial renal biopsies within a short period. (elsevierpure.com)
  • Dive into the research topics of 'Myeloperoxidase-antineutrophil cytoplasmic antibody-associated glomerulonephritis superimposed on biopsy-proven diabetic nephrosclerosis. (elsevierpure.com)
  • It can be labelled as primary malignant nephrosclerosis (NScl) or atypical HUS, based on primary thrombotic angiopathy. (jpgmonline.com)
  • The consequences of the markedly elevated blood pressure on the blood vessels throughout the body are known as malignant arteriolosclerosis, and the renal disorder is referred to as malignant nephrosclerosis. (slideserve.com)
  • In a 2015 review, Meyrier cites clinical and experimental evidence that nephrosclerosis, especially in blacks, can be explained by a genetic renovasculopathy that precedes the rise in blood pressure. (medscape.com)
  • Nephrosclerosis leads to renal ISCHEMIA. (mcw.edu)
  • Benign nephrosclerosis refers to the renal changes most commonly occurring in association with long-standing hypertension. (wikipedia.org)
  • Hypertensive arteriolar nephrosclerosis is progressive renal impairment caused by chronic, poorly controlled hypertension. (msdmanuals.com)
  • However, because chronic hypertension and hypertensive nephrosclerosis are common, hypertensive arteriolar nephrosclerosis is one of the most common diagnoses in patients with end-stage renal disease. (msdmanuals.com)
  • Benign arteriolar nephrosclerosis is closely related to primary hypertension. (journalofchinesemedicine.com)
  • CONCLUSIONS: Untreated high-grade hypertension and severe "benign'' nephrosclerosis represent a microvascular ischemic nephropathy (similar to critical bilateral RAS) in which a relatively minor insult can deteriorate the patient into ESRD.While being non-adherent to different anti hypertensive medications, patient did take omeprazole which triggered acute interstitial nephritis on the background of advanced ischemic nephropathy, leading to permanent loss of renal function. (bgu.ac.il)
  • Hypertension-cardiac hypertrophy-nephrosclerosis. (nih.gov)
  • Hypertensive renal disease is due to the presence of chronic hypertension leading to nephrosclerosis and renal damage. (elitelearning.com)
  • Hypertensive arteriolar nephrosclerosis progresses to end-stage renal disease in only a small percentage of patients. (msdmanuals.com)
  • Diabetic nephropathy , a common sequela of diabetes mellitus, is manifested as severe arteriolar nephrosclerosis, glomerulosclerosis, and acute or chronic pyelonephritis. (pharmacology2000.com)
  • The patient had acute kidney injury with hematuria and proteinuria, and kidney biopsy showed hypertensive arteriolar nephrosclerosis and fibrinoid arteriolar necrosis consistent with thrombotic microangiopathy. (amjcaserep.com)
  • Renal tubular lysosomal enzyme activities like alanine aminopeptidase (AAP) and N-acetyl- -D-glucosaminidase (NAG) have been shown to increase in patients developing diabetic nephropathy and nephrosclerosis. (hindawi.com)
  • Diabetic nephropathy (DN) and nephrosclerosis are clinical conditions characterized by persistent albuminuria, arterial blood pressure elevation, and an increasing decline in glomerular filtration rate (GFR) [ 1 - 4 ]. (hindawi.com)
  • According to the studies, nephrosclerosis is the most frequent nephropathy. (scirp.org)
  • Besides HIV-associated nephropathy, a number of different types of immune complex and non-immune complex-mediated processes have been identified on kidney biopsies, including vascular disease (nephrosclerosis), diabetes, and drug-related renal injury. (elsevierpure.com)
  • for example, a lower volume of the cortex in relation to the medulla is indicative of poor glomerular function, CKD, aging, and potential nephrosclerosis. (nih.gov)
  • Died of gastro-intestinal haemorrhage with nephrosclerosis and hypertensive vascular disease. (edu.au)
  • A total of 918 patients (19%) had biopsy-verified hypertensive nephrosclerosis (i.e., arterionephrosclerosis). (uib.no)
  • The most common biopsy-verified diagnoses in patients fulfilling the clinical criteria for hypertensive nephrosclerosis were arterionephrosclerosis (40%), glomerulonephritis (22%), and interstitial nephritis (14%), reflecting that the criteria had low sensitivity (0.17) and high specificity (0.94). (uib.no)
  • We hypothesized that TLS-associated inflammatory gene signatures are present in AIN and performed NanoString-based gene expression and multiplex 12-chemokine profiling on paired kidney tissue, urine and plasma specimens of 36 participants who developed acute kidney injury (AKI) on ICI therapy: AIN (18), acute tubular necrosis (9), or HTN nephrosclerosis (9). (jci.org)
  • Arterionephrosclerosis is a high-risk disease, often with an atypical phenotype with proteinuria and hematuria contributing to low accuracy for current clinical criteria for hypertensive nephrosclerosis. (uib.no)
  • The death certificate, completed by the Medical Examiner, and the autopsy, completed by the Forensic Pathologist, listed "oxycodone intoxication" as the cause of death with "mild thickening of the mitral valve" and "mild diffuse nephrosclerosis" as other conditions. (cdc.gov)
  • There were also changes consistent with mild nephrosclerosis. (blogspot.com)
  • The outcome of chronic pyelonephritis depends on the presence and degree of violation of the outflow of urine from the renal pelvis: with normal passage of urine, nephrosclerosis (shrunken kidney) develops, with stasis of urine-pionephrosis. (ed-pillsss.com)
  • November 10, 2008 (Philadelphia, Pennsylvania) - African Americans with hypertensive nephrosclerosis (chronic kidney disease [CKD] caused by high blood pressure [BP]) have a higher risk of progressing to end-stage renal disease (ESRD) than of dying from a cardiovascular event. (medscape.com)
  • 2. Intrarenal expression of miRNAs in patients with hypertensive nephrosclerosis. (nih.gov)
  • Hypertensive nephrosclerosis is considered the second most common cause of end-stage renal disease (ESRD), but it is still an insufficiently studied and controversial disease entity. (uib.no)
  • To identify risk factors for nephrosclerosis in a hypertensive patient. (medicalalgorithms.com)
  • The risk for nephrosclerosis increases if certain factors are present in a hypertensive patient. (medicalalgorithms.com)
  • The more risk factors that are present, the greater the risk that the patient will develop nephrosclerosis. (medicalalgorithms.com)