diabetic nephropathy

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nephropathy

 [nĕ-frop´ah-the]
1. any disease of the kidneys. adj., adj nephropath´ic.
2. any disease of the kidneys; see also nephritis. Called also nephrosis. adj., adj nephropath´ic.
AIDS nephropathy former name for HIV-associated nephropathy.
analgesic nephropathy interstitial nephritis with renal papillary necrosis, seen in patients with a history of abuse of analgesics such as aspirin or acetaminophen alone or in combination.
diabetic nephropathy the nephropathy that commonly accompanies later stages of diabetes mellitus; it begins with hyperfiltration, renal hypertrophy, microalbuminuria, and hypertension; in time proteinuria develops, with other signs of decreasing function leading to end-stage renal disease.
gouty nephropathy any of a group of chronic kidney diseases associated with the abnormal production and excretion of uric acid.
heavy metal nephropathy the kidney damage resulting from any of various forms of heavy metal poisoning, usually in the form of tubulointerstitial nephritis. The most common metals involved are cadmium, lead, and mercury.
HIV-associated nephropathy renal pathology in patients infected with the human immunodeficiency virus, similar to focal segmental glomerulosclerosis, with proteinuria, enlarged kidneys, and dilated tubules containing proteinaceous casts; it may progress to end-stage renal disease within weeks.
hypokalemic nephropathy nephropathy with hypokalemia, interstitial nephritis, swelling and vacuolization of proximal renal tubules, and progressive renal failure, resulting from conditions such as oncotic overloading of the kidney filtration mechanisms by sugars. See also potassium-losing nephropathy.
IgA nephropathy a chronic form marked by hematuria and proteinuria and by deposits of IgA immunoglobulin in the mesangial areas of the renal glomeruli, with subsequent reactive hyperplasia of mesangial cells. Called also Berger's disease and IgA glomerulonephritis.
ischemic nephropathy nephropathy resulting from partial or complete obstruction of a renal artery with ischemia, accompanied by a significant reduction in the glomerular filtration rate.
lead nephropathy the kidney damage that accompanies lead poisoning; lead deposits appear in the epithelium of the proximal tubules and as nuclear inclusions in cells. In time this leads to tubulointerstitial nephritis with chronic renal failure and other symptoms.
membranous nephropathy membranous glomerulonephritis.
minimal change nephropathy minimal change disease.
obstructive nephropathy nephropathy caused by obstruction of the urinary tract (usually the ureter), with hydronephrosis, slowing of the glomerular filtration rate, and tubular abnormalities.
potassium-losing nephropathy hypokalemic nephropathy after persistent potassium loss; it may be seen in metabolic alkalosis, adrenocortical hormone excess, or in intrinsic renal disease such as renal tubular acidosis or hyperplasia of juxtaglomerular cells. Called also potassium-losing nephritis.
reflux nephropathy childhood pyelonephritis in which the renal scarring results from vesicoureteric reflux, with radiological appearance of intrarenal reflux.
salt-losing nephropathy intrinsic renal disease causing abnormal urinary sodium loss in persons ingesting normal amounts of sodium chloride, with vomiting, dehydration, and vascular collapse. Called also salt-losing nephritis.
urate nephropathy (uric acid nephropathy) any of a group of kidney diseases occurring in patients with hyperuricemia, including an acute form, a chronic form (gouty nephropathy), and nephrolithiasis with formation of uric acid calculi.

diabetic nephropathy

a syndrome characterized by albuminuria, hypertension, and progressive renal insufficiency.

Diabetic nephropathy is a major cause of morbidity and mortality in people with diabetes mellitus (DM). Patients with DM make up the largest number (50%) of those who start renal dialysis for end-stage renal disease (ESRD) each year in the U.S. The prevalence of ESRD approaches 50% among people who have had Type 1 DM for 20 years. The risk of diabetic nephropathy is higher in males, blacks, Hispanics, and Native Americans. Within 3 years after the diagnosis of DM is made, histologic study shows thickening of glomerular basement membrane, capsular drop deposits, and mesangial proliferation, changes characteristic of diabetic glomerulosclerosis (Kimmelstiel-Wilson disease). The kidneys increase in size and weight because of both hypertrophy and hyperplasia of parenchymal cells, and renal blood flow and glomerular filtration rate (GFR) are increased; as a result, serum creatinine and urea nitrogen levels are slightly reduced. After 10-15 years, the first evidence of renal damage may appear as microalbuminuria, a persistent excretion of albumin in concentrations not detected by routine tests for urinary protein. An albumin excretion rate of 20-200 mcg/min (30-300 mg/day) heralds the onset of diabetic nephropathy and strongly predicts eventual ESRD. Further progression of renal damage leads to frank albuminuria and a decline in glomerular filtration rate and nitrogen clearance. The prevalence of hypertension is markedly greater in people with microalbuminuria, and hypertension accelerates the progression of renal disease. Diabetic nephropathy can lead to hyperkalemia, metabolic acidosis, nephrotic syndrome, papillary necrosis, and increased susceptibility to acute renal failure after exposure to radiographic contrast media. The onset of microalbuminuria indicates increased risk of cardiovascular disease; myocardial infarction and stroke are statistically more likely to cause death than renal disease in people with microalbuminuria. Current practice guidelines for the treatment of DM call for annual assessment of 24-hour albumin excretion, prompt treatment of urinary tract infections, and avoidance of nephrotoxic drugs (including nonsteroidal antiinflammatory drugs and COX-2 inhibitors) and radiographic dyes. No interventions have been shown to reverse clinical diabetic nephropathy. However, prospective randomized studies have established that improved metabolic control, maintaining plasma glucose as near normal as possible at all times, can markedly retard the development and progression of diabetic nephropathy, as well as of other long-term microvascular complications of diabetes (retinopathy and neuropathy). In addition, aggressive management of hypertension with ACE inhibitors or angiotensin II receptor blockers has been shown to delay progression of nephropathy by mechanisms independent of blood pressure control, and limitation of daily protein intake to 0.8 g/kg of body weight (not appropriate in pregnancy) has been shown to delay progression of both diabetic and nondiabetic renal disease. ESRD is treated with kidney transplantation, hemodialysis, or peritoneal dialysis. Because diabetic retinopathy and neuropathy progress more rapidly with the onset of renal failure, dialysis is usually instituted early (when serum creatinine reaches about 6 mg/dL) in diabetic nephropathy.

diabetic nephropathy

Diabetic kidney disease The constellation of renal changes attributed to DM–eg Armanni-Ebstein lesion, arterionephrosclerosis, arteriolonephrosclerosis, chronic interstitial nephritis, diabetic glomerulosclerosis, fatty changes in renal tubules, glomerulonephritis, Kimmelstiel-Wilson disease—focal and segmental glomerulosclerosis, nephrotic syndrome, papillary necrosis, and pyelonephritis; DN is the most common cause of ESRD in the West Diagnosis Microalbuminuria Management Antihypertensives–eg, ACE inhibitors–eg, captopril, protect kidneys against further deterioration in type 1 DM, and a 50% ↓ risk in end points–death, dialysis, and transplantation; if renal failure is in an early stage, the Pts are good transplant candidates; ESRD requires dialysis and protein restriction. See End-stage renal disease.

di·a·bet·ic ne·phrop·a·thy

(dī-ă-bet'ik nĕ-frop'ă-thē)
A syndrome occurring in people with diabetes mellitus; associated with damage to blood vessels that supply the glomeruli of the kidney; characterized by albuminuria, hypertension, and progressive renal insufficiency.

diabetic nephropathy

; diabetic kidney disease persistent proteinuria (urinary excretion of >500 mg of protein in 24 hours) with hypertension (secondary to microvascular [arteriolar nephrosclerosis] and macrovascular [arterial nephrosclerosis] disease, and glycation of kidney tissue proteins) associated with long-term diabetes mellitus; a precursor to end-stage renal failure; note: patients with persistent proteinuria tend to have increased incidence of cardiovascular disease (see microalbuminuria)

di·a·bet·ic ne·phrop·a·thy

(dī-ă-bet'ik nĕ-frop'ă-thē)
Syndrome characterized by albuminuria, hypertension, and progressive renal insufficiency.

diabetic nephropathy (nəfro´pəthē´),

n the negative effects on the kidneys or renal system caused by diabetes mellitus. The condition may necessitate dialysis or kidney transplant.
diabetic neuropathy,
n the complications to the nervous system that can be caused by diabetes mellitus, some of which may necessitate amputation or result in oral or facial symptoms.
References in periodicals archive ?
We are confident that by harnessing the most modern approaches in stromal cell therapeutics there may well be a way to halt the progression of diabetic kidney disease using this therapy.
Diabetic kidney disease is a common complication of diabetes and the most frequent cause of end-stage renal disease (ESRD) in Western countries.
Diabetic kidney disease is a common complication of diabetes It is estimated that by 2040 it may affect around 200 million people -in most cases there is no effective medical treatment for it.
When they stimulated the mitochondria by activating a key energy-sensing enzyme called AMPK, superoxide production increased but evidence of diabetic kidney disease markedly declined.
It aimed to alert governments, health organisations, providers, doctors and patients to the increasing health and socioeconomic problems due to diabetic kidney disease and its sequelae, end-stage kidney disease requiring dialysis and death from cardiovascular causes.
Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for preventing the progression of diabetic kidney disease.
The incidence of diabetic kidney disease is expected to double by the year 2030.
Pharmacopeia's most advanced internal program is a dual-acting angiotensin and endothelin receptor antagonist for hypertension and diabetic kidney disease for which Phase 1 clinical trials are underway.
Diabetic kidney disease is the most prevalent cause of end-stage renal disease.
7) A large majority of patients with diabetic kidney disease are also hypertensive; however, the prevalence of hypertension (when defined as blood pressure >140/90 mm Hg) is consistently higher among patients with type 2 diabetic nephropathy (78-96%) than in patients with type 1 diabetic nephropathy (65-88%).
Researchers found a 50 percent decrease in both development and progression of early diabetic kidney disease (stages I and II) in participants who followed an intensive regimen for controlling blood glucose levels.
The risk of developing diabetic kidney disease is much higher if one or both parents had it, so these individuals should be especially careful about their diet and blood pressure.