diabetic nephropathy


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Related to diabetic nephropathy: diabetic retinopathy, diabetic neuropathy

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.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

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.

Farlex Partner Medical Dictionary © Farlex 2012

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.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

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.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

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.
Medical Dictionary for the Dental Professions © Farlex 2012
References in periodicals archive ?
Thus, serum KIM-1 may be recommended as a biomarker for detecting early diabetic nephropathy.14,16,17-20 KIM-1 levels in this study showed strong positive association with blood urea nitrogen as a marker for kidney function both at baseline (r= 0.728; p value = 0.000) and follow up (r=0.843; p value = 0.001).
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Identifying parameters to distinguish non-diabetic renal diseases from diabetic nephropathy in patients with type 2 diabetes mellitus: A meta-analysis.
As far as treatment is concerned; Angiotensin converting enzyme (ACE) inhibitors and Angiotensin receptor blockers (ARB) both are equally effective in the treatment of diabetic nephropathy in patients with type 1 or type 2 diabetes mellitus.
Lupus nephritis was the most common among secondary GN (68.6%), followed by diabetic nephropathy (22.5%); membranous nephropathy was the most common primary GN (30.0%), followed by IgA nephropathy (16.6%) (Figure 2).
Blood urea nitrogen, serum creatinine, formulas to estimated glomerular filtration rate (GFR), proteinuria, and albuminuria are measures currently used to assess the presence and progress of diabetic nephropathy [2,3].
Diabetic nephropathy affects the African-American population about 3-5 times more than the Caucasian population.
Glycosylation of tissue proteins may contribute to diabetic nephropathy apart from other microvascular complications.
announced that it will initiate a Phase II clinical trial investigating IW-1973 in diabetic nephropathy. IW-1973 is an investigational soluble guanylate cyclase (sGC) stimulator which plays an important role in regulating diverse physiological processes such as blood flow, inflammation, fibrosis, and metabolism.
Diabetic nephropathy is the leading cause of End Stage Renal Disease (ESRD) worldwide and a leading cause of DM-related morbidity and mortality.
Diabetic nephropathy (DN) is one of the most important microvascular complications of DM and is responsible for 40-50% of all cases of end stage renal disease (ESRD) [1].