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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.