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| AuthorGeorge L Bakris, MD | Section EditorsRichard J Glassock, MD, MACPDavid M Nathan, MD | Deputy EditorAlice M Sheridan, MD |
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Diabetic nephropathy is a common problem that is most likely to occur in patients who have worse glycemic control, hypertension, glomerular hyperfiltration or a genetic predisposition. The lifetime risk of nephropathy is roughly equivalent in type 1 and type 2 diabetes [1]. (See "Overview of diabetic nephropathy".)
The earliest clinical manifestation of renal involvement in diabetes is an increase in albumin excretion (microalbuminuria), a stage at which renal histology may be relatively normal or may reveal glomerulosclerosis [2-5]. However, regression of microalbuminuria to normoalbuminuria occurs spontaneously in a substantial proportion of patients with type 1 and type 2 diabetes. (See "Microalbuminuria in type 1 diabetes mellitus" and "Microalbuminuria in type 2 diabetes mellitus".)
Proteinuria in diabetes mellitus is occasionally due to a glomerular disease other than diabetic nephropathy. The major clinical clues suggesting nondiabetic glomerular disease are onset of proteinuria less than five years from the documented onset of diabetes in type 1 diabetes, acute onset of renal disease, presence of an active urine sediment containing red cells (particularly acanthocytes) and cellular casts, and in type 1 diabetes, the absence of diabetic retinopathy or neuropathy. (See "Overview of diabetic nephropathy", section on 'Nondiabetic renal disease'.)
This review will address the treatment of diabetic nephropathy, particularly the importance of glycemic control and of rigorous antihypertensive therapy, with emphasis on the use of angiotensin converting enzyme inhibitors or angiotensin II receptor blockers. In addition to data from controlled trials, further proof of benefit from these therapies is the observation that the incidence of end-stage renal disease among patients with type 1 diabetes may be decreasing [6].
The efficacy of strict glycemic control depends in part upon the stage at which it is begun and the degree of normalization of glucose metabolism; the evidence is best established in type 1 diabetes. (See "Glycemic control and vascular complications in type 1 diabetes mellitus" and "Glycemic control and vascular complications in type 2 diabetes mellitus".)
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