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Overview of diabetic nephropathy

George L Bakris, MD
Section Editors
Richard J Glassock, MD, MACP
David M Nathan, MD
Deputy Editor
John P Forman, MD, MSc


Diabetic nephropathy occurs in type 1 (formerly called insulin-dependent or juvenile onset) and type 2 (formerly called non-insulin-dependent or adult onset) diabetes mellitus, and in other secondary forms of diabetes mellitus, for example after pancreatitis or pancreatectomy, in which duration of diabetes is long-enough and level of glycemia high enough to result in complications. (See "Classification of diabetes mellitus and genetic diabetic syndromes".)

The following data concerning the epidemiology of renal disease may not represent the current clinical course of the disease. Some of the evidence was obtained before the availability of data supporting the efficacy of tight glycemic control, aggressive blood pressure and lipid control, and the specific benefit of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs).

This topic provides an overview of diabetic nephropathy; treatment issues are discussed separately. (See "Treatment of diabetic nephropathy".)


Diabetic kidney disease is defined by characteristic structural and functional changes. The predominant structural changes include mesangial expansion, glomerular basement membrane thickening, podocyte injury, and, ultimately, glomerular sclerosis [1-3]. (See 'Pathology' below.)

The major clinical manifestations of diabetic nephropathy are albuminuria, hematuria (less often), and, in many patients, progressive chronic kidney disease, which can be slowed with optimal therapy. (See "Treatment of diabetic nephropathy".)

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Literature review current through: Nov 2017. | This topic last updated: Feb 28, 2017.
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