George L Bakris, MD
Richard J Glassock, MD, MACP
David M Nathan, MD
Alice M Sheridan, MD
Last literature review version 18.2: May 2010 | This topic last updated: May 21, 2010 (More)
INTRODUCTION — Diabetic nephropathy occurs in both type 1 (formerly called insulin-dependent or juvenile onset) and type 2 (formerlycalled non-insulin-dependent or adult onset) diabetes mellitus, including diabetes due to genetic defects of beta-cell function (which was previously called maturity onset diabetes of the young, or MODY). (See "Classification of diabetes mellitus and genetic diabetic syndromes".)
The following data concerning the epidemiology of renal disease are confounded since they may or may not represent thecurrent "natural history" 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 the epidemiology, pathogenesis, and riskfactors for diabetic nephropathy. The importance of microalbuminuria and the treatment of diabetic nephropathy are discussed separately. (See "Microalbuminuria in type 1 diabetes mellitus" and "Microalbuminuria in type 2 diabetes mellitus" and "Treatment of diabetic nephropathy".)
Type 1 diabetes — The epidemiology of diabetic nephropathy has been best studied in patients with type 1disease, since the time of clinical onset is usually known. Approximately 20 to 30 percent will have microalbuminuria after a mean duration of diabetes of 15 years [1,2]. Less than half of these patients will progress to overt nephropathy; microalbuminuria may regress or remain stable in a substantial proportion, probably related to glycemic and blood pressure control. (See "Microalbuminuria intype 1 diabetes mellitus", section on 'Prevalence' and "Microalbuminuria in type 1 diabetes mellitus", section on 'Regression to normoalbuminuria'.)
Prior to the current period of intensive monitoring and treatment, it was suggested that 25 to 45 percent of diabetic patients will develop clinically evident disease (the minimal criterion for which is a persistently positive urine dipstick forprotein) [1,3-5].
The overall incidence of end-stage renal disease (ESRD) was also substantial, with reported rates of 4 to 17 percent at 20 years from time of initial diagnosis and approximately 16 percent at 30 years [6-8]. In comparison to these findings, subsequent studies have found that the renal prognosis of type 1 diabetes, including the rate of progression to ESRD, has dramatically improvedover the last several decades [9,10]:
* A study from Sweden noted a dramatic reduction in clinically evident diabetic nephropathy to 8.9 percent at 25 years, a presumed reflection of better glycemic control . The average hemoglobin A1c concentration in the later part of this follow-up period was 7.0 percent; patients without overt proteinuria had a lower hemoglobin A1c concentration than thosewith proteinuria (7.1 versus 8.1 percent). A similar decline in incidence was not noted in another report in which this degree of glycemic control was not achieved .
* One study from Finland evaluated the long-term outcomes of 20,005 patients over the period 1965 to 1999 . During the median follow-up period of 17 years (maximum of 37 years), progression to ESRD occurred in only 632patients, with the cumulative incidence being 2.2 and 7.8 percent at 20 and 30 years, respectively. In addition, the rate of ESRD was relatively lower among patient cohorts diagnosed at later time points, and the incidence of ESRD was lowest among those diagnosed prior to the age of 5 years.
* 33 of 480 patients (7%) with type I diabetes and normal GFR developed ESRD after 16 years of...