Volume 1, Number 1, March 2000

Blockade of the renin-angiotensin-aldosterone system and renal protection in diabetes mellitus
Hans-Henrik Parving

A clinical diagnosis of diabetic nephropathy is made in patients with diabetes on the basis of persistent albuminuria (>300 mg/24-hour), the presence of diabetic retinopathy, and the absence of any clinical or laboratory evidence of other kidney or renal tract disease. This definition is valid in patients with either Type 1 or Type 2 diabetes. The clinical syndrome termed diabetic nephropathy is characterised by persistent albuminuria, early arterial blood pressure elevation, a relentless decline in glomerular filtration rate (GFR), and high risk of cardiovascular morbidity and mortality. Previous studies have found a cumulative incidence of diabetic nephropathy of 25–40% after diabetes duration of at least 25 years in both Type 1 and Type 2 diabetes. Diabetic nephropathy has become the leading cause (25–42%) of end-stage renal disease (ESRD) in Europe, Japan, and the United States. Unfortunately, the proportion of ESRD patients suffering from diabetes, particularly Type 2, is expected to rise significantly because the worldwide prevalence of diabetes is expected to double within the next 15 years, and because the individual diabetic patient lives longer and consequently has a greater risk of developing late complications including diabetic nephropathy.
This editorial reviews the evidence for the benefit of blockade of the renin-angiotensin-aldosterone system (RAAS) on the development and the progression of diabetic nephropathy. The renin-angiotensin-system plays an important role in the initiation and progression of diabetic kidney disease. Blockade of the RAAS reduces the progressive rise in albuminuria, diminishes the loss of glomerular filtration power, postpones end-stage renal failure and prolongs survival in patients with diabetic kidney disease.

JRAAS 2000;1:30-31.

View full PDF article (open in new window)
Email this article

Right click on this DOI link and copy link to cite this article (What is a DOI link?)