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

Accepted for publication 26th November 1999 A clinical diagnosis of diabetic nephropathy is made in patients with diabetes on the basis of persistent albuminuria (>300 mg/24h), 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. A beneficial effect on kidney function (and structure) above and beyond that expected from the blood pressure lowering effect alone is defined as renoprotection, as originally demonstrated in experimental diabetic and non-diabetic glomerulopathies by Brenner’s group.