Prevalence of microalbuminuria in type 2 diabetes: lessons learned from the ROADMAP study

It is plausible to assume that the earlier the stage of diabetic nephropathy the greater is the chance of successful intervention; this is suggested e.g. by the observation of Siragy and Carey [1], who report that in diabetic nephropathy the efficacy of delayed RAS blockade is limited. In the past, it had commonly been assumed that kidney disease in diabetes starts with an increase in albuminuria and progresses to the stages of microalbuminuria and subsequently to overt proteinuria and progressive loss of renal function. Although recent observations indicate that this is not true in all cases of type 2 [2, 3] or type 1 [4] diabetes, this scheme is certainly valid in the majority of patients. The urinary albumin excretion in diabetes constitutes a continuum so that the diagnosis of microalbuminuria is somewhat arbitrary––which led to the proposal to abandon the concept of microalbuminuria [5], because in type 2 diabetics renal and cardiovascular (CV) risks increase progressively with increasing albumin excretion even within the normal range [6]. Nevertheless, the onset of microalbuminuria remains [1] a valid parameter for intervention studies. The currently available interventions to reduce albuminuria are mainly based on two interventions, i.e. lowering of blood pressure (BP) and blockade of the renin–angiotensin system by ACE inhibitors (ACEi) or angiotensin receptor blockers (ARB). In the BENEDICT trial, Ruggenenti and Remuzzi [7] documented the efficacy of RAS blockade with ACE inhibitors (ACEi) for the prevention of microalbuminuria in patients with type 2 diabetes. The situation had remained less clear for the effect of angiotensin receptor blockers (ARB), because negative outcomes had been reported by several authors [8, 9].