Diabetic nephropathy: from micro- to macroalbuminuria

This brief review will focus on the major factors leading to incipient diab etic nephropathy (i.e. microalbuminuria) progressing to overt nephropathy ( i.e, macroalbuminuria) and particularly on the role of glycaemic control an d hypertension. Both experimental and cohort studies support the role of hyperglycaemia in the development of diabetic nephropathy. Some recent long-term intervention al studies in microalbuminuric patients show conflicting results regarding the role played by good metabolic control in reducing the incidence of over t nephropathy. However, strict metabolic control, which is fundamental in n ormoalbuminuric patients, is of little use even in microalbuminuric patient s. In general, levels of glycosylated haemoglobin less than two standard de viations above the upper normal range, commonly <7.5-8%, seem to protect pa tients from developing nephropathy. The results of many cross-sectional studies have shown that the progression of renal damage regularly is accompanied by arterial hypertension both in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabet es mellitus (NIDDM). Many longterm interventional studies have been perform ed in order to understand the effect of antihypertensive treatment on the i ncidence of proteinuria in both normotensive and hypertensive patients with IDDM or NIDDM. These data show a marked effect of antihypertensive therapy in preventing the onset of overt nephropathy, and suggest the superiority of angiotensin-converting enzyme (ACE) inhibitors. We believe that optimal blood pressure values are similar to 120/70-75 mmHg in younger patients and 125-130/80-85 mmHg in older patients. In conclusion, antihypertensive trea tment, ACE inhibitors per se and possibly strict metabolic control reduce t he development of nephropathy, thus playing a striking role in the secondar y prevention of renal failure.