ABSTRACT
Microalbuminuria, defined as urinary excretion of albumin in the range of 30-300 mg/g creatinine, affects 20-30 percent of the type 2 diabetic (DM2) patients and 30-40 percent of type 1 diabetic (DM1) patients who, without intervention, progress to macroalbuminuria at rates of 5 and 7.5 percent per year, respectively. Hyperglycemia, by activating different metabolic pathways and the renin-angiotensin-aldosterone system, determines an increase in reactive oxygen species (ROS) which finally causes endothelial dysfunction. Albuminuria reflects a generalized endothelial dysfunction, that is related to cardiovascular disease in diabetic patients. Therefore, microalbuminuria becomes a predictor of renal damage, a coronary risk factor and a predictor of cardiovascular diseases. Several studies have demonstrated that progression of albuminuria can be prevented in normotensive and hypertensive DM1 and DM2 patients with the use of an inhibitor of angiotensin converting enzyme II or an antagonist of the angiotensin II receptor. These measures also provide cardiovascular protection in diabetic patients, an effect that is independent of the hypotensive action of the drug. In microalbuminuric diabetic patients, treatment should be oriented to diminish or avoid progression of microalbuminuria, and to maintain blood pressure, glucose and lipids within the recommended limits to avoid vascular and renal damage.