[Microalbuminuria, hypertension, and cardiovascular risk]

A growing interest in the study of microalbuminuria (Mi) in essential hypertension (EH) has recently emerged. While clinical proteinuria is found with a low frequence (between 4 and 16%) in patients with EH, a variable but generally higher prevalence (10-40%) of Mi has been reported, even in the absence of diabetes and nephropathy. Mi is defined as an abnormal urinary excretion of albumin (20-200 micrograms/min), undetectable by conventional tests. Variations in the prevalence of Mi in different studies may be attributed to different selection criteria, techniques for detection of albuminuria, the severity of hypertension, age, race, coexistence of renal disease as well as the number of patients studied and the presence or absence of antihypertensive treatment. It is unknown whether the predictive value of albuminuria reflects its association with more severe hypertension and target organ damage, or whether albuminuria serves as an indicator of capillary leakiness which causes detectable abnormalities in the renal microcirculation but reflects more generalized endothelial barrier dysfunction predisposing to accelerated atherogenesis. Mi has been associated with higher blood pressure levels, a worse lipid profile as well as the presence of target organ damage, namely peripheral artery disease and left ventricular hypertrophy in patients with EH. Several studies have shown a correlation between Mi and/or proteinuria and cardiovascular diseases independently of other risk factors and cardiovascular mortality to be ten times higher in patients with Mi than in normoalbuminuric patients. Long-term prospective studies are needed in order to clarify the exact prevalence of Mi, its predictive value for the development of clinical proteinuria and renal function deterioration as well as the effect of different antihypertensive drugs.