Clinical and epidemiologic data have demonstrated that microalbuminuria (MA) may legitimately be an integrated marker of cardiovascular risk in nondiabetic hypertensive patients. The relation of augmented urinary albumin excretion rate (UAER) with the other surrogates of the atherosclerotic process, such as carotid artery intima-media thickness, large artery elasticity, and left ventricular hypertrophy gives further support to this view. Available evidence so far indicate that MA possibly reflects a state of increased renal endothelial permeability and may be an easily measured marker of a rather diffuse endothelial dysfunction, low-grade inflammation, and vascular disease burden. Whether management of hypertensive populations may be improved by UAER monitoring and whether the reduction of UAER can decrease cardiovascular morbidity and mortality remains to be determined in the future.