Abstract
Microalbuminuria, i.e., abnormal urinary excretion of albumin detectable by sensitive, low cost, and widely available tests, can be found in up to one third of non diabetic patients with primary hypertension. Microalbuminuria has been shown to predict an increased probability of suffering a cardiovascular event or death. The pathogenetic mechanisms leading to the development of microalbuminuria are not yet fully known: blood pressure load and increased systemic vascular permeability, possibly due to early endothelial damage, seem to play a major role. Increased urinary albumin excretion has been associated with several unfavorable metabolic and non metabolic risk factors and sub-clinical organ damage, such as left ventricular hypertrophy and carotid atherosclerosis. Microalbuminuria itself has recently been recognized as a sign of hypertensive target organ damage and since it reflects the influence of so many clinically relevant parameters, it can rightly be considered an integrated marker of cardiovascular risk, a unique feature among the several available prognostic predictors for stratifying risk in hypertensive patients. While microalbuminuria has proven to be a forerunner of overt renal damage in the presence of diabetes mellitus, conflicting clinical evidence makes this hypothesis tempting at the moment, but speculative in non diabetic hypertensives. Effective antihypertensive treatment, especially with drugs counteracting the renin angiotensin system, has been found to reduce urinary albumin excretion. More recently, regression from microalbuminuria to normoalbuminuria has been associated with an amelioration of cardiovascular outcome, regardless of achieved blood pressure levels and type of drug. This evidence emphasizes the usefulness of evaluating urinary albumin excretion not only to assess cardiovascular risk, but also to monitor the efficacy of treatment in clinical practice.
Keywords: Microalbuminuria, primary hypertension, target organ damage, cardiovascular risk
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