The emerging role of subclinical inflammation in hypertension-associated early renal dysfunction: focus on microalbuminuria.

M icroalbuminuria (MA), the presence of low but abnormal levels of albumin in the urine, is the earliest clinical sign of diabetic nephropathy and for hypertensive patients it is also a marker for greatly increased cardiovascular risk, regardless of the presence of diabetes. The association of MA with elevated blood pressure (BP) is consistent and independent, and increased urinary albumin excretion (UAE) has also been linked to lipid abnormalities, reduced insulin sensitivity, impaired endothelial function, peripheral vascular disease, diffuse inflammatory processes and prothrombotic state. All the above define MA as a marker of generalised vascular dysfunction beyond the renal glomerulus. Cumulative evidence suggests that hypertension is an inflammatory disease and that diverse inflammatory and pro-atherogenic mechanisms may be involved in both the pathogenesis of hypertension and the progression of target organ damage. The observed interrelationships of MA with inflammatory mediators provide further support to the notion that in the vicious circle connecting essential hypertension, microalbuminuric state and atherosclerotic cardiovascular events, subclinical inflammation participates in all stages of this deleterious process. The purpose of this article is to review the available data regarding the role of proinflammatory processes in the context of hypertensive cardiovascular disease and to focus on their relation with MA, a promising marker of subclinical atherosclerosis. A better understanding of MA could clarify the link between increased UAE and unfavourable outcome and underscore the value of screening for MA in the setting of non-diabetic essential hypertension.