Renal Abnormalities in Essential Hypertension. From the Genetics to the Renoprotective Effect of the Antihypertensive Treatment

pp 329-336

Abstract

Essential hypertension is a frequent cause of chronic renal damage. Even though the underlying patho­genic mechanisms remain mainly unknown, the ge­netic factors are decisive to establish salt-sensitiv­ity and it has been postulated that the number of functional nephrons at birth determines which will be the individual bias for the eventual development of hypertension. Furthermore, low birth weight can impede the renal development, reduce the glomeruli number and/or diminish the filtration surface with the development of glomerular hypertension. The alteration of the selfregulatory mechanism accom­panies the reduction of the renal blood :flow. Sev­eral neurohumoral factors contribute to this distur­bance. Prominent among them are the plasmatic concentrations of angiotensin II (Ali) which are higher than the expected according to the blood pres­sure measurements (BP). AII produces intense vaso­ constriction mainly of the efferent arteriole as well as reduction of the renal blood: flow and in crease of tubular reabsorption ofNa⁺. This imbalance among vasopressor factors -as sympathetic activity, endothelins, digitalics-like factors- and vasorelaxant factors -as renal prostaglandins, ni­trie oxide, kallikreins-kinins and atrial natriuretic peptide- acquires great importance in the genera­tion of renal alterations associated to hypertension. Aldosterone stimulates fibrosis and renal dysfunc­tion. Furthermore, it exerts a facilitator effect on the vascular receptors of AII. From a renoprotective perspective, there is no conclusive evidence that the antihypertensivedrugs whichreducetheproteinuria constitute the first election. Nevertheless the reduc­tion ofthe BP is effective to decrease the progres­sion ofthe renal functional and structural alter­ations, independently of the pharmacological therapy chosen.