Preclinical Cardiorenal Interrelationships in Essential Hypertension

• Published in: Cardiorenal medicine Vol. 3; no. 1; pp. 38 - 47
• Main Authors: Tsioufis, Costas, Tsiachris, Dimitrios, Kasiakogias, Alexandros, Dimitriadis, Kyriakos, Petras, Dimitris, Goumenos, Dimitris, Siamopoulos, Konstantinos, Stefanadis, Christodoulos
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01-04-2013
• Subjects: Review; Hypertension; Cardiorenal syndrome; Preclinical organ damage
• ISSN: 1664-3828; 1664-5502
• DOI: 10.1159/000346817

A diseased heart causes numerous adverse effects on kidney function, and vice versa renal disease can significantly impair cardiac function. Beyond these heart-kidney interrelationships at the clinical level, a reciprocal association has been suggested to exist even in the early stages of those organs' dysfunction. The aim of the present review is to provide evidence of the presence of a preclinical cardiorenal syndrome in the particular setting of essential hypertension, focusing on the subsequent hypertensive sequelae on heart and kidneys. In particular, a plethora of studies have demonstrated not only the predictive role of kidney damage, as expressed by either decreased glomerular filtration or increased urine albumin excretion, for adverse left ventricular functional and structural adaptations but also preclinical heart disease, i.e. left ventricular hypertrophy that is associated with deterioration of renal function. Notably, these reciprocal interactions seem to exist even at the level of microcirculation, since both coronary flow reserve and renal hemodynamics are strongly related with clinical and preclinical renal and cardiac damage, respectively. In this preclinical setting, common pathophysiological denominators, including the increased hemodynamic load, sympathetic and renin-angiotensin system overactivity, increased subclinical inflammatory reaction, and endothelial dysfunction, account not only for the reported associations between overt cardiac and renal damage but also for the parallel changes that occur in coronary and renal microcirculation.