Pathogenesis of Renovascular Hypertension: Challenges and Controversies

Abstract

With an aging population, renovascular hypertension has become a major public health problem (Safian & Textor, 2001). Although various forms of fibromuscular disease of the renal arteries and/or traumatic disruption of renal vessels are the most common cause of RVH among the younger individuals, atherosclerotic renal artery disease (ARAD) is the most common lesion producing hypertension by far (Garovic & Textor, 2005). ARAD is present in over 6.8% of individuals over 65 years of age and is found in up to 49.1% of patients with coronary artery disease or aortoiliac disease (Iglesias et al. 2000; Valabhji et al. 2000; Hansen et al. 2002; Rihal et al. 2002; Weber-Mzell et al. 2002; Textor 2003). Although many patients with asymptomatic renovascular disease do not develop progressive renal dysfunction, overall morbidity and mortality is significantly increased (Chabova et al. 2000; Textor 2002; Textor 2003; Textor 2003; Foley et al. 2005; Foley et al. 2005). On the other hand, some studies suggest that from 10% to 40% of elderly hypertensive patients with newly discovered end stage renal disease and no identifiable parenchymal renal disease have significant RAS (Textor and Wilcox 2001). As in other forms of renal disease, the severity of interstitial fibrosis, tubular atrophy, interstitial inflammation, and glomerular sclerosis are important predictors of renal outcome (Wright et al. 2001). It has been postulated that this acquired tubulointerstitial injury may contribute to at least some forms of essential hypertension (Raghow 1994). Mechanisms underlying vascular and renal dysfunction in RAS have not been well delineated, despite intense study (Textor 2004). This information is essential for the development of therapies – surgical or medical – to treat RAS.