An Outline of Renal Artery Stenosis Pathophysiology—A Narrative Review

Abstract

Renal artery stenosis (RAS) is conditioned mainly by two disturbances: fibromuscular dysplasia or atherosclerosis of the renal artery. RAS is an example of renovascular disease, with complex pathophysiology and consequences. There are multiple pathophysiological mechanisms triggered in response to significant renal artery stenosis, including disturbances within endothelin, kinin–kallikrein and sympathetic nervous systems, with angiotensin II and the renin–angiotensin-aldosterone system (RAAS) playing a central and key role in the pathogenesis of RAS. The increased oxidative stress and the release of pro-inflammatory mediators contributing to pathological tissue remodelling and renal fibrosis are also important pathogenetic elements of RAS. This review briefly summarises these pathophysiological issues, focusing on renovascular hypertension and ischemic nephropathy as major clinical manifestations of RAS. The activation of RAAS and its haemodynamic consequences is the primary and key element in the pathophysiological cascade triggered in response to renal artery stenosis. However, the pathomechanism of RAS is more complex and also includes other disturbances that ultimately contribute to the development of the diseases mentioned above. To sum up, RAS is characterised by different clinical pictures, including asymptomatic disorders diagnosed in kidney imaging, renovascular hypertension, usually characterised by severe course, and chronic ischemic nephropathy, described by pathological remodelling of kidney tissue, ultimately leading to kidney injury and chronic kidney disease.