Pathophysiology

The pathophysiology of unilateral renal artery stenosis provides a clear example of how hypertension develops. Narrowing of the renal artery, due to atherosclerosis or, rarely, fibromuscular dysplasia, leads to reduced renal perfusion. The consequent activation of the renin-angiotensin system causes hypertension (mediated by angiotensin II), hypokalaemia, and hyponatraemia (which are features of secondary hyperaldosteronism). Although these features may be reversed by correcting the stenosis, a classic presentation is uncommon, and hypertension is rarely cured in patients with atheromatous renal artery stenosis. In addition, it is now known that renal artery stenosis is underdiagnosed and may present as a spectrum of disease from secondary hypertension to end stage renal failure, reflecting variation in the underlying disease process. Thus, the presence of overt, or coincidental, renal artery stenosis usually reflects widespread vascular disease, with the associated implications for cardiovascular risk and patient survival.