Renal artery stenosis (RAS) is a relatively common condition in the elderly, especially in the setting of concomitant vascular disease in other anatomical sites and is most often of atheromatous origin. Rarely is it encountered in young women as a result of fibromuscular dysplasia. RAS is considered responsible for refractory or accelerated hypertension, progressive loss of renal function and deterioration of patients??? cardiovascular status, with episodes of angina or pulmonary oedema disproportional to the extent of coronary artery disease and left ventricle functional capacity, dominating the clinical presentation. This article summarizes the pathophysio logical implications and diagnostic methods and attempts a review of the current literature on indications and efficacy of the available therapeutic options for RAS, focusing on interventional treatment. Renal artery stenosis (RAS) is most commonly due to atherosclerosis (???90%) or fibromuscular dysplasia (10%) and rarely to extrinsic compression, neurofibromatosis type I or Williams syndrome. Fibromuscular dysplasia predominates in young women (30-50 years old), is a nonatherosclerotic, noninflammatory vascular disease that causes stenosis in medium and small arteries, most commonly involving the distal 2/3 of the renal artery and carotid arteries. Atherosclerotic renal artery stenosis is usually encountered in males over 55 years old and often occurs at the ostium or the proximal 2 cm of the artery. [1,2] Refractory hypertension, progressive renal function deterioration and recurrent episodes of decompensated heart failure or flash pulmonary oedema are the most common clinical manifestations of the disease Both conservative and interventional treatment have been proposed and applied with comparable efficacy, as far as atherosclerotic disease is concerned and thus certain controversies have arisen regarding the treatment of choice.[3
