The predominant cause of renal artery stenosis (RAS) is atherosclerosis. Clinical manifestations of atherosclerotic RAS are both direct (hypertension and kidney dysfunction) and indirect (increased cardiovascular events and mortality). However, in many cases, atherosclerotic RAS seems to be an incidental finding with no discernable effects. Antihypertensive medications such as renin-angiotensin-aldosterone system inhibitors, along with statins and aspirin, have significantly improved the medical treatment of atherosclerotic RAS. However, revascularization is still advocated in a variety of clinical settings such as the preservation of renal function, recurrent episodes of "flash" pulmonary edema, and in patients with refractory hypertension. Current management guidelines indicate "resistant hypertension" as an indication for renal artery revascularization. A large number of observational studies support revascularization for both control of high blood pressure and/or preservation of renal function. Unfortunately, the favorable effects of revascularization on these end points seen in the observational studies were not reproduced in randomized controlled trials compared to medical therapy alone. The ability for revascularization to improve control of congestive heart failure or to prevent hard cardiovascular end points (eg, myocardial infarction or stroke) has not been tested in the randomized clinical trials published to date. Hence, the efficacy of intervention remains controversial, which poses a dilemma, especially given the large number of elderly patients with resistant systolic hypertension.