Atherosclerotic renal artery stenosis (RAS) is a relatively common problem, affecting from 1% to 5% of patients with hypertension.1,2 Given the high prevalence of hypertension, it follows that there are from 2 million to 4 million individuals with RAS in the United States alone. Autopsy data demonstrate that the incidence of RAS increases with age affecting 18% of individuals between the ages 65 to 74 years and >40% of those more than age 75.3 RAS is also common in individuals with vascular disease in other beds and is present in ≤40% of those with overt coronary artery disease, aortoiliac disease, or peripheral vascular disease.4–6 At present, the best treatment for RAS is unknown, and, in particular, whether or not revascularization, typically accomplished by angioplasty and stenting, improves clinical outcomes for patients with RAS is unclear. Nevertheless, it is estimated that &40 000 renal artery angioplasties procedures are performed in the United States each year, which, depending on whether or not the procedure is beneficial, is either far too many or far too few. The purpose of this article is to review current knowledge about atherosclerotic RAS and to discuss the Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) trial, which is examining the best treatment for this disease. The pathophysiology of hypertension is different in patients with unilateral and bilateral RAS. In both, a drop in perfusion pressure to a kidney distal to a stenosis induces an increase in the activity of the renin–angiotensin–aldosterone system (RAAS). Salt and water retention and vasoconstriction contribute to the initial rise in systemic blood pressure, which tends to raise perfusion pressure of the poststenotic kidney toward normal. In patients with unilateral disease, perfusion pressure also rises in the contralateral, nonstenotic kidney to supra normal levels, inducing a pressure natriuresis response. Salt and …