Atherosclerotic renal artery stenosis (ARAS) represents a common manifestation of systemic atherosclerosis and remains an underrecognized cause of secondary hypertension, chronic kidney disease, and cardiovascular morbidity. Although often clinically silent, progressive narrowing of the renal artery may result in renovascular hypertension, ischemic nephropathy, or cardiac destabilization syndromes such as recurrent pulmonary edema. The pathophysiology of ARAS extends beyond simple flow limitation, involving renin-angiotensin-aldosterone system activation, oxidative stress, microvascular rarefaction, and parenchymal fibrosis, thereby explaining the limited reversibility of renal damage after revascularization. Over the past decades, management strategies have evolved considerably. While initial enthusiasm for surgical or endovascular revascularization was supported by observational reports of improved blood pressure and renal function, randomized controlled trials-including ASTRAL and CORAL-failed to demonstrate a consistent benefit of stenting over optimal medical therapy in unselected patients. These findings have shifted current practice toward medical therapy as the cornerstone of management, integrating renin-angiotensin system inhibitors, statins, antiplatelet agents, and, more recently, SGLT2 inhibitors. Nevertheless, accumulating evidence indicates that specific high-risk subsets-patients with resistant hypertension, recurrent pulmonary edema, or progressive ischemic nephropathy-may derive meaningful clinical benefit from timely revascularization. In the post-CORAL era, the central challenge is therefore accurate patient selection to identify the small group in whom revascularization remains appropriate, leveraging advanced imaging, physiological indices, and risk stratification.
