Renovascular disease remains among the most prevalent and important causes of secondary hypertension and renal dysfunction. Many lesions reduce perfusion pressure including fibromuscular diseases and renal infarction, but most are caused by atherosclerotic disease. Epidemiologic studies establish a strong association between atherosclerotic renal-artery stenosis (ARAS) and cardiovascular risk. Hypertension develops in patients with renovascular disease from a complex set of pressor signals, including activation of the renin-angiotensin system (RAS), recruitment of oxidative stress pathways, and sympathoadrenergic activation. Although the kidney maintains function over a broad range of autoregulation, sustained reduction in renal perfusion leads to disturbed microvascular function, vascular rarefaction, and ultimately development of interstitial fibrosis. Advances in antihypertensive drug therapy and intensive risk factor management including smoking cessation and statin therapy can provide excellent blood pressure control for many individuals. Despite extensive observational experience with renal revascularization in patients with renovascular hypertension, recent prospective randomized trials fail to establish compelling benefits either with endovascular stents or with surgery when added to effective medical therapy. These trials are limited and exclude many patients most likely to benefit from revascularization. Meaningful recovery of kidney function after revascularization is limited once fibrosis is established. Recent experimental studies indicate that mechanisms allowing repair and regeneration of parenchymal kidney tissue may lead to improved outcomes in the future. Until additional staging tools become available, clinicians will be forced to individualize therapy carefully to optimize the potential benefits regarding both blood pressure and renal function for such patients.