Renal Artery Stenting

Renal Artery Stenosis (RAS) is a narrowing of one or both renal arteries, most commonly caused by atherosclerosis (80-90%, typically ostial/proximal, in older adults) or fibromuscular dysplasia (FMD) (10-20%, mid-distal artery, “string of beads” appearance, in young women). RAS reduces blood flow to the kidneys, activating the renin-angiotensin-aldosterone system (RAAS). This triggers vasoconstriction, sodium retention, and fluid overload, leading to secondary hypertension and/or renal impairment.

Renal Artery Stenosis typically presents with refractory hypertension (sudden onset before age 30 or after 60, resistant to ≥3 medications, or malignant/accelerated patterns) and unexplained renal dysfunction—most notably acute worsening of kidney function after initiating ACE inhibitors or ARBs. A critical red flag is recurrent flash pulmonary edema (cardiogenic-like pulmonary edema without cardiac cause), often triggered by renal ischemia activating the renin-angiotensin-aldosterone system (RAAS). RAS is strongly suspected in hypertensive patients with coexisting coronary or peripheral artery disease.