Clinical meaning
Renovascular hypertension results from renal artery stenosis (RAS) causing reduced renal perfusion pressure. The juxtaglomerular apparatus senses decreased afferent arteriolar pressure and releases renin, converting angiotensinogen to angiotensin I, which ACE converts to angiotensin II. Angiotensin II causes systemic vasoconstriction, stimulates aldosterone release (promoting sodium/water retention), and activates sympathetic nervous system — all elevating BP. In unilateral RAS, the contralateral kidney experiences hypertension-induced natriuresis ('pressure natriuresis'), partially compensating. In bilateral RAS, both kidneys retain sodium and water without compensation, causing volume-dependent hypertension with flash pulmonary edema. Atherosclerotic RAS (90% of cases) involves ostial plaque extension from the aorta, while FMD (10%) affects mid-to-distal segments.
Diagnosis & workup
Diagnostics & workup: - Duplex ultrasound of renal arteries: peak systolic velocity > 200 cm/s, renal-to-aortic ratio > 3.5 (sensitivity 85-92%) - CTA renal arteries: excellent anatomic detail, distinguishes atherosclerotic (ostial) from FMD (mid-distal); IV contrast required - MRA with gadolinium: alternative to CTA if CKD with eGFR > 30 (avoid gadolinium if eGFR < 30 — nephrogenic systemic fibrosis risk) - Captopril renal scan (renography): functional test showing delayed uptake and excretion in affected kidney; largely replaced by CTA/MRA - Renal artery catheter angiography: gold standard for diagnosis and simultaneous intervention - Plasma renin activity: elevated in renin-dependent RVH (may be suppressed in bilateral RAS) - BMP: creatinine (renal function), potassium (hypokalemia from secondary aldosteronism) - Kidney size assessment on ultrasound: < 9 cm suggests chronic ischemic nephropathy with limited revascularization benefit