Renal Artery Stenosis
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Direct answer
Two diseases hide behind one angiographic label: atherosclerotic renal artery stenosis, an ostial lesion of the older smoker with diffuse vascular disease, accounting for about nine in ten cases; and fibromuscular dysplasia, a mid-to-distal string-of-beads lesion of young women that responds to angioplasty beautifully. Screening begins with duplex ultrasound — peak systolic velocity above roughly 200 cm/s and a renal-to-aortic ratio above 3.5 — and management of the atherosclerotic form is overwhelmingly medical, because the CORAL trial found stenting added nothing to statin, antiplatelet, smoking cessation and blood pressure therapy. Revascularisation is reserved for refractory hypertension, recurrent flash pulmonary oedema, a rapidly failing kidney, or the dysplastic patient, in whom it is often curative.
What you must remember
- Atherosclerotic disease: ostium and proximal third, over 55 years, smoking, diabetes and coronary or peripheral disease; bilateral in a fifth to a third; progresses slowly to ischaemic nephropathy.
- Fibromuscular dysplasia: women aged 15–50, mid and distal artery, medial fibroplasia with the string-of-beads angiogram; hypertension often cured or markedly improved by angioplasty, restenosis modest.
- Bedside clues: resistant hypertension on three drugs, an abdominal bruit, spontaneous hypokalaemia from secondary hyperaldosteronism, asymmetric kidneys beyond 1.5 cm, and a creatinine that jumps over 30 per cent on starting an ACE inhibitor or ARB.
- Flash pulmonary oedema: recurrent acute pulmonary oedema with clean coronaries points to bilateral stenosis or stenosis of a solitary kidney — a classic image-based viva.
- CORAL message: stenting plus medical therapy did not beat medical therapy alone for atherosclerotic stenosis — the trial that ended routine stenting.
- Medical bundle: statin, antiplatelet, smoking cessation, and an ACE inhibitor or ARB with careful creatinine and potassium monitoring — protective for the contralateral kidney.
- Revascularisation indications: refractory hypertension, flash pulmonary oedema, rapidly declining GFR or bilateral critical disease, intolerance of medical therapy, and fibromuscular dysplasia itself.
- Goldblatt models: the two-kidney one-clip model is renin-dependent and ACE inhibitor-responsive; the one-kidney one-clip model is volume-dependent — a perennial physiology viva.
Flash pulmonary oedema at two in the morning
A 68-year-old smoker with known coronary disease is admitted twice in a month with acute pulmonary oedema; echocardiography shows only mild diastolic dysfunction and the coronaries are unremarkable. Step one: the pattern — flash oedema with a modest cardiac substrate — puts renovascular disease on the shortlist, and the examination finds a soft epigastric bruit and a blood pressure of 168/96 on three agents, with a recent potassium of 3.2. Step two: duplex ultrasound reports peak systolic velocities above 300 cm/s at both ostia with a right-sided renal-to-aortic ratio of 4.1, kidneys 9.4 and 9.0 cm. Step three: CT angiography confirms bilateral ostial stenosis, 80 per cent right and 60 per cent left. Step four: the decision — CORAL says medicine first, and his medicine is intensified: atorvastatin, aspirin, smoking support, and cautious ACE inhibitor introduction with a creatinine check inside the fortnight; but he returns a third time with oedema, which is precisely the escape hatch CORAL allows — recurrent flash pulmonary oedema is an accepted indication for revascularisation, and a right renal artery stent is placed with blood pressure improvement. Step five: contrast stewardship throughout — staged imaging, hydration and the lowest adequate dose, because this kidney has no reserve for a contrast insult on top of ischaemia.
How the exam frames it
The stem is usually the ACE inhibitor trap: creatinine rising from 1.2 to 1.8 within two weeks of starting ramipril. A rise under 30 per cent is expected pharmacology — the efferent arteriole opens — and therapy continues; beyond 30 per cent, withhold and image for bilateral disease or a solitary functioning kidney. The second framing is age and sex: a 34-year-old woman with abrupt hypertension and a beaded artery on the angiogram image is fibromuscular dysplasia, and the answer is percutaneous angioplasty without a stent in most cases — the one setting where revascularisation is first-line. The third is the trial question, asked bluntly: what did CORAL show? Stenting offered no superiority over medical therapy for atherosclerotic disease — and quoting it, with the exceptions, is what distinguishes a current answer from a 2005 one.
Frequently asked questions
Which screening test comes first?
Duplex ultrasonography — peak systolic velocity above about 200 cm/s and renal-to-aortic ratio above 3.5 indicate significant stenosis.
What did the CORAL trial conclude?
Renal artery stenting added no benefit to comprehensive medical therapy in atherosclerotic renal artery stenosis, settling management as predominantly medical.
How is fibromuscular dysplasia treated?
Percutaneous transluminal angioplasty, usually without stenting — hypertension is cured or improved in the majority, unlike the atherosclerotic form.
What creatinine rise on an ACE inhibitor mandates investigation?
An increase above 30 per cent from baseline suggests bilateral stenosis or stenosis of a solitary functioning kidney.
When is revascularisation indicated despite CORAL?
Refractory hypertension, recurrent flash pulmonary oedema, rapidly progressive renal dysfunction, or fibromuscular dysplasia.
Why does hypokalaemia accompany renal artery stenosis?
Renin-driven angiotensin II and aldosterone excess drive potassium wasting — one of the silent bedside clues.