Renal artery stenosis
Renal artery stenosis causes renovascular hypertension through renal hypoperfusion and renin-angiotensin activation, most often from atherosclerosis in older patients or fibromuscular dysplasia in young women. Most patients are managed with optimal medical therapy (an ACE inhibitor or ARB plus risk-factor control), reserving revascularization for medically refractory hypertension, recurrent flash pulmonary edema, or progressive kidney impairment from bilateral or solitary-kidney disease.
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What this article covers
- Overview
Renal artery stenosis narrows one or both renal arteries, causing renal hypoperfusion that activates the renin-angiotensin-aldosterone system and produces renovascular hypertension, a potentially curable secondary cause of hypertension.
- Epidemiology
Atherosclerotic renovascular disease is the more common form overall, occurring in patients over 45 years, particularly those with coronary, cerebrovascular, or peripheral arterial disease.
- Risk factors
Diffuse atherosclerosis: coexisting coronary artery, cerebrovascular, or peripheral vascular disease is the strongest risk factor for the atherosclerotic form.
- Pathophysiology
Renal hypoperfusion from arterial narrowing activates the renin-angiotensin-aldosterone system, with increased renin release driving systemic vasoconstriction, sodium retention, and hypertension.
- Clinical features
Severe hypertension with onset after age 55 years, or abrupt-onset hypertension before age 35 years, are the classic age-based clues for atherosclerotic disease and fibromuscular dysplasia respectively.
- Differential diagnosis
Essential hypertension: the most common cause of hypertension overall, lacking the age-of-onset extremes, bruit, AKI-after-ACE-inhibitor pattern, or asymmetric kidney size that suggest renovascular disease.
- Diagnosis
The diagnosis is confirmed by renal artery imaging showing a stenosis of more than 75% in one or both renal arteries, or more than 50% with post-stenotic dilatation; renal intra-arterial angiography…
- Management
First, start medical therapy for essentially all patients: an ACE inhibitor or ARB, plus treatment of underlying cardiovascular risk factors (hypercholesterolemia, diabetes, smoking cessation); do…
- Complications
Progressive loss of kidney function, from chronic hypoperfusion-related parenchymal damage, especially with bilateral disease or a solitary kidney.
- Prognosis
Medical therapy alone achieves outcomes similar to revascularization in atherosclerotic disease with stable kidney function, as shown consistently across the STAR, ASTRAL, and CORAL randomized trials.
- Prevention
Control standard atherosclerotic risk factors (blood pressure to guideline target, LDL cholesterol with a statin, glycemic control in diabetes, smoking cessation) to reduce progression of the atherosclerotic form.
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Secondary hypertension is high blood pressure from an identifiable, often correctable cause, such as primary aldosteronism, renal or renovascular disease, obstructive sleep apnea, or endocrine tumors. It should be suspected with resistant, early-onset, or abrupt hypertension, and identifying the cause can cure or greatly improve control.
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