- Clinical science
Renal artery stenosis is the narrowing of one or both renal arteries. It is most commonly caused by atherosclerosis. In young women, fibromuscular dysplasia is an important underlying cause. Decreased renal blood flow due to renal artery stenosis causes activation of the renin-angiotensin-aldosterone system, which in turn results in secondary hypertension. Physical examination may reveal an abdominal bruit. Patients with progressive renal artery stenosis develop renal insufficiency and progressive renal atrophy. Hypokalemia in a newly diagnosed case of hypertension or an abrupt increase in creatinine after initiating ACE inhibitors or angiotensin receptor blockers is suggestive of renal artery stenosis. The diagnosis is confirmed by duplex ultrasonography or angiography. Treatment of mild renal artery stenosis primarily consists of antihypertensive therapy. The antihypertensives of choice are paradoxically ACE inhibitors and angiotensin receptor blockers; calcium channel blockers or beta blockers can also be used. Patients on ACE inhibitors or angiotensin receptor blockers should be closely monitored for an increase in serum creatinine, especially if they have bilateral renal artery stenosis. Patients with severe renal artery stenosis will require renal angioplasty.
- Accounts for 1–10% of all hypertension cases.
- 5–25% of pediatric cases of secondary hypertension cases have a renovascular etiology.
- Age and sex preponderance depend on the underlying cause (see “Etiology” below).
Epidemiological data refers to the US, unless otherwise specified.
- Atherosclerosis (∼ 90% of cases): occurs more often in men > 50 years of age
- (∼ 10% of cases): mostly affects women < 50 years of age
- Narrowing of one or both renal arteries → obstruction of renal blood flow → ischemia → renin release and activation of the → hyperreninemic hyperaldosteronism → increased sodium retention and peripheral vascular resistance → renovascular hypertension ()
- Prolonged renal hypoperfusion → chronic stimulation of the juxtaglomerular apparatus to secrete renin → hyperplasia of the juxtaglomerular apparatus
- No improvement in renal blood flow → ischemic renal injury → renal insufficiency and progressive renal atrophy
- Decreased kidney function (see “ Diagnostics” in )
- ↑ Serum creatinine > 30% after antihypertensive treatment with ACE inhibitors or is a strong indication of renal artery stenosis.
Imaging (confirmatory test)
- Indications 
Imaging modality 
First-line: non-invasive imaging
- CT or MR angiography
- Duplex ultrasonography
- Second-line: invasive catheter angiography
- First-line: non-invasive imaging
- Tubular stenosis of the proximal renal artery segment → typically atherosclerotic disease
- Stenosis of the distal renal artery segment with a “string-of-beads” appearance → typically fibromuscular dysplasia 
- Significant renal artery stenosis: > 60% reduction in the diameter of the renal artery
- Increased systolic flow velocity in the renal artery (Duplex)
- Decrease in kidney size
- Patients with atherosclerosis: reduce risk factors by statin therapy and lifestyle modification
- Antihypertensive therapy: ACE inhibitors, angiotensin receptor blockers, , beta blockers 
Closely monitor serum creatinine especially in patients with bilateral renal artery stenosis. ACE inhibitor or ARB treatment should be terminated if rapid and/or severe worsening of kidney function occurs.
Revascularization procedures 
- > 60% unilateral stenosis with any of the following:
- > 60% bilateral stenosis
- Progressive renal insufficiency
First-line: percutaneous transluminal renal angioplasty
- Atherosclerotic disease: with stenting
- Fibromuscular dysplasia: typically without stenting
- Second-line: aortorenal bypass surgery
- First-line: percutaneous transluminal renal angioplasty