• Clinical science

Renal artery stenosis


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.





Clinical features

  • Abdominal bruits heard over the flank or epigastrium; present during both systole and diastole
  • Hypertension that is often resistant to therapy
  • Features of renal insufficiency (e.g., nausea, edema)

References: [4][5][6][7][8]


Laboratory findings

Imaging (confirmatory test)

  • Indications [12][13]
    • Onset of hypertension before the age of 30 years or after 55 years
    • New onset renal dysfunction or worsening of renal function with ACEi or ARBs
    • Unexplained renal atrophy or asymmetry of > 1.5 cm between kidneys
    • Hypertension that is resistant to a 3-drug antihypertensive regimen
  • Imaging modality [12][14][13]
    • First-line: non-invasive imaging
      • Duplex ultrasonography
      • CT or MR angiography
    • Second-line: invasive catheter angiography
  • Findings
    • 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 [4][5]
    • 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

References: [4][5][6][7][8]


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 [12][15]
    • Indications
    • Procedures
      • First-line: percutaneous transluminal renal angioplasty
        • Atherosclerotic disease: with stenting
        • Fibromuscular dysplasia: typically without stenting
          • A stent would be placed if angioplasty is complicated by arterial dissection or renal artery perforation occur during angioplasty.
      • Second-line: aortorenal bypass surgery
        • Bypass surgery may be considered as the first-line revascularization procedure in the following situations
          • Patients with fibromuscular dysplasia affecting small renal arteries or branch renal arteries, or extensive intimal fibrodysplasia
          • Concomitant conditions require open surgical repair (e.g., aortic aneurysm).