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 may develop renal insufficiency and renal atrophy. Duplex ultrasonography and/or angiography are used for screening and to confirm the diagnosis. Treatment of renal artery stenosis primarily consists of antihypertensive therapy, including ACE inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers, or beta blockers. Antihypertensive therapy may need to be continued indefinitely. Patients on ACE inhibitors or ARBs should be closely monitored for an increase in serum creatinine, especially if they have bilateral renal artery stenosis. Patients with may require revascularization. Treatment of the underlying cause is essential to prevent disease progression.
- Atherosclerosis (∼ 90% of cases): occurs more often in men > 50 years of age; increased risk in smokers 
- (∼ 10% of cases): mostly affects women < 50 years of age
- Other causes (∼ 1%) 
- Narrowing of one or both renal arteries → obstruction of renal blood flow → ischemia → renin release and activation of the system → hyperreninemic hyperaldosteronism (increased renin → increased angiotensin → increased aldosterone) → 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 (unilateral or bilateral depending on laterality of RAS) 
- Family history of hypertension is often absent.
- Hypertension: severe (i.e., resistant to therapy) and/or early-onset (i.e, hypertension in individuals < 30 years of age) 
- Abdominal bruit heard over the flank or epigastrium: present during both systole and diastole 
- Flash pulmonary edema
- Features of atherosclerosis in other parts of the body (e.g., peripheral artery disease, coronary artery disease, carotid stenosis)
- Features of renal insufficiency (e.g., nausea, edema)
Imaging is required to confirm a clinical suspicion of renal artery stenosis. Laboratory findings may provide supportive evidence but are not diagnostic.
- Onset of hypertension before the age of 30 years
- Severe hypertension after the age of 55 years
- Hypertension resistant to a 3-drug antihypertensive regimen (resistant HTN)
- New-onset or worsening of renal dysfunction (↑ serum creatinine) after initiating ACE inhibitors or ARBs
- Acute worsening of previously controlled hypertension
- Hypertension with acute end-organ damage (hypertensive emergency)
- Unexplained renal atrophy or asymmetry of > 1.5 cm between the kidneys
- Unexplained acute pulmonary edema
The choice of modality depends on the presence and severity of renal dysfunction. Consider a nephrology and/or radiology consult in patients with significant renal dysfunction (eGFR < 30 mL/min/1.73 m2) to help guide this decision.
- First-line (screening) tests
- Second-line test: catheter angiography (diagnostic gold standard) 
- Additional imaging (not recommended for establishing a diagnosis) 
In patients with renal dysfunction, there is a risk of contrast-induced nephropathy with CT/catheter angiography and a risk of nephrogenic systemic fibrosis with MR angiography with gadolinium contrast.
- Increased systolic flow velocity in the renal artery (on duplex US) 
- Segmental narrowing of one or both renal arteries
- Stenotic segment(s) can be complete or partial and solitary or multiple.
- Hemodynamically significant renal artery stenosis 
- The site of renal artery stenosis differs according to the underlying etiology.
- Ipsilateral renal atrophy (decrease in kidney size) 
- Idiopathic cause
- Cardiovascular disease: atrial fibrillation, endocarditis, valvular or ischemic heart disease
- Renal artery disease: renal artery dissection, Marfan syndrome, polyarteritis nodosa, fibromuscular dysplasia
- Hypercoagulable states: antiphospholipid syndrome, polycythemia vera, factor V Leiden
Diagnosis is based on the presence of clinical features. Imaging confirms the diagnosis.
- Laboratory studies
Imaging studies (confirmatory)
- Abdominal CT scan
- Color Doppler ultrasound: decreased or absent blood flow
- Other: Assess for cardiovascular causes.
- Antihypertensive therapy (e.g., ACE inhibitors, ARBs)
- Anticoagulation (e.g., direct oral anticoagulants, warfarin)
- Percutaneous endovascular therapy (e.g., thrombolysis, thrombectomy with or without angioplasty)
- Medical therapy: preferred initial therapy in all patients
- Good response to optimal medical therapy : Continue medical therapy indefinitely.
- Poor response to optimal medical therapy: Consider revascularization procedures (endovascular/surgical).
- HTN, chronic renal insufficiency, or a solitary functional kidney: Revascularization is typically required to control HTN and prevent worsening of renal function. with cardiac disease, complicated
Treatment of associated hypertension 
- Multiple agents may be required to achieve blood pressure control.
- Regimens including an ACE inhibitor or an ARB are preferable.
- Monitor renal function if ACE inhibitors or ARBs are initiated ; discontinue these medications if renal function worsens. 
- Avoid hypotension, especially in patients who do not undergo revascularization. 
- Antihypertensive therapy may need to be continued indefinitely. 
Closely monitor serum creatinine and K+ after initiating ACE inhibitors or ARBs, especially in patients with bilateral renal artery stenosis. Onset or rapid worsening of renal dysfunction can often be reversed by promptly discontinuing the agent.
Treatment of atherosclerosis 
- Lifestyle modification (see “Treatment of atherosclerosis” for details)
- High-intensity statin therapy (i.e., atorvastatin or rosuvastatin ) unless contraindicated 
- Glycemic control in patients with diabetes
- Consider antiplatelet therapy.
Revascularization procedures 
- Not routinely recommended for patients with well-controlled HTN on optimal medical therapy 
- Only of moderate benefit in patients with fibromuscular dysplasia and of uncertain benefit in patients with atherosclerotic renal artery stenosis 
- Unlikely to be beneficial in patients with small, nonviable kidneys 
- Should be reserved primarily for patients with poor response to optimal medical therapy or those with severe bilateral disease or stenosis affecting a solitary functioning kidney
with any of the following:
- Heart failure with recurrent acute decompensations
- Sudden unexplained acute pulmonary edema
- Uncontrolled unstable angina despite maximal medical therapy
- Complicated or severe hypertension
Bilateral stenosis or stenosis of a single functioning kidney:
- With progressive renal insufficiency
- Or asymptomatic patients with
Endovascular revascularization: percutaneous transluminal renal angioplasty
- Indications: appropriate for most patients who require intervention
- Potential risks: injury at the vascular access site, atheroembolism, retroperitoneal hematoma, and renal artery dissection or rupture
Surgical revascularization: aortorenal bypass surgery
- Disadvantages: potential morbidity and mortality risks of open surgical repair
Further management 
- Dose reduction of antihypertensive agent(s) as required
- Serial postprocedural duplex US to monitor response to therapy and identify restenosis