Renal artery stenosis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Renal artery stenosis is most often ostial atherosclerosis in older people with systemic vascular disease; fibromuscular dysplasia usually affects younger patients and the mid-to-distal artery. Reduced renal perfusion activates renin, angiotensin and aldosterone, producing vasoconstriction and sodium retention. In unilateral disease the other kidney can excrete sodium, while bilateral severe disease or stenosis to a solitary functioning kidney makes global filtration more pressure-dependent. This explains resistant hypertension, fluid-sensitive pulmonary oedema and the potential fall in filtration after ACE inhibition. Yet many stenoses coexist with essential hypertension and chronic parenchymal kidney disease without causing either, so an anatomical lesion is not itself an indication for repair.

Current management starts with clinical phenotype and optimal medical therapy. Duplex provides velocities, waveforms, kidney size and resistance indices without contrast. CTA or MRA confirms anatomy and guides intervention when duplex is limited. For stable controlled hypertension and renal function, ESVS 2025 specifically recommends against angioplasty or stenting regardless of stenosis degree. Revascularisation is concentrated in populations often excluded from routine trials: repeated flash pulmonary oedema from bilateral disease, truly resistant hypertension with severe stenosis, and severe declining renal function when the kidney still appears viable. Even then, a multidisciplinary discussion weighs embolisation, dissection, contrast injury and restenosis against a realistic blood-pressure, pulmonary-oedema or renal objective.

Key points

Suspect RAS in resistant or abrupt-onset hypertension, unexplained renal decline, asymmetric kidneys, recurrent flash pulmonary oedema, diffuse atherosclerosis or deterioration after renin–angiotensin blockade; many anatomical stenoses are incidental.
Use renal artery duplex first. If it is inconclusive, use CTA or MRA for diagnosis and planning; ESVS recommends cross-sectional angiography over diagnostic catheter angiography.
Do not stent any RAS degree when blood pressure and renal function are controlled. Consider selected atherosclerotic stenting only for resistant hypertension on at least three drugs plus >70% stenosis, bilateral >50% disease with flash pulmonary oedema from acute fluid retention/AKI, or >70% disease with severe renal decline and preserved kidney viability.
For unilateral RAS with hypertension, ESVS recommends an ACE inhibitor or ARB first line, then a calcium-channel blocker and thiazide as first additions. Check baseline and early creatinine, eGFR, potassium and blood pressure.
Do not silently extend that instruction to bilateral severe disease: ESVS says monitored ACEI/ARB may be considered, but the selected UK ramipril SmPC contraindicates significant bilateral RAS or stenosis of a single functioning kidney; choose therapy with renal/specialist input and the actual product licence.
Consider atherosclerotic renal artery stenting only in selected high-risk groups: resistant hypertension on at least three drugs plus >70% stenosis; bilateral >50% disease causing flash pulmonary oedema with acute fluid retention/AKI; or >70% disease with severe renal decline and preserved kidney viability.
Preserved viability before renal rescue includes kidney length >8 cm, cortex >0.5 cm, albumin:creatinine ratio <20 mg/mmol and renal resistance index <0.8 in the ESVS discussion; absence of these features weakens expected renal benefit.
Treat the whole vascular risk: stop smoking, control diabetes and lipids, use antiplatelet therapy when otherwise indicated, and monitor renal function and blood pressure rather than judging success by angiographic diameter alone.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Atherosclerosis

Aortic ostial plaque commonly coexists with coronary and peripheral arterial disease, producing the characteristic older systemic-atherosclerosis phenotype.

Fibromuscular dysplasia

Fibromuscular dysplasia produces alternating narrowing and dilatation in mid-to-distal renal arteries, often presenting as hypertension in younger adults.

Inflammatory or structural disease

Vasculitis, arterial dissection, radiation injury and external compression are uncommon mechanisms that require cause-specific specialist treatment.

Transplant or procedural stenosis

Anastomotic narrowing after transplantation and iatrogenic arterial injury have distinct imaging appearances and procedural treatment pathways.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
RAAS activation
Reduced afferent pressure releases renin, increasing angiotensin and aldosterone to raise vascular tone and retain sodium.
2
Filtration dependence
Angiotensin constricts the efferent arteriole to preserve GFR; ACE inhibition can expose bilateral or solitary-kidney perfusion failure.
3
Pressure natriuresis failure
Bilateral perfusion failure impairs pressure natriuresis, permitting episodic sodium retention, severe hypertension and flash pulmonary oedema.
4
Ischaemic nephropathy
Persistent hypoperfusion, microembolisation and fibrosis cause parenchymal atrophy that eventually cannot recover after restored arterial inflow.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Resistant hypertension

Confirm adherence, correct cuff technique, home or ambulatory readings and removal of pressor drugs before calling hypertension resistant. The ESVS intervention threshold requires failure despite at least three antihypertensive medicines plus >70% atherosclerotic RAS.

Flash pulmonary oedema

Sudden recurrent pulmonary oedema with severe hypertension and fluctuating renal function suggests bilateral perfusion-dependent renin activation, especially when systolic function alone does not explain episodes.

Renal trajectory

Unexplained rapid eGFR loss, asymmetric kidney size or a substantial deterioration after ACEI/ARB raises causal suspicion. Long-standing small scarred kidneys are less likely to recover after stenting.

Atherosclerotic phenotype

Older age, smoking, coronary, carotid or peripheral arterial disease and calcified ostial plaque favour atherosclerotic RAS and high systemic cardiovascular risk.

Fibromuscular dysplasia phenotype

Younger patients, often women, may have hypertension with beading of mid-to-distal renal arteries. Angioplasty is primary intervention, with stenting only as bailout when the current resistant-hypertension and >70% selection criteria are met.

Red flags requiring action

Recurrent flash pulmonary oedema, rapidly accumulating fluid or otherwise unexplained acute kidney injury with bilateral disease requires urgent vascular and renal review.
A marked creatinine rise, oliguria, hyperkalaemia or hypotension after starting an ACE inhibitor or ARB suggests dependence on angiotensin-mediated efferent tone; stop and reassess urgently.
Resistant hypertension means blood pressure remains uncontrolled despite three or more appropriately chosen antihypertensive drugs; with atherosclerotic RAS >70%, this is a selected stenting indication rather than a reason to stent lesser incidental disease.
A small kidney, thinned cortex, heavy proteinuria or high renal resistance index suggests irreversible parenchymal loss and a low chance that revascularisation will restore function.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Renal artery duplex ultrasoundFirst stepFirst line
Why
First-line imaging to assess ostial flow velocities, renal-aortic ratio, intrarenal waveforms, renal size and resistance indices.
Interpretation and limitations
A technically adequate abnormal study raises suspicion, but obesity, bowel gas, accessory arteries and operator dependency limit exclusion. Kidney length and cortex help estimate viability.
02
CT angiography
Why
Confirm location, degree and length of stenosis, aortic calcification, accessory vessels and feasibility of endovascular treatment.
Interpretation and limitations
Relate >50% or >70% thresholds to the exact clinical phenotype; calcification can overestimate luminal narrowing and contrast requires an individual renal-risk plan.
03
MR angiography
Why
Cross-sectional alternative when iodinated contrast or radiation is unsuitable and MRI is feasible.
Interpretation and limitations
It can overestimate stenosis and gadolinium choice matters in severe renal impairment; use CTA or MRA over catheter angiography for establishing diagnosis.
04
Renal function, potassium, urine ACR and urinalysis
Why
Establish parenchymal disease, baseline treatment safety and probability of renal recovery.
Interpretation and limitations
Heavy proteinuria favours intrinsic kidney damage. ESVS cites ACR <20 mg/mmol among preserved-viability features; creatinine and potassium must be rechecked after RAAS blockade.
05
Ambulatory/home blood pressure and adherence review
Why
Confirm sustained resistant hypertension and document response to an adequate multidrug regimen.
Interpretation and limitations
White-coat effect, missed doses, NSAIDs, stimulants and excess salt can mimic resistance; revascularisation evidence applies only after these are addressed.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Essential hypertension

Essential hypertension is far more common and often coexists with incidental stenosis; a causal high-risk phenotype must be demonstrated.

Primary renal disease

Heavy proteinuria, active urine sediment and diffuse parenchymal imaging change favour intrinsic nephropathy over flow-limiting renovascular disease.

Primary aldosteronism

Hypokalaemia with suppressed renin suggests primary aldosteronism and requires endocrine testing instead of an assumed renovascular mechanism.

Medication or adherence problem

NSAIDs, stimulants, excess dietary salt, inaccurate measurement and missed doses can all create apparent treatment resistance without renovascular causation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Worked controlled caseIncidental severe stenosis with stable controlFirst stepCTA obtained for another reason shows 80% unilateral ostial RAS, but blood pressure is controlled and renal function stable.

1Confirm the clinical history, kidney function, potassium, urine ACR and vascular risk; do not infer causality from the percentage alone.
2Continue optimal medical therapy and surveillance: ESVS says angioplasty with or without stenting is not indicated at any stenosis degree when blood pressure and renal function are controlled.
3Use an ACEI or ARB for unilateral RAS hypertension if indicated, monitor creatinine and potassium, and optimise lipid, smoking and antiplatelet management according to overall atherosclerotic disease.
4Verify continued control through blood pressure and renal trends; investigate if pulmonary oedema, resistance or rapid renal decline develops.

02Preferred stable medical pathwayUnilateral RAS with hypertensionPreferredHaemodynamically relevant unilateral stenosis is associated with hypertension but no high-risk revascularisation phenotype.

1Start a renin–angiotensin system blocker if tolerated; with the selected ramipril product, usual hypertension initiation is 2.5 mg orally once daily, or 1.25 mg with marked RAAS activation, frailty, diuretic-related depletion or creatinine clearance 10–30 mL/min.
2Check blood pressure, creatinine/eGFR and potassium before treatment and within the early treatment period and after dose changes; stop and urgently reassess for major renal decline, hyperkalaemia, hypotension or oliguria.
3Titrate ramipril at two-to-four-week intervals toward control, within product renal maxima: 10 mg/day if creatinine clearance ≥60, 5 mg/day if 30–60 or 10–30 mL/min; never combine ACEI and ARB routinely.
4Add a calcium-channel blocker and thiazide-type therapy as needed and individualise the ESVS age-based tolerated BP target.

03Selected revascularisationHigh-risk phenotype despite medical careUse only after CTA/MRA confirms threshold disease and specialists agree the lesion plausibly drives the syndrome.

1For resistant hypertension despite at least three medicines, consider stenting only when atherosclerotic stenosis is >70%; verify true resistance first.
2For flash pulmonary oedema from acute fluid retention/AKI, consider stenting when bilateral atherosclerotic RAS is >50%; stabilisation of the pulmonary emergency remains immediate.
3For severe renal decline, >70% atherosclerotic RAS may justify stenting only when kidney viability is preserved; review length >8 cm, cortex >0.5 cm, ACR <20 mg/mmol and resistance index <0.8 alongside the full picture.
4Use surgical reconstruction only when revascularisation is clinically indicated and endovascular treatment is impossible or has failed; monitor the predefined clinical objective after either approach.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

ACE inhibitor for hypertension in unilateral RAS, with a defined blood-pressure goal and renal/potassium surveillance; long-term while effective and tolerated.

Ramipril 2.5 mg tablets

For hypertension, start 2.5 mg orally once daily; consider 1.25 mg once daily with strongly activated RAAS, old/frail status, or creatinine clearance 10–30 mL/min. Double at 2–4-week intervals if tolerated, to a product maximum 10 mg/day when CrCl ≥60 and 5 mg/day when CrCl 10–60; haemodialysis patients start 1.25 mg after dialysis, maximum 5 mg/day.

Check renal function and potassium before and soon after initiation/titration. Stop and reassess with major renal decline, hyperkalaemia, hypotension or angioedema. The product SmPC contraindicates significant bilateral RAS or RAS in a single functioning kidney, despite ESVS allowing carefully monitored class use in selected patients. Stop immediately if pregnancy occurs; contraindicated in second/third trimesters and avoid planned pregnancy.

Lipid lowering in atherosclerotic RAS as part of systemic cardiovascular prevention; ESVS targets LDL-C <1.4 mmol/L and at least 50% reduction from baseline.

Atorvastatin 10 mg film-coated tablets

Usual starting dose 10 mg orally once daily, taken any time with or without food; individualise to LDL response at intervals of at least four weeks, maximum 80 mg once daily. Continue long term for atherosclerotic risk reduction while tolerated.

No renal dose adjustment is required. Check liver tests before treatment and if symptoms occur; active liver disease or persistent transaminases >3 times ULN contraindicate use. Stop for clinically important myopathy/rhabdomyolysis and review CYP3A4 interactions. Contraindicated in pregnancy, breastfeeding and women of child-bearing potential without contraception.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Flash pulmonary oedema

Abrupt pressure and sodium loading can cause recurrent life-threatening pulmonary congestion, particularly with bilateral severe disease.

Progressive kidney failure

Bilateral hypoperfusion, repeated acute injury or cholesterol embolisation can progressively reduce viable renal mass and filtration.

Cardiovascular events

Systemic atherosclerosis creates substantial myocardial infarction, stroke, limb ischaemia and vascular death risk beyond the renal arteries.

Procedure-related injury

Angioplasty and stenting can cause access bleeding, dissection, contrast-associated injury, cholesterol embolisation, thrombosis and later restenosis.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Measure home or ambulatory blood pressure and medication adherence; define whether the intended outcome is BP control, prevention of pulmonary oedema or renal stabilisation.
Check creatinine/eGFR and potassium before and after ACEI/ARB initiation or titration and during intercurrent dehydration, NSAID exposure or acute illness.
Trend eGFR, urine ACR and kidney size rather than expecting an angiographic result to restore scarred parenchyma.
After stenting, assess access-site bleeding, cholesterol embolisation, renal injury, dissection and restenosis, then compare the prespecified BP, renal or pulmonary-oedema outcome.
Continue systemic vascular prevention and review smoking, lipids, diabetes and antiplatelet indication because cardiovascular events dominate long-term risk.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Controlled disease should not be stented

This is an explicit all-degrees ESVS recommendation. A visually severe stenosis does not overcome stable renal function and controlled pressure.

Trial populations and high-risk phenotypes differ

Routine stenting failed to improve outcomes in broadly selected stable patients. Flash pulmonary oedema, true drug-resistant hypertension and rapid renal decline with viability are narrower specialist indications.

The product licence can be stricter

ESVS allows monitored ACEI/ARB consideration in bilateral severe RAS or a solitary kidney, while the selected ramipril SmPC contraindicates that anatomy. Prescribing must respect the actual product and specialist alternatives.

Viability predicts plausible renal gain

A kidney longer than 8 cm with cortex over 0.5 cm, low ACR and resistance index below 0.8 is more likely to contain recoverable tissue than a small proteinuric scarred kidney.

FMD is a different lesion

Fibromuscular dysplasia is treated with angioplasty when selected; stenting is bailout rather than the routine atherosclerotic ostial approach.

11Common pitfallsFrequent interpretation and management errors.

01
Stenting an incidental stenosis solely because it exceeds 70% ignores whether blood pressure or renal function is uncontrolled.
02
Calling hypertension resistant without confirming adherence, ambulatory readings and an adequate three-drug regimen over-selects procedures.
03
Starting or escalating RAAS blockade without early creatinine and potassium monitoring can precipitate avoidable kidney injury or hyperkalaemia.
04
Quoting ESVS class advice while overlooking the chosen ramipril product contraindication in significant bilateral or solitary-kidney RAS silently mixes authority levels.
05
Expecting renal recovery from a small, thin-cortex, heavily proteinuric kidney overstates the biological reserve available after revascularisation.

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