Suspected renovascular hypertension / renal artery stenosis

ACR AC Renovascular Hypertension; ESC 2024 hypertension guideline; NICE NG136; ACR/NKF 2020

Two questions, in this order. First, does this patient warrant imaging at all — which means genuinely resistant hypertension, recurrent flash pulmonary oedema, deterioration in renal function after starting an ACE inhibitor or angiotensin receptor blocker, unexplained asymmetric kidney size, or young-onset hypertension where fibromuscular dysplasia is in play. Second, which test — and here the awkward fact drives the answer: the people most likely to have atherosclerotic renal artery stenosis are the people whose kidneys make iodinated contrast and gadolinium least attractive, which is what makes an operator-dependent duplex genuinely the right first study rather than a compromise.

A hypertensive adult in whom a secondary cause is being sought, or a patient whose renal function or fluid balance has behaved in a way that points at the renal arteries — a creatinine that jumped after an ACE inhibitor was started, pulmonary oedema that keeps recurring with preserved ventricular function, or a kidney that is measurably smaller than its neighbour.

Referenced decision support — confirm against your local protocol.

Decision support, not a directive. Protocols and timings shown are typical published ones — your local protocol takes precedence, and the vetting radiologist decides.

The request in front of you

Everything is optional. Leave a field alone and the answer assumes nothing — the verdict updates as you go.

Study requested

What the referrer actually asked for. It is evidence of intent, not a constraint on the right answer.

Contrast as written

What the request form says, not what it should say.

Age

Pick a band, or type an exact age if it matters.

years

Pregnancy status

eGFR

Only needed where the pathway itself changes with renal function — not as a routine gate.

Renal risk factors

The question a vetter can actually answer from the request. An explicit “none known” is a real answer, and it removes checks rather than deferring them.

Previous contrast reaction

The pathway — tap anything already done

Marking a study complete moves the answer on. A patient arrives partway through a pathway far more often than at the start of one.

Accept as requested

Renal artery duplex — haemodynamic assessment

Arterial duplex ultrasound

What we'd amend, and why

Renal artery duplex is the first study because it is the only one that measures the thing the diagnosis is actually about. Renal artery stenosis is a haemodynamic diagnosis, not a morphological one — an ostial plaque on a CT angiogram tells you a vessel is narrow, not that the narrowing is driving this patient's blood pressure — and duplex answers the haemodynamic question directly: peak systolic velocity in the stenosis, the renal-aortic ratio against the suprarenal aorta, and the intrarenal tardus-parvus waveform with its prolonged acceleration time downstream. It costs no contrast and no radiation, it can be repeated as often as the clinical course demands, and it returns kidney length, cortical thickness and resistive index in the same sitting, which is the information that decides whether a kidney is salvageable at all. Its weaknesses are real and are about the operator and the patient rather than the physics: bowel gas, body habitus, a long examination, and accessory renal arteries that are present in a substantial minority and are routinely not found. Those are reasons to send the patient to a laboratory that does the study regularly and to report an inadequate study as inadequate — not reasons to open at CT.

Nothing needs resolving before this goes ahead. Routine checks below are owned downstream.

How was this decided?

pathwayadult — Adults with preserved renal function

Decision support only. Local protocol takes precedence.

Worth asking the referrer (5)

None of these hold the request up. They sharpen the protocol or the plan that follows.

Is the hypertension genuinely resistant — above target on three agents including a diuretic at optimal or maximally tolerated doses, with adherence confirmed and out-of-office readings?
It is the difference between an indicated investigation and imaging a compliance problem. Apparent resistance from non-adherence or white-coat effect is common, and a renal artery study does not detect either.
Which specific trigger is present — flash pulmonary oedema, a rise in creatinine after starting an ACE inhibitor or angiotensin receptor blocker, asymmetric kidney size, an abdominal bruit, or onset under 40?
These are the features that lift the pre-test probability out of the range where a positive study is more likely to be incidental atherosclerosis than the cause of the hypertension. Onset under 40 additionally changes which test comes first, because fibromuscular dysplasia sits where duplex is weakest.
If a significant stenosis is found, is this patient a candidate for angioplasty or stenting, or would management be optimal medical therapy either way?
The revascularisation trials were largely negative, so the value of the study is set almost entirely by what follows it. Where nothing would change, the honest answer is that the imaging is not indicated — and saying so is more useful than protocolling it well.
What is the current eGFR, and is the trajectory stable or falling?
It selects the pathway rather than merely modifying it. It also frames the trade-off honestly: the risk of contrast-associated acute kidney injury has been revised down substantially, but in a patient approaching dialysis the calculus is different, and duplex answers the screening question with no contrast at all.
Has this patient had previous renal artery angioplasty, stenting or bypass?
A stent changes both the anatomy and the velocity thresholds that apply on duplex, and it produces beam-hardening on CT and a susceptibility void on MR. In-stent restenosis is a different measurement problem from native-vessel stenosis and the report has to say which one it is answering.

Pathways

Big forks are separate pathways; the first whose conditions match is the one used.

Established chronic kidney disease or eGFR-limited

Role	Study & protocol	Why this answers the question
First line	Arterial duplex ultrasound Renal artery duplex — haemodynamic assessment usually appropriate	This is the arm where duplex stops being the cheap option and becomes the right one. The population that harbours atherosclerotic renal artery stenosis is the population with chronic kidney disease, diabetes and diffuse atheroma, and a renal artery duplex gives a haemodynamic answer with no iodinated contrast, no gadolinium and no radiation in exactly that group. The examination is a specific one: direct interrogation of each main renal artery from origin to hilum with peak systolic velocity and the renal-aortic ratio, plus intrarenal segmental and interlobar waveforms looking for the tardus-parvus pattern — a slow systolic upstroke with prolonged acceleration time — that says a proximal narrowing is haemodynamically significant rather than merely present. Kidney length, cortical thickness and the resistive index come free in the same sitting and are what actually decide whether a kidney is worth salvaging: a small kidney with a thin cortex and a high resistive index does not recover after revascularisation, and knowing that before anyone reaches for a wire is often the most useful thing the study contributes. The honest limitations belong in the request conversation rather than in a refusal — it is operator- and habitus-dependent, bowel gas defeats it, it takes 45 to 60 minutes of a skilled sonographer's time, and accessory renal arteries are routinely missed.
Second line	Ultrasound renal tract Ultrasound renal tract	Where a full arterial duplex is not achievable — habitus, bowel gas, no vascular sonographer available — a grey-scale renal tract study still answers part of the question and answers it cheaply. Asymmetry of more than about 1.5 cm in kidney length, unilateral cortical thinning and a difference in resistive index between the two kidneys are all indirect evidence of a haemodynamically significant unilateral lesion, and a small scarred kidney with a resistive index above roughly 0.8 predicts a kidney that will not recover function whatever is done to its artery. It is a weak rule-out and a useful rule-in, and it should be reported as such rather than as a negative renal artery study.
Problem solving	CT Angiogram — Aorta CT Aorta — Aneurysm Assessment and Planning	Reserved for the patient in whom duplex was non-diagnostic or discordant with the clinical picture AND a positive result would actually lead to intervention. It is worth being precise about the risk being weighed, because it is routinely overstated: the ACR/NKF consensus concluded that the incidence of acute kidney injury genuinely caused by intravenous iodinated contrast has been substantially exaggerated by uncontrolled studies, and that for a patient with eGFR at or above 30 the risk is low enough that a needed examination should not be withheld. Below 30, and in the patient close to needing dialysis but not yet on it, the calculation is different and a nephrology conversation belongs in it — a patient already established on dialysis has, by contrast, very little left to protect. What CT angiography buys is a definitive anatomical map: ostial calcified plaque, accessory arteries that duplex never saw, the aortic disease that would complicate access, and the branch-vessel detail no ultrasound can reach.

The paradox worth naming out loud on this arm: the patients with the highest prevalence of renal artery stenosis are the patients in whom the definitive tests are least attractive, and that is the whole reason an operator-dependent ultrasound holds its place in a modern pathway.
A technically limited duplex is a result, and it must be reported as inadequate rather than as normal. "Renal arteries not visualised" and "renal arteries normal" are opposite findings and they are confused constantly.
Contrast-enhanced MR angiography is the other contrast-sparing route where local practice supports it; group II gadolinium agents carry a very low risk of nephrogenic systemic fibrosis even at low eGFR. This knowledge base has no renal MR angiography node, so that option has to be arranged directly rather than selected here.

Young-onset hypertension — fibromuscular dysplasia in play

Role	Study & protocol	Why this answers the question
First line	CT Angiogram — Aorta CT Aorta — Aneurysm Assessment and Planning usually appropriate	The reason the young patient gets cross-sectional angiography first is anatomical, not enthusiastic. Fibromuscular dysplasia lives in the mid and distal renal artery and in the first-order branches, which is precisely the territory duplex interrogates worst — insonation angles are poor, the vessel is deep and small, and the classic string-of-beads is a morphological finding that velocity measurements do not reproduce. A thin-section arterial-phase acquisition through the abdominal aorta and both renal arteries, reconstructed at sub-millimetre thickness with curved and maximum-intensity reformats along each vessel, shows the beading, the focal tubular type, any dissection and any microaneurysm, and it finds the accessory arteries that carry the lesion in a meaningful minority. The dose and contrast arguments that dominate the atherosclerotic arm largely fall away here: renal function in this group is usually normal, the diagnosis is potentially curable by angioplasty without stenting, and the alternative is decades of antihypertensive therapy in someone with a long life ahead. A positive study should also prompt imaging of the cervicocerebral arteries, because fibromuscular dysplasia is a systemic arteriopathy and dissection and aneurysm elsewhere are what actually kill these patients.
Reasonable alternative	Arterial duplex ultrasound Renal artery duplex — haemodynamic assessment	Reasonable where cross-sectional angiography must be avoided, and a positive duplex in a young hypertensive is informative. A negative one is not: duplex misses distal and branch fibromuscular disease often enough that a normal study in a young patient with genuinely unexplained hypertension should escalate to angiography rather than close the question. It remains the natural test for follow-up after angioplasty, where the comparison is against the patient's own post-procedural baseline.

Fibromuscular dysplasia is the one renovascular diagnosis where intervention has a good record: angioplasty without stenting improves or cures hypertension in a substantial proportion, and the younger the patient and the shorter the duration of hypertension, the better the response.
Young-onset hypertension is not automatically fibromuscular dysplasia. Coarctation, primary aldosteronism, phaeochromocytoma, thyroid disease, oral contraceptives, sympathomimetics and renal parenchymal disease all belong in the same work-up, and some of them are excluded before any imaging is booked.
This arm is entered on age alone. In a patient under 40 who has established chronic kidney disease, the contrast-sparing arm above is selected first and that ordering is deliberate.
Age alone also means this arm is reachable by children and adolescents, and in a child the calculus changes. Paediatric renovascular hypertension is usually mid-aortic syndrome, neurofibromatosis type 1 or Takayasu arteritis rather than classical fibromuscular dysplasia; the differential is different, the vessels are smaller, and the lifetime dose consequence of a thin-section arterial-phase CT is larger. Contrast-enhanced MR angiography or a duplex performed by a paediatric vascular laboratory should be preferred wherever the local service can deliver them, and catheter angiography remains the reference standard in children and is often what the interventionalist wants in any case. A CT angiogram in a child should be a considered decision with a paediatric dose protocol, not the default this arm would otherwise imply.

Adults with preserved renal function

Matches your inputsDefault

Role	Study & protocol	Why this answers the question
First line	Arterial duplex ultrasound Renal artery duplex — haemodynamic assessment usually appropriate	Renal artery duplex is the first study because it is the only one that measures the thing the diagnosis is actually about. Renal artery stenosis is a haemodynamic diagnosis, not a morphological one — an ostial plaque on a CT angiogram tells you a vessel is narrow, not that the narrowing is driving this patient's blood pressure — and duplex answers the haemodynamic question directly: peak systolic velocity in the stenosis, the renal-aortic ratio against the suprarenal aorta, and the intrarenal tardus-parvus waveform with its prolonged acceleration time downstream. It costs no contrast and no radiation, it can be repeated as often as the clinical course demands, and it returns kidney length, cortical thickness and resistive index in the same sitting, which is the information that decides whether a kidney is salvageable at all. Its weaknesses are real and are about the operator and the patient rather than the physics: bowel gas, body habitus, a long examination, and accessory renal arteries that are present in a substantial minority and are routinely not found. Those are reasons to send the patient to a laboratory that does the study regularly and to report an inadequate study as inadequate — not reasons to open at CT.
Second line	CT Angiogram — Aorta CT Aorta — Aneurysm Assessment and Planning	CT angiography is the confirmatory and planning study, and the sequencing matters: it is what you do once duplex has raised the question and an intervention is genuinely on the table, or when duplex could not answer it. Arterial phase only — there is no reason to carry the unenhanced series from the dissection protocol into this question, and that omission is the main dose saving available. Reconstruct thin and reformat along each renal artery; measure the stenosis against a normal segment of the same vessel rather than eyeballing the maximum-intensity projection, which systematically overcalls. Two caveats travel with every report: dense ostial calcification blooms and exaggerates severity, and anatomical narrowing is not haemodynamic significance — a lesion that looks tight on CT with a normal intrarenal waveform on duplex is a lesion nobody should be stenting.
Reasonable alternative	Ultrasound renal tract Ultrasound renal tract	A plain renal tract ultrasound is not a renal artery study and requesting one for this question usually reflects the two examinations sharing a booking code rather than a clinical choice. It still earns its place: asymmetric kidney length, unilateral cortical thinning and an interside difference in resistive index all support a haemodynamically significant unilateral lesion, and it excludes the obstructive and parenchymal causes of renal impairment that sit in the same differential. What it cannot do is exclude renal artery stenosis, and a normal renal tract ultrasound reported against a renovascular question is a false reassurance the referrer will act on.

Before this pathway starts, confirm the hypertension is genuinely resistant and that the more prevalent secondary causes — primary aldosteronism above all — have been addressed biochemically. Imaging a renal artery is not a substitute for an aldosterone-to-renin ratio.
ASTRAL and CORAL both failed to show that stenting atherosclerotic renal artery stenosis beats optimal medical therapy in the broad population. The study is justified by the subgroup in front of you — flash pulmonary oedema, a solitary functioning kidney, deteriorating function, truly uncontrollable pressure — not by the diagnosis being findable.
Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are not contraindicated in renovascular disease. A modest, stable creatinine rise after starting one is expected; a large or progressive rise is the clue that brought the patient here, and it is a reason to investigate rather than an emergency to reverse.

Pitfalls

Imaging apparently resistant hypertension without first excluding non-adherence, an unmeasured white-coat effect and suboptimal dosing. A large proportion of "resistant" hypertension is one of those three, and no renal artery study detects any of them.
Requesting the study when nothing would be done with a positive result. ASTRAL and CORAL were both negative for the broad atherosclerotic population, so a finding that leads only to the medical therapy the patient is already on is a finding that did not need looking for.
Treating a plain renal tract ultrasound as a renal artery study. They frequently share a booking code and they answer different questions; a normal renal tract ultrasound does not exclude renal artery stenosis, and reporting it against a renovascular request creates a false negative the referrer will act on.
Reporting a technically limited duplex as normal. Bowel gas, habitus and a rushed examination produce non-visualisation, and "renal arteries not seen" must be reported as inadequate rather than negative — this is the commonest way renal artery stenosis is missed on this pathway.
Missing accessory renal arteries. They are present in a substantial minority, they can carry the stenosis, and ultrasound finds them unreliably — so a negative duplex in a patient with a strong clinical trigger should escalate rather than reassure.
Confusing anatomical narrowing with haemodynamic significance. An ostial plaque on CT in a 75-year-old with diffuse atheroma is an expected finding; it becomes the cause of the hypertension only when the downstream waveform and the clinical course agree, and stenting a lesion that fails that test exposes the patient to the procedure without the benefit.
Over-calling stenosis on maximum-intensity projections and in densely calcified ostia. Calcium blooms and the projection hides the residual lumen — measure on thin axial and centreline reformats against a normal segment of the same artery.
Applying native-vessel velocity criteria to a stented artery. A stent stiffens the vessel and raises baseline velocities, so in-stent restenosis has different thresholds and is best judged against the patient's own post-procedural study.
Concentrating on the ostium in a young patient. Fibromuscular dysplasia is a mid-to-distal and branch disease, and a study or a report focused proximally will miss it in exactly the group where the diagnosis is most worth making.
Stopping at the kidneys once fibromuscular dysplasia is confirmed. It is a systemic arteriopathy and cervicocerebral dissection and aneurysm are the complications that matter — a positive renal study should prompt imaging of the head and neck vessels.
Withholding a genuinely needed CT angiogram from a patient with chronic kidney disease on the strength of a contrast risk that the ACR/NKF consensus concluded has been substantially overstated. The correct move is a considered trade-off with nephrology, not a reflex refusal.
Treating an expected modest creatinine rise after starting an ACE inhibitor as evidence in itself. It is normal physiology; it is the large or progressive rise, particularly with bilateral disease or a single functioning kidney, that points at the renal arteries.

Priors — what to pull first

Find a previous kidney measurement. A kidney that has lost 1.5 cm or more in length over a few years is far more persuasive than a single cross-sectional measurement, and it is often already recorded in an ultrasound report done for another reason.
Any previous abdominal CT with arterial-phase coverage may already have imaged the renal arteries adequately — an unnecessary repeat is common on this pathway.
A record of previous angioplasty or stenting changes both the anatomy and the duplex velocity thresholds. Retrieve the procedural report before booking, and state on the request which vessel was treated.
The creatinine trend, and specifically its relationship to starting or increasing an ACE inhibitor or angiotensin receptor blocker, is more informative than any single value and belongs on the request.

What makes a good request

Resistant hypertension has a definition and it is worth applying before imaging anything: blood pressure above target on three antihypertensives including a diuretic at optimal or maximally tolerated doses, with adherence checked and white-coat effect excluded by out-of-office measurement. A large share of apparently resistant hypertension is non-adherence, an unmeasured white-coat effect, or a drug interaction, and imaging none of those.
Renovascular disease is not the commonest secondary cause and should not be the only one considered. Primary aldosteronism is more prevalent in this population and is a biochemical diagnosis; obstructive sleep apnoea, chronic kidney disease, thyroid disease and prescribed or recreational drugs all belong on the same list, and several are answered without any imaging at all.
The randomised evidence for revascularising atherosclerotic renal artery stenosis is largely negative — ASTRAL and CORAL both failed to show benefit over optimal medical therapy for the broad population studied. That does not make the diagnosis worthless, but it does move the burden onto the request: what will be done differently if the artery is narrowed? For most atherosclerotic disease the answer is optimal medical therapy either way, and the honest vetting conversation says so.
The situations where the answer does change management are the ones worth imaging for: recurrent flash pulmonary oedema with bilateral disease or stenosis to a single functioning kidney, rapidly deteriorating renal function attributable to the stenosis, hypertension that genuinely cannot be controlled on maximal therapy, and fibromuscular dysplasia in a young patient — where angioplasty without stenting has a real chance of curing or substantially improving the hypertension, and where the patient has decades of drug therapy ahead of them otherwise.
Fibromuscular dysplasia is a different disease with a different imaging target. It affects the mid and distal renal artery and its branches rather than the ostium, it is commonest in women under about 50, and it travels with disease elsewhere — so a positive renal study is a reason to image the cervicocerebral arteries for dissection and aneurysm, not the end of the work-up.

Scoring this once it is done

The classification and risk tools this question ends in.

Doppler Resistive Index (Pourcelot)eGFR (CKD-EPI 2021 Creatinine)Ankle-Brachial Index (ABI)Rutherford Classification TASC II Classification

How these studies are acquired

Contrast, phases and timing for every study on the pathways above.

Renal artery duplex — haemodynamic assessment Ultrasound renal tract CT Aorta — Aneurysm Assessment and Planning

Confirm locally

Renal artery duplex — haemodynamic assessment: timings are typical — confirm against local protocol.
Timings, contrast volumes and rates above are typical published values. Your department's protocol, scanner and patient population decide the actual numbers.
Safety thresholds and premedication policy follow local policy where it differs from the cited guidance.

References

ACR Appropriateness Criteria — Renovascular Hypertension · ACR Appropriateness Criteria
2024 ESC Guidelines for the management of elevated blood pressure and hypertension — secondary hypertension and renovascular disease · Other
NICE NG136 — Hypertension in adults: diagnosis and management · NICE
Cooper CJ, et al. Stenting and medical therapy for atherosclerotic renal-artery stenosis (CORAL). N Engl J Med 2014;370:13-22. · Primary literature
ASTRAL Investigators. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009;361:1953-62. · Primary literature
ACR/NKF consensus statement on the use of intravenous iodinated contrast media in patients with kidney disease (Radiology 2020) · ACR/NKF consensus
ACR Manual on Contrast Media — gadolinium-based agents and nephrogenic systemic fibrosis risk groups · ACR Contrast Manual

Implemented from the cited published sources. Educational and workflow support only; confirm against current guidelines and local policy before clinical use.