Renovascular disease and renal artery stenosis

• Renovascular disease is narrowing of one or both renal arteries. It is a secondary cause of hypertension and a reversible source of kidney injury.
• Two main forms exist: atherosclerotic renal artery stenosis (common, older patients with vascular risk factors) and fibromuscular dysplasia (non-atherosclerotic, mainly women, any age).
• Severe (high-grade) narrowing activates the renin-angiotensin-aldosterone system, causing resistant hypertension, falling kidney function, and in bilateral or solitary-kidney disease recurrent flash pulmonary oedema (Pickering syndrome).
• ACE inhibitors and ARBs are often needed to control blood pressure, but in high-grade or bilateral disease they can precipitate acute kidney injury by removing angiotensin II support from a kidney that depends on it.
• First-line management is medical therapy and risk-factor control. Revascularisation (stenting or angioplasty) is reserved for high-risk phenotypes such as flash pulmonary oedema, progressive chronic kidney disease, or ACE inhibitor intolerance; in uncomplicated disease trials showed no added benefit. ^[1]

By the end of this page you should be able to:

1. Distinguish atherosclerotic renal artery stenosis from fibromuscular dysplasia by patient profile, lesion site and natural history.
2. Explain how a renal artery stenosis produces renovascular hypertension, ischaemic nephropathy and flash pulmonary oedema.
3. Predict when an ACE inhibitor or ARB will be well tolerated and when it will precipitate acute kidney injury.
4. Choose and interpret the imaging tests used to investigate a suspected renal artery stenosis, including duplex ultrasound, CT and MR angiography and catheter angiography.
5. Decide which patients should be treated medically and which should be considered for revascularisation, using current consensus criteria.
6. Recognise renovascular disease in children and adapt management for pregnancy.
7. Cross-check renovascular hypertension against other secondary causes of raised blood pressure.

Classification follows the underlying arterial disease.

• Atherosclerotic renal artery stenosis (ARAS). Atherosclerotic plaque, usually ostial or proximal, on the background of systemic atherosclerosis. This is the common form in older adults with hypertension, diabetes, dyslipidaemia, smoking or known cardiovascular disease.
• Fibromuscular dysplasia (FMD). A non-atherosclerotic, non-inflammatory arteriopathy of medium-sized vessels that most often involves the mid and distal renal artery (and the carotid/vertebral arteries). It produces multifocal "string of beads" lesions or, less often, a focal tubular stenosis. It is the commonest cause in younger adults and in children.
• Other causes. Vasculitides (Takayasu arteritis, polyarteritis nodosa, Kawasaki disease), neurofibromatosis type 1, Williams syndrome, radiation, thromboembolism and middle aortic syndrome occur mainly in children and young adults.

The stenosis may be unilateral or bilateral, may involve a solitary or transplanted kidney, and may be accompanied by aneurysm or dissection.

Renovascular disease is common in selected populations but is usually silent or mild.

• Atherosclerotic disease is evident in 14.1% of all patients with hypertension and in 20% of patients with hypertension and diabetes. Among patients with severe or refractory hypertension, prevalence ranges between 10% and 40%. ^[1]
• In patients with suspected peripheral arterial disease, radiological renal artery stenosis is found in 22% to 45%; in patients evaluated for coronary artery disease, in 14% to 30%. ^[2][1]
• 54% of patients with systolic heart failure who undergo magnetic resonance imaging screening have renal artery stenosis, rising to 68% when heart failure coexists with chronic kidney disease. ^[1]
• In patients over 50 years with advanced chronic kidney disease, prevalence varies between 5% and 22%; in dialysis patients, between 11% and 22%. ^[1]
• Renovascular disease accounted for a diagnosis in 9.2% of patients in the two years before dialysis initiation in US registry data. ^[1]
• Fibromuscular dysplasia affects the renal arteries in an estimated 3% to 4% of the general population based on living kidney donor screening; the CORAL renal artery stenting trial reported an FMD prevalence of 5.8% among patients with renovascular hypertension. FMD is the commonest non-syndromic cause of renovascular hypertension in children. ^{[1][4] [3]}
• Women make up about 92% of registered FMD patients (early reports from the US Registry). Men with FMD present at a younger age with more renal and vascular complications. ^[4]
• In children, renovascular hypertension is responsible for 5% to 25% of hypertension; fibromuscular dysplasia is the commonest non-syndromic cause. ^[6]

Renovascular disease carries a high mortality. The risk of death markedly exceeds the risk of progression to dialysis, 44% versus 16% over a median of 4 years, and patients with acute pulmonary oedema have hazard ratios for death and cardiovascular events of 2.2 and 3.1 respectively compared with lower-risk phenotypes. ^[1]

Atherosclerotic form. Renal atheroma is part of systemic atherosclerosis. Risk factors are the familiar vascular ones: age, hypertension, diabetes mellitus, dyslipidaemia, tobacco, and known coronary, cerebrovascular or peripheral arterial disease. Bilateral or solitary-kidney atherosclerotic disease is most likely to cause clinical problems.

Fibromuscular form. The cause is unknown. Current thinking is a combination of genetic susceptibility (PHACTR1 and other loci) with sex hormone and environmental modifiers (smoking, oestrogen). FMD is classically disease of small and medium arteries, is non-atherosclerotic and non-inflammatory, and clusters in young and middle-aged women. Smoking is associated with a more severe FMD phenotype and earlier presentation. Renal FMD lesions may be multifocal (the classic beading) or focal tubular stenoses; focal disease tends to occur in younger patients and in men, with a higher prevalence of smoking.

Risk modifiers that matter clinically in both forms include diabetes and dyslipidaemia, which amplify microvascular injury beyond the stenosis.

Everything in renovascular disease follows from one fact: reduced renal perfusion.

Modest narrowing has little haemodynamic effect. The renin-angiotensin-aldosterone system (RAAS), briefly the hormonal cascade in which the kidney releases renin to produce angiotensin II and aldosterone, activates when transluminal gradients develop at 70% to 80% luminal obstruction. ^[1] Angiotensin II raises systemic pressure and constricts the efferent glomerular arteriole, which preserves glomerular filtration in the face of a reduced afferent pressure. Aldosterone promotes sodium and water retention.

Initially the rise in blood pressure is driven by renin and is reversible: clearing the stenosis early can normalise pressure. Over time, sodium retention, sympathetic activation, arterial remodelling and renal microvascular injury make the hypertension self-sustaining even after the stenosis is treated. That transition is why late revascularisation often fails to cure blood pressure.

Glomerular filtration then depends, under some conditions and especially with marginal renal perfusion pressure or sodium depletion, on angiotensin II constricting the efferent arteriole. An ACE inhibitor or ARB dilates that efferent arteriole and acutely lowers filtration in the affected kidney. In unilateral disease the contralateral kidney maintains overall filtration, so creatinine changes little and the drugs are useful and safe. In bilateral disease, or disease of a solitary or transplanted kidney, the same dose can precipitate acute kidney injury. This is why a marked jump in creatinine soon after an ACE inhibitor is started or ARB is itself a clinical presentation of high-grade renovascular disease.

There is a further "multiplier" effect. Effective antihypertensive therapy that lowers systemic pressure widens the gradient between the aorta and the post-stenotic kidney and reduces renal blood flow for prolonged periods. The kidney can tolerate reductions in flow of 30% to 40% without worsening tissue hypoxia by reducing filtration and oxygen consumption, but beyond a critical level cortical hypoxia develops, with microvascular rarefaction, mitochondrial failure and interstitial inflammation and fibrosis (ischaemic nephropathy) that no longer reverses when flow is restored. ^[1]

Progressive loss of glomerular filtration rate follows prolonged critical hypoperfusion and is accelerated by diabetes, dyslipidaemia, smoking and other vascular risk factors. Proteinuria is usually modest; heavy proteinuria suggests a different diagnosis or a contralateral problem.

When both renal arteries are significantly stenosed, or a solitary kidney is affected, RAAS activation produces sodium and water retention, uncontrolled hypertension, left ventricular hypertrophy, progressive renal dysfunction and altered pulmonary vascular permeability. The result is sudden accumulation of fluid in the pulmonary interstitium and alveoli over minutes to hours, with acute dyspnoea, often without peripheral oedema, triggered by relatively small shifts in afterload. Recurrent episodes without clear cardiac cause should raise suspicion of renovascular disease. This syndrome is the phenotype excluded from most revascularisation trials and is the one most likely to benefit from restoring renal artery flow. ^[1][2]

Most patients are discovered incidentally during imaging for another reason. When symptomatic, renovascular disease produces a recognisable but non-specific pattern.

• Raised or resistant blood pressure, often needing three or more drugs.
• Breathlessness on exertion, orthopnoea or sudden severe breathlessness at night (flash pulmonary oedema).
• Fatigue, reduced exercise tolerance.
• Progressive tiredness from anaemia of chronic disease.
• In fibromuscular disease: headache, pulsatile tinnitus (a whooshing synchronous with the heartbeat), neck pain or flank/abdominal pain.
• Acute renal colic-like pain can indicate renal infarction in FMD.

• Blood pressure often markedly raised, sometimes with a disparity between arms.
• An abdominal or flank bruit (epigastric) may be heard, but it is insensitive, and absence does not exclude disease.
• Signs of left ventricular hypertrophy or heart failure.
• Pulmonary crackles if in pulmonary oedema.
• Asymmetry of kidney size on palpation is not reliable.
• Retinal, vascular or other evidence of atherosclerosis in the atherosclerotic form.

Signs can be subtle: one study found 5.6% of FMD patients were fully asymptomatic at diagnosis. ^[4]

Consider the diagnosis in:

• new-onset hypertension at an unusually young age, or new hypertension in older adults with vascular disease
• severe, accelerated or resistant hypertension
• creatinine that climbs unexpectedly once an ACE inhibitor or ARB is begun
• worsening renal function in a setting of good control of blood pressure elsewhere
• acute or recurrent pulmonary oedema without obvious cardiac cause
• renal ultrasound showing a kidney size difference over 1.5 cm or renal asymmetry ^[1]
• multiple vascular beds affected or a young woman with hypertension and migraine, pulsatile tinnitus or dissection/aneurysm

The stenosis must be distinguished from other kidney and vascular disease, and from other causes of secondary hypertension.

Renal artery stenosis is one of several secondary causes of raised blood pressure. Distinguishing it matters because the management differs.

Screening for secondary hypertension is part of the 2025 AHA/ACC hypertension guideline (summarised in 2026 review by Brown et al.), which expanded testing for primary aldosteronism and recommends systematic evaluation. ^[5] European Society of Cardiology and American College of Cardiology/American Heart Association guidance likewise recommends screening for renovascular disease in patients with severe or refractory hypertension, accelerated hypertension or heart failure. ^[1] Where primary aldosteronism is suspected, the aldosterone-to-renin ratio is used: a value of 30 or more with plasma aldosterone of at least 10 ng/dL and suppressed renin suggests the diagnosis. ^[5]

Choice of test depends on the question: screening, anatomic detail, functional significance or planning intervention.

• Duplex ultrasound. Non-invasive, cheap, widely available and gives flow data. It assesses peak systolic velocity, the renal-to-aortic velocity ratio (a value of 3.5 or greater correlates with stenosis above 60%) and the renal resistive index. Sensitivity for detecting a stenosis is 91-100% and specificity 82-91% in experienced hands. It is operator-dependent, limited by body habitus, bowel gas and high-grade obesity, and it performs poorly in branch lesions and FMD. ^[1]
• CT angiography. Rapid, multiplanar, excellent spatial resolution; sensitivity 64-96%, specificity 90-92%. It is the preferred first test for suspected FMD and reliably shows accessory arteries. It uses iodinated contrast (contrast-induced nephropathy risk is low, around 5%, even with GFR under 30 mL/min/1.73m2) and delivers ionising radiation. It also assesses aortic and other vascular beds. ^[1][3]
• MR angiography. Sensitivity 94-97%, specificity 85-93%; no radiation or iodinated contrast; gadolinium group II agents have excellent safety in chronic kidney disease. Long acquisition time (about one hour) and a tendency to overestimate stenosis severity. Useful when renal function is poor and CT contraindicated. ^[1]
• Catheter angiography. The gold standard: 100% sensitivity and specificity. It gives definitive anatomy, allows measurement of translesional pressure gradients (Pd/Pa under 0.90 is generally considered haemodynamically significant) and permits immediate treatment. It is invasive and carries the risk of atheroembolism. ^{[1] [3]}
• Other tests. Echocardiography to assess cardiac consequence; ECG and chest radiograph non-specific. Renal vein renin sampling (a ratio of 1.5 or greater between sides is considered significant) can lateralise disease but is rarely needed. Blood pressure measurement in both arms. Urinalysis and quantification of proteinuria as a marker of parenchymal viability. ^[1][6]

A renal resistive index under 0.7-0.8 before revascularisation correlates with a higher likelihood of blood pressure improvement. ^[1]

Before considering intervention, judge whether the kidney beyond the stenosis can recover:

• deterioration of function under 6 months favours viability; over 6 months makes non-viability more likely ^[1]
• modest proteinuria (albumin-to-creatinine ratio under 200 mg/g) favours viability; heavy proteinuria (ratio over 300 mg/g) suggests non-viability ^[1]
• cortical thickness over 0.5 cm with preserved corticomedullary differentiation favours recovery; loss of differentiation suggests atrophy ^[1]
• renal resistive index under 0.8 supports viability; over 0.8 suggests irreversibility ^[1]
• renal length over 8 cm favours viability; under 7 cm suggests advanced ischaemic atrophy ^[1]
• newer imaging (blood-oxygen-level-dependent MRI) may identify "hibernating" kidneys with preserved oxygenation despite reduced flow

There is no single score that establishes the diagnosis. "High-grade" stenosis is defined differently by different bodies: KDIGO uses greater than 75% (or haemodynamic significance), while ACC/AHA/SCAI/SIR/SVM uses 70% or more, or 50% to 69% with haemodynamic significance. ^[2] Severity of renovascular hypertension is judged clinically rather than by a score: resistant hypertension (failure to reach goal on an appropriate three-drug regimen including a diuretic), progressive chronic kidney disease, ACE inhibitor/ARB intolerance and flash pulmonary oedema define the higher-risk end. ^[1]

The most important distinction for prognosis is between lower-risk disease (isolated hypertension, unilateral stenosis, stable kidney function) and higher-risk disease (bilateral or solitary-kidney stenosis, recurrent pulmonary oedema, rapidly falling glomerular filtration rate). The latter is where revascularisation may change outcomes.

The foundation is aggressive medical therapy and risk-factor control. Most patients are managed medically. Revascularisation is an adjunct, not a routine first treatment.

• Treat hypertensive emergencies and flash pulmonary oedema conventionally: intravenous diuretics, nitrates, oxygen or ventilatory support, and controlled blood-pressure reduction.
• In suspected renovascular disease, avoid precipitous falls in systemic pressure that abolish the post-stenotic perfusion.
• If the patient is in acute kidney injury after starting an ACE inhibitor or ARB, stop the drug, rehydrate if volume-depleted, and image the renal arteries.

Medical therapy is the standard first-line management. ^[1] Under KDIGO consensus:

• Aim for blood pressure under 130/80 mm Hg (AHA/ACC and ESC targets) and, for KDIGO, systolic pressure under 120 mm Hg. ^[1]
• Use a renin-angiotensin-aldosterone system blocker (ACE inhibitor or ARB). These are physiologically rational in renovascular hypertension because the stenosis drives renin release, and observational series associate them with lower mortality. Several agents are usually required. ^[1]
• Start low and titrate slowly. Monitor creatinine and potassium after initiation or dose change. A rise in creatinine above 30-50% from baseline, hyperkalaemia, or haemodynamic symptoms should prompt stopping and imaging; a small rise can be acceptable and should not by itself be over-interpreted. ^[1]
• Lipid-lowering therapy to a very-high-risk atherosclerotic target, low-dose aspirin for secondary cardiovascular prevention, tobacco cessation and glycaemic control.
• Loop diuretics for volume and pulmonary oedema.

In fibromuscular dysplasia, ACE inhibitors or ARBs are widely considered first-line for renovascular hypertension, with blood pressure control and, where appropriate, low-dose antiplatelet therapy. ^[3] ACE inhibitors and ARBs are contraindicated in children until critical main renal artery or bilateral disease has been excluded. ^[6]

Weight reduction, dietary salt reduction, alcohol moderation, regular physical activity, sleep optimisation and smoking cessation. In FMD, high-impact or whiplash-prone activities and neck manipulation are best avoided because of dissection risk. Physical activity in general is encouraged.

Decide using three considerations: grade of stenosis, state of the kidney beyond the stenosis, and the clinical presentation attributable to the disease.

Atherosclerotic disease. Two pivotal trials changed practice:

• ASTRAL: no significant difference in renal function with stenting plus medical therapy versus medical therapy alone.
• CORAL: no significant benefit of renal artery stenting in preventing a composite of cardiovascular and renal events.

Both trials under-represented high-risk patients (excluded recent heart failure and recent myocardial infarction; many had stenosis under 75%). ^[2] Real-world and registry data suggest benefit in selected phenotypes, and KDIGO grades revascularisation for ARAS as class IIb (weak), level C-EO (expert opinion) in the 2017 AHA/ACC hypertension guideline. ^[1]

Definite indications (KDIGO consensus): acute pulmonary oedema or acute decompensations of heart failure with high-grade stenosis; progressive chronic kidney disease in high-grade (greater than 75%) stenosis of both kidneys or a solitary kidney; acute kidney injury due to acute occlusion or high-grade stenosis; ACE inhibitor/ARB intolerance in high-grade stenosis; renal artery stenosis of a transplant kidney. ^[1] Possible indications include chronic heart failure with high-grade stenosis, progressive chronic kidney disease with uncontrolled hypertension, asymptomatic high-grade (bilateral or solitary-kidney) disease with viable parenchyma, and dialysis started within three months with a possibly viable kidney. ^[1] Non-indications include moderate to severe hypertension alone and asymptomatic unilateral or bilateral stenosis under 75%. ^[1]

Fibromuscular dysplasia. Balloon angioplasty alone is preferred; routine stenting is discouraged because of stent kinking, fracture and a high rate of stent-related complications. Stenting is reserved for flow-limiting dissection, pseudoaneurysm or rupture. Hypertension cure rates after angioplasty are about 36% and after open surgery about 54% in a 2010 meta-analysis, with younger age and shorter hypertension duration predicting better outcomes. ^{[1] [3]}

Children. Angioplasty is the usual intervention and is often repeated rather than stented; angiography is the gold standard for diagnosis. ACE inhibitors and ARBs are avoided until critical or bilateral disease is excluded. ^[6]

Aftercare. Dual antiplatelet therapy (aspirin plus clopidogrel) after stenting, blood pressure control, surveillance imaging of the treated artery, annual follow-up. Intravascular ultrasound and translesional pressure gradients improve patient selection.

Refer urgently to a nephrologist and vascular or interventional specialist when:

• flash pulmonary oedema accompanies suspected high-grade (bilateral or solitary-kidney) disease
• there is ACE inhibitor/ARB intolerance with rising creatinine in a hypertensive patient
• progressive chronic kidney disease with uncontrolled hypertension is present
• a child or young adult has uncontrolled hypertension with syndromic features
• severe hypertension in pregnancy with rising creatinine

In children and pregnant patients, care belongs in a specialist centre with multidisciplinary expertise.

In patients on dialysis for under three months with non-functioning but possibly viable kidneys ("hibernating" kidneys), revascularisation may restore function. Beyond three months, parenchymal injury is generally considered irreversible and intervention futile. ^[1]

• Embolism and infarction from atherosclerotic plaque, occasionally precipitated by catheter manipulation.
• Progressive ischaemic nephropathy and eventual end-stage kidney disease.
• Pickering syndrome (recurrent flash pulmonary oedema).
• Heart failure and left ventricular hypertrophy from sustained hypertension.
• Complications of intervention: renal artery dissection, perforation, rupture, distal embolisation, contrast-induced kidney injury, restenosis (17% to 41% after angioplasty in children; high rate of stent-related complications in FMD). ^[6]
• Acute kidney injury on RAAS blockade where narrowing is severe and bilateral or solitary.
• Aneurysm or dissection in fibromuscular dysplasia, including intracranial aneurysms (screen once with CT or MR angiography of the head and neck). ^[1][3]

• Untreated high-risk renovascular disease (bilateral, solitary-kidney, or flash pulmonary oedema presentations) has high morbidity and mortality; major cardiovascular events in about one-third over 4 years. ^[1]
• In appropriately selected high-risk patients, revascularisation can restore kidney function (including liberation from dialysis, as in the case of flash pulmonary oedema with progressive kidney disease), improve blood pressure control and reduce hospitalisation. Revascularisation in uncomplicated disease does not improve long-term renal or cardiovascular outcomes over optimal medical therapy.
• In fibromuscular dysplasia, younger patients with shorter hypertension duration have the best chance of cure after angioplasty; older patients and those with long-standing hypertension are less likely to benefit. ^[3]
• In atherosclerotic disease, renal parenchymal damage becomes irreversible after sustained critical hypoperfusion, so timing matters more than grade alone.

• Because renovascular disease is systemic atherosclerosis in its common form, primary prevention of atheroma (control of blood pressure, glucose and lipids, smoking cessation) is also prevention of renal artery stenosis.
• Screening is recommended for severe or refractory hypertension, accelerated hypertension or hypertension with heart failure, rather than routine screening of all hypertensive patients, reflecting the high prevalence in these groups. ^[1]
• FMD is under-recognised: diagnostic delay averages nearly 5 years. A higher index of suspicion in young women with hypertension, plus high-quality vascular imaging, reduces this delay. ^[3]
• In FMD, once one vascular bed is affected, a one-time head-to-pelvis imaging study is used to screen for additional stenoses, aneurysms and dissections; intracranial aneurysm screening (with CT or MR angiography) is specifically recommended because prevalence is higher than in the general population. ^[3]
• Annual specialist follow-up for FMD: blood pressure review, symptoms and periodic imaging of affected beds (about every 2-3 years, extending to 5 years if mild and stable). ^[3]

Children. Renovascular hypertension is responsible for 5% to 25% of childhood hypertension. ^[6] Renal artery stenosis may be unilateral or bilateral (bilateral in 24% to 78% in paediatric series), may involve branch or accessory arteries, and may coexist with middle aortic syndrome (in about 60% of children with middle aortic syndrome). ^[6] FMD is the commonest non-syndromic cause; neurofibromatosis type 1 and Williams syndrome are the next most common, with Takayasu arteritis an important mimic. Present with severe, often malignant hypertension, growth failure or target-organ damage. Duplex ultrasound is a useful first test (sensitivity 65-88%, specificity 83-99%), but angiography remains the gold standard and allows treatment. ^[6] ACE inhibitors and ARBs are avoided until critical main renal or bilateral disease is excluded. ^[6] Management is best in specialist centres; repeat angioplasty is generally preferred to stenting.

Pregnancy. Pregnancy can be the first presentation of renovascular disease (atherosclerotic or FMD). FMD often predates pregnancy but may be diagnosed then. ACE inhibitors, ARBs, direct renin inhibitors and mineralocorticoid receptor antagonists are contraindicated; blood pressure targets follow pregnancy guidelines (under 140/90 mm Hg chronic, immediate treatment of severe hypertension). ^[5] In FMD registry data, about 40% of women had a pregnancy-related complication (most commonly gestational hypertension and preterm birth) and preeclampsia in 7.5%, higher than the general population but lower than with chronic essential hypertension; arterial complications were rare (under 1%). ^[3] Pre-conception counselling, multidisciplinary high-risk obstetric care and, where appropriate, pre-emptive treatment of aneurysms are advised. Pregnancy should not be systematically discouraged.

Older and frailer adults. Ischaemic nephropathy superimposed on long-standing vascular disease is common, and the kidneys are less likely to recover. Decisions are heavily weighted towards medical therapy, symptom relief and quality of life.

Diabetes and chronic kidney disease. Atherosclerotic stenosis is more common and repairable kidney function rarer; aim for guideline-directed blood pressure (under 130/80 mm Hg, encourage under 120 systolic when tolerated) and RAAS blockade when kidney function allows. ^[1] Work suspicious cases up promptly, especially with unexplained loss of eGFR on RAAS blocker.

Transplant recipients. Transplant renal artery stenosis (prevalence 1-23%) reduces allograft survival; angioplasty is usually effective and rarely needs stenting. ^[1]

• Suspect renovascular disease on clinical grounds (resistant/accelerated hypertension, young onset, ACE inhibitor intolerance, recurrent flash pulmonary oedema, paediatric hypertension) because confirmatory imaging (CT or MR angiography) may not be available.
• Duplex ultrasound by a trained operator is the most useful screening tool where available and can be repeated cheaply; it assesses velocity, renal-aortic ratio and resistive index.
• Refer patients with high-risk phenotypes to a centre able to image and revascularise (stenting or angioplasty) rather than trying repeated medical escalation alone.
• In children, non-invasive imaging is often inadequate; arrange transfer to a paediatric centre with interventional radiology if severe or syndromic hypertension is present.
• Medical therapy (RAAS blocker where not contraindicated, statin, aspirin, BP targets, smoking cessation) is universally applicable and should not be delayed waiting for imaging.

Atherosclerotic peripheral arterial disease; secondary hypertension; primary aldosteronism; chronic kidney disease; heart failure; hypertension in pregnancy; hypertension in children; fibromuscular dysplasia.