Synopsis
Recognise clinically important renovascular disease, investigate it proportionately and separate patients needing cardiovascular risk treatment from the small high-risk group who may benefit from revascularisation.
- Most renal-artery stenosis in older adults is ostial atherosclerotic disease; fibromuscular dysplasia more often affects younger women and the mid-to-distal artery, and is considered separately.
- Suspect a renovascular contribution when hypertension is genuinely resistant, starts abruptly or worsens unexpectedly, accompanies an abdominal bruit, or coexists with asymmetrical kidney size, widespread atherosclerosis or otherwise unexplained kidney decline.
- A creatinine rise of 30% or more, or eGFR fall of 25% or more, after starting or increasing an ACE inhibitor or ARB should prompt repeat testing and a search for depletion, NSAIDs and renovascular disease rather than an automatic lifelong drug-allergy label.
- Bilateral severe disease, or stenosis supplying a solitary functioning kidney, is the pattern most associated with salt retention, rapid loss of filtration and flash pulmonary oedema.
- Duplex ultrasound is a useful first-line anatomical and haemodynamic test when performed by an experienced vascular laboratory; an inconclusive scan does not exclude a technically difficult ostial or branch lesion.
- CT angiography usually gives the clearest arterial map, while contrast-enhanced or non-contrast MR angiography may be selected when iodinated contrast or radiation is problematic; modality choice belongs with renal and radiology teams.
- An imaging stenosis is not by itself proof that hypertension or CKD is caused by that lesion. Correlate severity, kidney viability, clinical trajectory and the physiological phenotype.
- For most atherosclerotic stenoses with stable kidney function and controlled blood pressure, optimal medical therapy and surveillance are preferred because routine stenting has not improved major renal or cardiovascular outcomes.
- Revascularisation is an expert-MDT decision for selected high-risk presentations, including recurrent flash pulmonary oedema, truly resistant hypertension with severe stenosis, or severe functional decline while the supplied kidney remains viable.
- Treat the whole vascular patient: confirm smoking status, blood pressure, lipids, diabetes, albuminuria and antithrombotic indication instead of focusing solely on the angiographic percentage.
Key red flags
Kidney function deteriorates substantially soon after ACE-inhibitor or ARB initiation or dose escalation, particularly with little albuminuria, no obvious hypovolaemia and bilateral disease or a solitary kidney on imaging.
Sudden pulmonary oedema recurs with severe hypertension and acute kidney injury, sometimes despite preserved left-ventricular systolic function. Bilateral haemodynamically important disease is a key, treatable possibility.
Investigation priorities
Confirm severity and distinguish sustained resistance from technique, adherence or white-coat effects.
Management branches
Abrupt pulmonary oedema with severe hypertension, acute kidney injury or recurrent unexplained episodes.
- Treat oxygenation, ventilation, blood pressure and congestion through the acute heart-failure pathway, obtain ECG and urgent biochemistry, and avoid an indiscriminate fluid challenge.
- Review prior kidney function, RAAS-blocker exposure and cardiac imaging; request urgent renal-artery imaging if bilateral disease or a solitary functioning kidney is plausible.
- Discuss the case during the same admission with renal, vascular and interventional specialists because selected bilateral atherosclerotic lesions may justify revascularisation once the patient is stabilised.
Difficult hypertension, progressive CKD, a bruit or asymmetric kidneys without acute organ injury.
- Validate blood-pressure technique and adherence, reconcile medicines, quantify ACR and chart eGFR so common pseudo-resistance and intrinsic kidney disease are not missed.
- Use experienced-laboratory duplex first where suitable, progressing to CTA or MRA when suspicion remains high, the scan is indeterminate or intervention planning requires an arterial map.
- If disease is stable, institute medical prevention and planned renal/BP surveillance; refer severe lesions with high-risk clinical features to a renal-vascular MDT rather than arranging routine
Key medicines
ACE inhibitor or angiotensin-receptor blockerChoose and titrate a licensed preparation to the highest tolerated dose under the indication-specific formulary.Check creatinine and potassium before treatment and usually within one to two weeks after starting or increasing; use particular caution in bilateral severe stenosis, a solitary kidney, hypovolaemia, hyperkalaemia or concurrent NSAID use.
Amlodipine and complementary antihypertensivesAmlodipine commonly starts at 5 mg once daily, then is titrated within its licence; combine according to NICE sequencing.Confirm adherence and postural tolerance before escalation; ankle oedema may confuse volume assessment, while beta-blockers, diuretics and alpha-blockers each require indication, electrolyte and comorbidity review.