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.
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.
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.
Difficult hypertension, progressive CKD, a bruit or asymmetric kidneys without acute organ injury.