skip to main content

Suspected renal artery stenosis causing ACE-inhibitor-associated deterioration in kidney function — MSRA MCQ

Instant feedback + full explanation. One question, done properly.

HardNephrologySuspected renal artery stenosis causing ACE-inhibitor-associated deterioration in kidney functionMSRA

A 76-year-old man is reviewed 10 days after ramipril 2.5 mg once daily was started for hypertension and CKD G3a A1. Before starting treatment, his creatinine was 104 micromol/L, eGFR 61 mL/min/1.73 m² and potassium 4.5 mmol/L. Today, creatinine is 145 micromol/L, eGFR 42 mL/min/1.73 m² and potassium 4.8 mmol/L. He is clinically euvolaemic and has had no diarrhoea, vomiting, sepsis, NSAID use, potassium supplements or recent contrast exposure. His blood pressure is 154/82 mmHg despite amlodipine 10 mg once daily. During the previous 6 months he has had 2 hospital admissions with acute pulmonary oedema despite preserved left ventricular systolic function. He has no urinary retention symptoms. What is the most appropriate management today?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: D — Stop ramipril, substitute an alternative antihypertensive if needed, and refer for nephrology assessment for suspected renal artery stenosis

Explanation lettering: E = shown as A · A = shown as C · C = shown as D · D = shown as E

This is a clinically significant deterioration in renal function after starting a renin–angiotensin system antagonist: creatinine has risen by approximately 39%, exceeding the NICE 30% threshold. NICE advises first considering reversible causes such as volume depletion and NSAID exposure; these have been specifically excluded. In the absence of another explanation, ramipril should be stopped or reduced to a previously tolerated dose, with alternative blood-pressure treatment used if required. The additional history is decisive. Recurrent acute pulmonary oedema with preserved systolic function, persistent hypertension and a marked ACE-inhibitor-associated fall in GFR together raise concern for haemodynamically significant, potentially bilateral renal artery stenosis. NICE lists suspected renal artery stenosis as an indication for nephrology referral. A is appropriate only when the creatinine increase is below 30% or eGFR reduction below 25%. B would be reasonable if there were a previously tolerated lower dose, but he has newly started ramipril and the stem supports an unmasked renovascular process requiring referral. D delays appropriate specialist assessment; renal ultrasound alone does not adequately assess renal artery stenosis. E does not address the drug-associated renal deterioration and may worsen renal perfusion if it causes volume depletion.

Reference: NICE NG203: Chronic kidney disease: assessment and management — referral criteria (Updated August 2025) — https://www.nice.org.uk/guidance/ng203/chapter/Recommendations NICE NG203: Chronic kidney disease: assessment and management — monitoring renin–angiotensin system antagonists (Updated August 2025) — https://www.nice.org.uk/guidance/ng203/chapter/Recommendations NICE NG203: Chronic kidney disease: assessment and management — management of significant renal function deterioration (Updated August 2025) — https://www.nice.org.uk/guidance/ng203/chapter/Recommendations