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Ciclosporin Nephrotoxicity — SCE Rheumatology MCQ

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ModerateRheumatology PharmacologyCiclosporin NephrotoxicitySCE Rheumatology

A 35-year-old woman with severe rheumatoid arthritis develops a blood pressure of 168/98 mmHg four weeks after her ciclosporin dose was increased. Her serum creatinine has risen from 75 to 115 micromol/L. She is clinically euvolaemic, has had no recent intercurrent illness or NSAID exposure, and urinalysis is negative for blood and protein. What is the most likely explanation for these findings?

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Correct answer: A — Ciclosporin-induced renal arteriolar vasoconstriction

The best answer is A. The close temporal relationship to ciclosporin dose escalation, new hypertension, approximately 53% creatinine rise, euvolaemia and bland urinalysis indicate calcineurin-inhibitor nephrotoxicity. Ciclosporin causes dose-dependent, initially reversible renal dysfunction through intrarenal arteriolar vasoconstriction and reduced glomerular filtration; hypertension is also very common. AA amyloidosis usually presents with substantial proteinuria in longstanding inflammatory disease. Prerenal acute kidney injury requires volume depletion. Essential hypertension would not ordinarily cause such an abrupt creatinine rise, while renal artery stenosis is less likely without suggestive vascular findings or a precipitant such as renin–angiotensin system blockade. The UK SmPC advises frequent renal-function and blood-pressure monitoring; a confirmed eGFR fall greater than 25% requires a 25–50% dose reduction.

Reference: Novartis Pharmaceuticals UK Ltd. Neoral Soft Gelatin Capsules, Summary of Product Characteristics, sections 4.2 and 4.4, revised 2026. https://www.medicines.org.uk/emc/product/1034/smpc