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Chemotherapy Nephrotoxicity — SCE Medical Oncology MCQ

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HardOncological EmergenciesChemotherapy NephrotoxicitySCE Medical Oncology

Four days after cycle 3 carboplatin for ovarian cancer, a patient with previously normal renal function has vomiting, poor oral intake and oliguria. She has continued naproxen. Creatinine rises from 90 to 420 micromol/L; urine sediment is bland, urate and creatine kinase are normal, blood count is stable and ultrasound shows no obstruction. What best explains the acute kidney injury?

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Correct answer: D — Hypovolaemic renal hypoperfusion compounded by NSAID haemodynamics and carboplatin nephrotoxicity

The temporal history and negative investigations support multifactorial AKI: gastrointestinal loss and poor intake reduce renal perfusion, naproxen impairs compensatory afferent arteriolar vasodilatation, and carboplatin adds nephrotoxic susceptibility. Carboplatin-associated thrombotic microangiopathy would require haemolysis and thrombocytopenia, which are absent. Tumour-lysis nephropathy would require biochemical lysis, particularly hyperuricaemia. Acute interstitial nephritis is less consistent with a bland sediment and no hypersensitivity features. Bilateral malignant obstruction is excluded by ultrasound.

Reference: Carboplatin 10 mg/mL UK summary of product characteristics (Current UK SmPC, accessed July 2026): https://www.medicines.org.uk/emc/product/3787/smpc; NICE NG148 acute kidney injury: prevention, detection and management (Updated October 2024; current NICE guidance): https://www.nice.org.uk/guidance/ng148/chapter/Recommendations