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TLS Calcium Phosphate Deposition AKI — ESENeph MCQ

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HardAcute Kidney InjuryTLS Calcium Phosphate Deposition AKIESENeph

A 43-year-old man develops AKI (creatinine 650 umol/L) 48 hours after starting tumour lysis syndrome prophylaxis with rasburicase. His uric acid level is paradoxically normal (120 umol/L). Urine microscopy shows abundant birefringent crystals. His phosphate is 4.2 mmol/L, calcium 1.70 mmol/L. What is the most likely mechanism of AKI?

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Correct answer: A — Calcium phosphate deposition from hyperphosphataemia and hypocalcaemia

In tumour lysis syndrome (TLS), the massive release of intracellular contents causes hyperphosphataemia, hyperkalaemia, hyperuricaemia, and secondary hypocalcaemia. While rasburicase effectively converts uric acid to allantoin (explaining the normal urate), the calcium-phosphate product elevation causes calcium phosphate crystal deposition in the renal tubules — this is the predominant mechanism of AKI in TLS when urate is controlled. The hypocalcaemia results from calcium binding to excess phosphate. Xanthine nephropathy can occur with rasburicase but is rare and would show xanthine crystals, not birefringent crystals. Management includes aggressive IV hydration, phosphate binders, and RRT if refractory.

Reference: Cairo & Bishop 2004 – Tumour Lysis Syndrome; Howard et al 2011 – TLS Prevention