• Vol. 36 No. 8, 679–683
  • 15 August 2007

Avoiding Dialysis in Tumour Lysis Syndrome: Is Urate Oxidase Effective? – A Case Report and Review of Literature



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Introduction: Hyperuricaemia in tumour lysis syndrome (TLS) can cause acute renal failure (ARF), necessitating dialysis. Recombinant urate oxidase (rasburicase) converts uric acid to soluble allantoin, which is excreted easily. Case Report: An 8-year-old boy with stage 3 Burkitt’s lymphoma, TLS was successfully treated with hyper-hydration, diuretics and rasburicase, without dialysis. This is the first paediatric case in Kandang Kerbau Women’s & Children’s Hospital (KKH) in which rasburicase was used. We review the literature on the effectiveness of urate oxidase in avoiding dialysis in TLS. Treatment and Outcome: Our patient developed rapidly rising serum uric acid (SUA) and progressive renal impairment. Hyper-hydration and rasburicase (0.2mg/kg) were administered. SUA rapidly decreased from 1308 to 437 mmol/L within 12 hours. Urate oxidase has shown better results than allopurinol. There was a need for dialysis in 0.4% to 1.7% of patients with haematological malignancies given rasburicase, compared to 20% in patients given allopurinol. Conclusions: Rasburicase can reverse renal insufficiency. Though expensive, it may be cost-effective by lowering incidence of dialysis, shortening the duration of intensive care and hospitalisation, allowing early chemotherapy.

Tumour lysis syndrome (TLS) is frequently associated with lymphoproliferative malignancies. It is the result of massive spontaneous or chemotherapy-induced cytolysis, leading to the release of intracellular metabolites. Hyperuricaemia from breakdown of large amount of nucleic acids in lysed tumour cells causes renal dysfunction from precipitation of uric acid leading to intraluminal tubular obstruction. This results in acute renal failure (ARF), necessitating dialysis. Standard treatment of TLS aims to clear high plasma levels of potassium, uric acid, phosphorus; correct acidosis; prevent ARF by hyper-hydration, and dialysis in ARF. The management of hyperuricaemia traditionally involves the use of allopurinol, hyper-hydration and urine alkalinisation.1 Allopurinol blocks the metabolic conversion of hypoxanthine and xanthine to uric acid, preventing the rise of uric acid, but does not degrade uric acid already present. It has to be given with alkaline hyperdiuresis to clear renal uric acid crystals, a process that takes about 10 days. A new modality is recombinant urate oxidase (rasburicase), which catalyses conversion of uric acid to more soluble allantoin (5 to 10 times more soluble than uric acid; excreted more easily); it acts at the end of the purine pathway and does not lead to the accumulation of intermediary metabolites (xanthine), hence limiting the risk of renal damage. It has a rapid onset of action of 4 hours, hence a potential role in reversing renal insufficiency which may avoid the need for dialysis2 (Fig. 1).

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