Excessive elevation of serum phosphate during tumor lysis syndrome: Lessons from a particularly challenging case

Burkitt’s lymphoma is a common cause of tumor lysis syndrome (TLS) and, in the era of aggressive utilization of prophylactic allopurinol and recombinant uricase enzyme, nephrologists are increasingly witnessing monovalent or divalent cation abnormalities without marked uric acid elevation. An 18-year-old male received his 1(st) cycle of intensive chemotherapy for Burkitt’s lymphoma and developed TLS as defined by the Cairo Bishop criteria. Lactate dehydrogenase peaked at 9,105 U/L (range: 130 – 250) and was accompanied by acute kidney injury, including serum creatinine 2.2 mg/dL on the 4(th) day with oliguria, hyperkalemia, extreme hyperphosphatemia (21.4 mg/dL), hypermagnesemia, and hypocalcemia. Renal replacement therapy decision was made based on life-threatening electrolyte disturbances. The competing necessity to effectively control hyperphosphatemia and avoid the complication of dialysis disequilibrium syndrome prompted us to perform an initial intermittent hemodialysis with simultaneous intravenous mannitol administration, followed by continuous hemodialysis to manage the continued production of phosphorus from cell lysis. Osmotic stability during the therapy session was affirmatively demonstrated (322, 319 mOsm/kg, respectively). The patient showed excellent tolerance for these therapies and eventually recovered renal function as demonstrated during follow-up visits.