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Kidney Week

Abstract: PO0119

Continuous Venovenous Hemofiltration for Hypouricemic Tumor Lysis Syndrome and Extreme Hyperphosphatemia Complicated by AKI

Session Information

Category: Trainee Case Report

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Saleem, Muhammad Omar, Augusta University Medical College of Georgia, Augusta, Georgia, United States
  • Chughtai, Ambreen, FMH College of Medicine and Dentistry, Lahore, Punjab, Pakistan
Introduction

Tumor lysis syndrome (TLS) is an oncological emergency and can cause Acute Kidney Injury (AKI) mostly by acute urate nephropathy. We present a case of hypouricemic TLS and severe hyperphosphatemia leading to AKI, effectively managed by Continuous Veno-Venous Hemofiltration (CVVH).

Case Description

44-year male with newly diagnosed Burkitt’s lymphoma and currently receiving first cycle of da-EPOCH chemotherapy, was found to have clinical TLS per Cairo-Bishop definition. Laboratory studies were significant for hyperkalemia (K 6.4 mEq/L), hyperphosphatemia (Phosphate 13.0 mg/dL), hypocalcemia (Ca 6.9 mg/dL) and high LDH in addition to oliguric AKI with elevated serum creatinine (2.5 mg/dL, baseline 0.8 mg/dL). Surprisingly Uric acid level was low (1.8mg/dL) as patient had been on prophylactic Allopurinol. Patient did not have any signs of hypovolemia or post renal obstruction. Urine microscopy was bland. Urgent Hemodialysis (HD) session was provided for malignant hyperkalemia. AKI was assumed to be hyperphosphatemia-induced rather than urate nephropathy in TLS. Renal biopsy was considered but deferred due to high risk of bleeding. Hyperkalemia resolved with one session of HD, but hyperphosphatemia rebounded with worsening of creatinine. So CVVH was initiated and carried out for 72 hours. It lowered serum phosphate level to normal range with resolution of AKI.

Discussion

With the broad use of hypouricemic agents, calcium phosphate deposition, rather than hyperuricemia is becoming the leading cause of AKI in TLS. Choosing an appropriate dialysis modality is crucial to prevent further phosphate nephrotoxicity. Intermittent HD followed by CVVH may be an effective approach. CVVH should be considered as a preferred modality to achieve a sustained lowering of phosphate level and prevent rebound hyperphosphatemia. Our case is an excellent example when HD followed by CVVH helped in early renal recovery by effectively lowering serum phosphate levels.