Fatal tumor lysis syndrome presenting with extreme hyperuricemia and dialysis-requiring acute kidney injury in blast-phase chronic myeloid leukemia

Abstract

Tumor lysis syndrome (TLS) is a life-threatening oncologic emergency characterized by hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia, and acute kidney injury (AKI). Although TLS most commonly occurs following initiation of cytotoxic therapy, it may rarely develop spontaneously in rapidly proliferating hematologic malignancies. Chronic myeloid leukemia (CML) is generally considered a low-risk malignancy for TLS; however, blast transformation can markedly increase tumor turnover and precipitate catastrophic metabolic complications. We report a 46-year-old woman with CML who defaulted treatment and follow-up for approximately 5 months and subsequently presented with decreased appetite, abdominal distension, and bilateral pedal edema. Prior molecular monitoring demonstrated disease progression with BCR-ABL transcript levels increasing from 2.5% to 40%. Laboratory evaluation revealed leukocytosis (174.3 × 10 9 /L), severe anemia (41 g/L), thrombocytopenia (26 × 10 9 /L), and 28% circulating blasts consistent with blast-phase transformation. She had severe metabolic derangements including serum creatinine 1379 µmol/L, blood urea nitrogen 64.0 mmol/L, uric acid 2718 µmol/L, potassium 5.8 mmol/L, phosphorus 1.84 mmol/L, calcium 1.85 mmol/L, lactate dehydrogenase 897 U/L, and arterial pH 7.0. The patient fulfilled Cairo–Bishop criteria for both laboratory and clinical TLS with dialysis-requiring AKI. Despite aggressive management with intravenous hydration, rasburicase, febuxostat, correction of electrolyte abnormalities, and urgent hemodialysis, progressive metabolic acidosis and renal failure culminated in death within 48 h of admission. This case highlights the potential for blast-phase CML to present with fulminant TLS-associated AKI and demonstrates the devastating consequences of extreme hyperuricemia, emphasizing the importance of early recognition and prompt intervention in patients with progressive CML.