TUMOUR LYSIS SYNDROME IN ACUTE LEUKEMIA: THE ROLE OF EARLY RENAL REPLACEMENT THERAPY

 

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TUMOUR LYSIS SYNDROME IN ACUTE LEUKEMIA: THE ROLE OF EARLY RENAL REPLACEMENT THERAPY

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Norazinizah
Ahmad Miswan
Sze Yin Lee sylee86@gmail.com Hospital Ampang Nephrology Unit, Department of Internal Medicine Ampang Malaysia -
Norazinizah Ahmad Miswan norazinizah@gmail.com Hospital Ampang Nephrology Unit, Department of Internal Medicine Ampang Malaysia *
Murugaiah Nadesan murunades@yahoo.com Hospital Ampang Nephrology Unit, Department of Internal Medicine Ampang Malaysia -
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Tumor Lysis Syndrome (TLS) is a potentially fatal oncologic emergency caused by rapid destruction of malignant cells, resulting in massive release of intracellular contents. The ensuing hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia can lead to acute kidney injury (AKI), cardiac arrhythmias, seizures, and sudden death. TLS most frequently occurs in high-grade hematologic malignancies such as acute leukemia and high-burden lymphomas. Early identification of at-risk patients, prophylactic hydration, and timely intervention are crucial to prevent morbidity and mortality. We report a case of severe TLS in a young woman with newly diagnosed T-acute lymphoblastic leukemia (T-ALL), successfully managed with aggressive supportive care and continuous venovenous hemodiafiltration (CVVHDF).

A 22-year-old woman presented with one week of dyspnea, gum bleeding, and significant weight loss. Examination revealed petechiae and scleral icterus. Chest X-ray demonstrated a large mediastinal mass with left pleural effusion, initially treated as pneumonia. Her full blood count showed white cell count 96 ×10⁹/L, hemoglobin 8.1 g/dL, and platelet count 3 ×10⁹/L. Peripheral smear revealed 78% blast cells suggestive of acute leukemia. Initial renal and electrolyte parameters were normal. She received IV dexamethasone 4 mg and IV rasburicase 3 mg while on oxygenation support for respiratory distress. Subsequent investigations revealed lactate dehydrogenase (LDH) 7247 U/L, uric acid 113.7 µmol/L, potassium 5.8 mmol/L, phosphate 1.68 mmol/L, and calcium 1.76 mmol/L, fulfilling TLS diagnostic criteria. She was also started on allopurinol 300 mg daily along with aggressive hydration.

Despite optimal medical therapy, her potassium level rose to 7.1 mmol/L with persistent TLS features. Urgent nephrology input was obtained, and CVVHDF was initiated. Following initiation of CVVHDF, her potassium improved steadily (5.4 → 4.7 → 4.0 → 3.5 mmol/L). The dialysis circuit ran continuously for 44 hours, with final potassium 3.8 mmol/L. She remained hemodynamically stable throughout. LDH level peaked at 13,441 U/L before trending down in parallel with normalization of phosphate, calcium, and renal function. Flow cytometry later confirmed T-ALL, and induction chemotherapy was commenced after metabolic stability was achieved.

This case highlights the critical importance of early recognition, close biochemical surveillance, and prompt renal support in the management of TLS. Even with adequate prophylaxis, metabolic deterioration may occur rapidly, necessitating timely escalation to renal replacement therapy to prevent fatal complications. Key learning points include the need for early risk identification in acute leukemia to enable prompt TLS prophylaxis, and the importance of frequent biochemical monitoring to detect evolving electrolyte and metabolic abnormalities. CVVHDF provides effective and stable correction of refractory electrolyte disturbances while maintaining hemodynamic stability. Multidisciplinary collaboration among oncology, nephrology, and critical care teams is essential to achieve optimal patient outcomes.

Kewords