Background Tumor lysis syndrome (TLS) is an oncologic emergency that most commonly follows cytotoxic treatment of highly proliferative hematologic malignancies; spontaneous TLS as the presenting manifestation of chronic lymphocytic leukemia (CLL) is rare but can cause life-threatening metabolic disturbance and acute kidney injury (AKI). Case presentation A 68-year-old man from rural Oromia presented with 48 hours of progressive weakness, oliguria, and confusion, and a several-month history of weight loss and painless lymphadenopathy. Initial testing showed leukocytosis (WBC 148 ×10 9 /L; absolute lymphocyte count 130 ×10 9 /L), marked hyperuricaemia (14.5 mg/dL), hyperphosphataemia (8.5 mg/dL), severe hyperkalaemia (6.8 mmol/L) with peaked T-waves, elevated LDH (980 U/L), and AKI (serum creatinine 4.9 mg/dL). Flow cytometry confirmed CLL; there was no prior cytotoxic therapy. Management and outcome The patient received emergent cardioprotective and potassium-lowering measures, aggressive isotonic fluids, serial monitoring, and oral allopurinol. Oliguria and progressive uraemia prompted urgent haemodialysis on the day of admission. Rasburicase was not available. After stabilization, inpatient cytoreduction with oral chlorambucil and a short steroid taper was started on day 8. The patient was discharged clinically improved on day 10 with monitoring and outpatient follow-up. Renal function and metabolic parameters progressively normalized, with serum creatinine 1.4 mg/dL and marked hematologic improvement at 6 weeks. Conclusion This case illustrates that spontaneous TLS can unmask previously undiagnosed CLL and cause severe, but potentially reversible, AKI. Early recognition, prompt metabolic stabilization, and timely renal replacement therapy, adapted to local resource availability, are critical to optimize renal and overall outcomes.
Asfaw et al. (Fri,) studied this question.