1 - Central Lisbon University Hospital Centre, Lisbon, Portugal, Paediatric Nephrology Unit
2 - Central Lisbon University Hospital Centre, Lisbon, Portugal, Paediatric Intensive Care Unit
3 - Portuguese Oncology Institute Francisco Gentil, Lisbon, Portugal, Paediatric Unit
4 - Central Lisbon University Hospital Centre, Lisbon, Portugal, Nephrology Department
5 - Central Lisbon University Hospital Centre, Lisbon, Portugal, Pathology Department
- 56th Annual Meeting of the European Society for Paediatric Nephrology, 24-26/9/2024, Valência, Espanha, Poster
- Resumo publicado em: Pediatr Nephrol 2024;39(Suppl 1):S146-S147.
Abstract:
Aims/Purpose: Acute kidney injury (AKI) in acute lymphoblastic leukaemia (ALL) is usually multifactorial and associated with tumour lysis syndrome, drug-induced nephrotoxicity, and sepsis. Symptomatic AKI due to leukemic infiltration of the kidneys as the initial presentation of ALL is rare. We report a case of a T-cell ALL presenting as symptomatic AKI to highlight this rare and severe disease presentation.
Case description: A 17-year-old previously healthy male was admitted to the hospital in his homeland country, Cape Verde, with an eight-day history of left flank pain, vomiting and fever. The patient was edematous, hypertensive, and oliguric. Laboratory workup was positive for anaemia, metabolic acidosis, hyperkalemia and altered renal function (serum creatinine 13 mg/dL, urea 230 mg/dL). Kidneys were enlarged, echogenicity was increased and corticomedullary differentiation was decreased. Assuming a presumptive diagnosis of AKI due to acute glomerulonephritis, haemodialysis and methylprednisolone pulses were initiated. After two weeks, he was discharged home asymptomatic, with normal renal function. After six weeks, he was readmitted due to vomiting, fatigue, and facial oedema. Hypertension (140/75 mmHg) and cervical adenopathies were noted. Haemodialysis was restarted and the patient was transferred to our hospital. Laboratory workup showed anaemia (10 g/dL), leucocytosis (13870/uL) and lymphocytosis (8670/uL) with 20% of blast cells on the peripheral blood smear. Serum creatinine was 6 mg/dL (eGFR 20 mL/min/1.73 m2). The patient promptly underwent a bone marrow aspirate and renal biopsy. Acute T-cell lymphoblastic leukaemia with diffuse and extensive infiltration of the renal parenchymal was diagnosed. With the first dose of dexamethasone, tumour lysis syndrome developed. Continuous venous-venous haemodiafiltration was needed for 36h. Chemotherapy initiation (vincristine and daunorubicin) was withheld for two days. Two weeks after chemotherapy initiation, serum creatinine was within the normal range for age (0.88 mg/dL). One month later, the patient passed away due to refractory septic shock (OXA-48-producing Klebsiella pneumoniae). Post-mortem histopathology showed a normal kidney parenchyma with no neoplastic infiltration.
Conclusions: T-cell ALL presenting as severe AKI due to kidney leukaemic infiltration is rare and leads to delayed diagnosis and treatment. The normalization of kidney function two weeks after treatment initiation suggested a reduction in the initial extensive and diffuse leukaemic neoplastic infiltration of the kidneys, which was documented by post-mortem histopathology.
Keywords: acute kidney injury, acute lymphoblastic leukaemia, haemodialysis