1 - General Paediatrics Department, Hospital Dona Estefânia, Centro Hospitalar de Lisboa Central, Lisbon, Portugal
2 - Paediatric Nephrology Unit, Hospital Dona Estefânia, Central Lisbon University Hospital Center , Lisbon, Portugal
- 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):S106-S107.
Abstract:
Purpose: Ifosfamide (IFO)-induced renal toxicity often presents as Fanconi syndrome (FS) and/or reduction in glomerular filtration rate (GFR). While most cases resolve after completion of chemotherapy (CTX), FS may be detected several months after exposure. If left untreated, metabolic bone disease may develop. We present 3 cases of FS secondary to IFO.
Methods: We collected data from patients over the last ten years who presented with ifosfamide-induced Fanconi Syndrome at our hospital.
Results: Case 1: A 2-year-old boy with Burkitt lymphoma and GFR of 60 mL/min/1.73m2 was treated with vincristine (VCR), cyclophosphamide, doxorubicin, and prednisone. He relapsed 3 months later, which prompted a salvage regimen with rituximab, IFO, carboplatin and etoposide, followed by allogeneic stem cell transplantation. During relapse treatment, downward crossing of weight and height centiles, metabolic acidosis and electrolyte disturbances were noted. FS was diagnosed and adequate supplementation was initiated with improvement of the patient’s condition. Treatment was stopped 5 years later. Case 2: A 17-month-old boy with bladder rhabdomyosarcoma causing bilateral obstructive kidney disease underwent decompressive percutaneous nephrostomy and 4 cycles of IFO, VCR, actinomycin and doxorrubicin. GFR before CTX initiation was 75 mL/min/1.73m2. Following treatment, tumor enlargement occurred. Biochemical disturbances consistent with FS were noted and the patient started oral supplementation. A second CTX protocol with VCR, irinotectan and temozolamide was performed. To date, the patient maintains osteopenia, supplemented with vitamin D and phosphorus. Case 3: A 6-year-old boy with anaplastic nephroblastoma and preserved renal function underwent nephroureterectomy and CTX protocol with VCR, dactinomycin, and doxorubicin. After one year, he relapsed and was treated with 6 rounds of IFO, carboplatin and etoposide. One year after finishing CTX he reported general malaise, and biochemical workup was consistent with FS, with plasma phosphate of <0,7 mg/dL. However, the patient lost follow up. At 15 years of age, he presented multiple pathologic fractures and weight and height at -6,2 and -7,6 SDS, respectively. Rickets secondary to previous FS was assumed, currently with normal plasma phosphate. The patient was started on vitamin D and zoledronic acid.
Conclusions: These cases illustrate the importance of close monitoring to identify renal toxicity of IFO as early as possible to allow adequate supplementation. Follow up must include detailed CTX protocols, growth, blood pressure evaluation, and laboratorial surveillance of kidney function and signs of tubulopathy.
Keywords: congenital nephrotic syndrome, rivaroxaban