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Reversible acute renal failure following single administration of fludarabine

Bone Marrow Transplantation volume 33, page 671 (2004)Cite this article

Fludarabine is a purine analogue with high activity in lymphoid malignancies and a frequent component of reduced-intensity conditioning regimens, due to its immunosuppressive properties. Renal toxicity of fludarabine occurs in less than 5% of patients,1 usually in the context of tumor lysis syndrome.2 In one case report of fludarabine-associated nephrotoxicity occurring after the administration of a cumulative dose of 500 mg/m2 of fludarabine, renal biopsy showed the presence of mesangiocapillary glomerulonephritis.3 Another report described the occurrence of crescentic glomerulonephritis, with p-ANCA positivity, after three courses of treatment with this drug.4 We report a case of acute renal failure developing after the first administration of fludarabine, without associated tumor lysis syndrome.

A 34-year-old male patient with relapsed heavily pretreated Hodgkin's disease was admitted to our transplant unit for an allogeneic reduced-intensity conditioning stem cell transplantation. The patient had previously been treated with several lines of conventional dose chemotherapy, as well as with prior high-dose chemotherapy with autologous stem cell support. Preadmission medication included acyclovir, NSAIDs and corticosteroids. Serum creatinine was 0.7 mg/ml and the EDTA clearance was 108 ml/min. The prescribed conditioning regimen was fludarabine, 30 mg/m2/day for 5 days, and melphalan, 160 mg/m2 on day 5. Prophylactic intravenous acyclovir, 750 mg/m2/day, was given. Less than 24 h after the first dose of fludarabine, serum creatinine level increased to 1.6 mg/ml. By the time this result was available, the second dose of fludarabine had already been administered. Intravenous hydration was increased with monitoring of renal function and volume status. Further deterioration of renal function was seen, with an increase in serum creatinine to 3.7 mg/dl over the following 24 h, after a cumulative fludarabine dose of only 60 mg/m2. Chemotherapy and acyclovir were suspended. Peak creatinine level was 4.1 mg/ml, 4 days after starting fludarabine. There was no evidence of volume depletion or tumor lysis syndrome. Urinalysis showed nine red blood cells per high-power field, without proteinuria, casts or eosinophiluria. Antiglomerular basement membrane and antistreptolysin O antibodies were negative; complement levels were normal. An ultrasound showed normal kidneys and no urinary tract obstruction. Over the following days, renal function improved gradually, with moderate polyuria. Serum creatinine level eventually decreased to 0.9 mg/ml by day 10 and an EDTA clearance on day 42 was 78 ml/min. After 2 months, the patient underwent a reduced-intensity conditioning allogeneic stem cell transplant with TBI (400 cGy)–cyclophosphamide (60 mg/kg for 2 days) conditioning and cyclosporine, mofetil mycofenolate prophylaxis of graft-versus-host disease as well as acyclovir (750 mg/m2/day) as prophylaxis of herpesvirus infection, without renal toxicity.

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References

  1. McEvoy GK (ed). American Hospital Formulary Service – Drug Information. American Society of Health-System Pharmacists: Bethesda, 2001, pp 972–978.

    Google Scholar 

  2. List AF, Kummet TD, Adams JD et al. Tumor lysis syndrome complicating treatment of chronic lymphocytic leukemia with fludarabine phosphate. Am J Med 1990; 89: 388–390.

    Article  CAS  Google Scholar 

  3. Macheta MP, Parapia LA, Gouldesbrough DR . Renal failure in a patient with chronic lymphocytic leukemia treated with fludarabine. J Clin Pathol 1995; 48: 181–182.

    Article  CAS  Google Scholar 

  4. Tisler A, Pierratos A, Lipton JH . Crescentic glomerulonephritis associated with p-ANCA positivity in fludarabine-treated chronic lymphocytic leukemia. Nephrol Dial Transplant 1996; 11: 2306–2308.

    Article  CAS  Google Scholar 

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  1. Instituto Portugues de Oncologia, Lisboa, Portugal

    R Nunes, J L Passos-Coelho, N Miranda, M Nave, F Leal da Costa & M Abecasis

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  1. R Nunes
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  2. J L Passos-Coelho
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  3. N Miranda
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  4. M Nave
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  5. F Leal da Costa
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  6. M Abecasis
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Nunes, R., Passos-Coelho, J., Miranda, N. et al. Reversible acute renal failure following single administration of fludarabine. Bone Marrow Transplant 33, 671 (2004). https://doi.org/10.1038/sj.bmt.1704404

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