Gentamicin/tenofovir alafenamide
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Gentamicin/tenofovir alafenamide Renal proximal tubulopathy: case report
A 46-year-old man developed renal proximal tubulopathy during treatment with tenofovir alafenamide for HIV infection and gentamicin for febrile neutropenia [not all routes and durations of treatments to reactions onsets stated]. The man, who had a 17-year history of HIV infection, had been receiving antiretroviral therapy (ART) with oral tenofovir alafenamide 10 mg/day, emtricitabine, darunavir and cobicistat. He was diagnosed with Hodgkin lymphoma in 2011 and achieved a complete remission after treatment with bleomycin, doxorubicin, dacarbazine and vinblastine. In July 2019, he presented with febrile neutropenia and anaemia. Hodgkin lymphoma relapse was confirmed. He started receiving cytarabine, dexamethasone and carboplatin (DHAC regimen). Along with ART, he had been receiving various concomitant medications. Prior to initiation of DHAC chemotherapy, he had normal serum potassium, phosphate and bicarbonate levels. Eighteen days after initiation of chemotherapy, he was admitted with febrile neutropenia and hypotension. Upon admission, his WBC count was 0.7 × 109/L. He started receiving piperacillin/tazobactam and gentamicin for febrile neutropenia. The source of sepsis was unclear. He received two daily doses of gentamicin at 3.8 mg/kg, and a third dose of 5.8 mg/kg on day 4 of the admission in the context of sepsis and persistent hypotension. Within 24 hours of receiving gentamicin, he developed marked hypophosphataemia and hypokalaemia. Hypophosphataemia and hypokalaemia were difficult to correct despite unspecified oral and IV replacement therapies. The serum bicarbonate levels were normal. Despite hypokalaemia and hypophosphataemia, the urinary potassium concentration was 24 mmol/L with a fractional excretion of 21.5%, and the urinary phosphate concentration was 8 mmol/L with a fractional excretion of 60.4%. The man had proteinuria, with increased urinary protein creatinine ratio. There was glycosuria, with a urine glucose concentration of >107 mmol/L in the setting of a blood glucose concentration of 18 mmol/L. The hypophosphataemia persisted for 11 days and the hypokalaemia persisted for 7 days. His clinical presentation was consistent with renal proximal tubulopathy. Therefore, gentamicin was discontinued. Eleven days following the last dose of gentamicin and following normalisation of the serum biochemistry, his urinary potassium level was 40 mmol/L, with a fractional excretion of >24.6%. The urinary phosphate concentration was 6 mmol/L, with a fractional excretion of 13.9%. The urine glucose concentration was 0.2 mmol/L. The urine protein creatinine ratio had decreased. Due to improvement in his biochemical parameters, tenofovir alafenamide was continued with close monitoring. He continued treatment for relapsed Hodgkin lymphoma without recurrence of proximal tubulopathy. It was hypothesised that sepsis and lymphopenia might have led to the accumulation of both tenofovir alafenamide and gentamicin in proximal tubular cells lea
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