Methotrexate
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Methotrexate Nephrotoxicity and acute kidney injury secondary to toxic methotrexate concentration: case report
A 20-year-old man developed nephrotoxicity and acute kidney injury (AKI) secondary to toxic methotrexate concentration during treatment with methotrexate for non-Hodgkin lymphoma (NHL). The man, who had been diagnosed with NHL for 2 months, was admitted to hospital for his scheduled IV infusion of high-dose methotrexate at 3 g/m2 for 24 hours, along with unspecified IV hydration for urine alkalinisation. Twelve hours after initiation of methotrexate infusion, he complained of discomfort with oliguria (urine volume of 400mL) and oedema, indicative of nephrotoxicity. AKI due to methotrexate was thus considered. The man’s methotrexate infusion was therefore stopped, and a quick check for methotrexate concentration and renal function was performed. Serum methotrexate concentration analysis performed using chemiluminesent micropaticle immunoassay revealed increased methotrexate concentration of 148.7µM (after 12 hours of infusion). Meanwhile, an increase in serum creatinine level from 76 µmol/L to 169 µmol/L was also observed (consistent with AKI). With continued hydration, his urine pH remained between 7 and 8 and urine output remained appropriately high. Considering the serum creatinine levels over the baseline by 50%, AKI due to toxic methotrexate concentration was considered. After referring the literature, the clinical pharmacists recommended two doses of folinic acid [leucovorin] 150mg micro pump every 3 hours or 300mg micro pump every 6 hours. Eventually, he was treated with folinic acid 150mg micro pump every 3 hours along with oral hydrotalcite tablets 500mg every 3 hours and oral sodium bicarbonate tablets 0.9g every 3 hours for urine alkalisation. Despite this treatment, his methotrexate concentration was found to be at toxic level, 82µM (toxic range >20µM; consistent with methotrexate toxicity). At 36 hours, his methotrexate concentration was 49.5 µmol/L and serum creatinine was 300 µmol/L. Thereafter, haemodiafiltration was initiated based on the methotrexate characteristics. After HDF (10 times), a decrease in methotrexate concentration to 1.06 µmoL and serum creatinine to 272 µmol/L was observed. At 444 hours after the methotrexate infusion, liver injury, oral mucositis or other side-effects were not observed. A decline in methotrexate concentration to 0.5 µmoL and serum creatinine to 195 µmol/L was noted. His urine output also returned to normal (urine volume of 3750mL). His chemotherapy was continued without methotrexate, and his kidney parameters remained in normal ranges. Yang Y-Y, et al. How to rescue high-dose methotrexate induced nephrotoxicity and literature review about hemodiafiltration?. Pakistan Journal of Pharmaceutical Sciences 33: 803503824 1163-1167, No. 3, May 2020. Available from: URL: http://www.pjps.pk/wp-content/uploads/pdfs/33/3/Paper%2033.pdf
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Reactions 26 Sep 2020 No. 1823
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