This is the report of a case of methotrexate nephrotoxicity for which glucarpidase was used. We use the case to review a number of teaching points related to this new treatment option.
TreviñoLRShimasakiNYangW. Germline genetic variation in an organic anion transporter polypeptide associated with methotrexate pharmacokinetics and clinical effects. J Clin Oncol2009; 27: 5972–5978.
2.
ChristensenAMPauleyJLMolinelliAR. Resumption of high-dose methotrexate after acute kidney injury and glucarpidase use in pediatric oncology patients. Cancer2012; 118: 4321–4330.
WidemannBCBalisFMMurphyRF. Carboxypeptidase-G2, thymidine, and leucovorin rescue in cancer patients with methotrexate-induced renal dysfunction. J Clin Oncol1997; 15: 2125–2134.
5.
BuchenSNgampoloDMeltonRG. Carboxypeptidase G2 rescue in patients with methotrexate intoxication and renal failure. Br J Cancer2005; 92: 480–487.
6.
WidemannBCBalisFMKimA. Glucarpidase, leucovorin, and thymidine for high-dose methotrexate-induced renal dysfunction: clinical and pharmacologic factors affecting outcome. J Clin Oncol2010; 28: 3979–3986.
7.
TuffahaHWAl OmarS. Glucarpidase rescue in a patient with high-dose methotrexate-induced nephrotoxicity. J Oncol Pharm Pract2011; 17: 136–140.
8.
SalandJMLeaveyPJBashRO. Effective removal of methotrexate by high-flux hemodialysis. Pediatr Nephrol2002; 17: 825–829.
