Introducción: múltiples agentes quimioterapéuticos que se usan comúnmente pueden causar síndrome de Fanconi (SF) completo o parcial. El SF es una tubulopatía proximal que produce alteraciones electrolíticas y ácido-básicas, donde se evidencia pérdida de glucosa, aminoácidos, calcio, fósforo, potasio, ácido úrico y se produce acidosis metabólica por pérdida de bicarbonato. El SF usualmente no es reportado y muchas veces no se realiza el diagnóstico. Objetivo: resaltar la importancia del monitoreo urinario y sérico en pacientes que estén sometidos a quimioterapia, así como describir la literatura reciente acerca de la asociación entre agentes quimioterapéuticos y síndrome de Fanconi parcial o completo. Presentación de los casos: se presenta una serie de casos de pacientes pediátricos oncológicos con función renal preservada, donde se produjeron diferentes manifestaciones de nefrotoxicidad tubular proximal secundaria a agentes quimioterapéuticos como antimetabolitos, agentes alquilantes y antraciclinas. Discusión y conclusión: el espectro del SF puede ir de una tubulopatía proximal generalizada o completa a alteraciones parciales en la reabsorción de electrolitos. Se debe reconocer la importancia del monitoreo sérico y urinario en pacientes con lesiones tumorales que van a ser sometidos a quimioterapias con agentes potencialmente nefrotóxicos; asimismo, tener en cuenta la dosis, la frecuencia y la combinación de agentes quimioterapéuticos, con el fin de prevenir y tratar complicaciones de toxicidad renal, incluyendo SF completo o parcial.
Introduction: Methotrexate is a drug with chemotherapeutic properties frequently used for the treatment of certain types of cancer. The following is a clinical case which, to the best of the authors’ knowledge, is the first report in Colombia on nephrotoxicity caused by this drug and describes the consequences as well as the treatment provided at a quaternary care hospital. Case report: A 71-year-old patient with a diagnosis of non-Hodgkin’s lymphoma with normal renal function underwent chemotherapy (high-dose methotrexate intravenously) and developed stage 3 acute renal failure according to the KDIGO guidelines, which was most likely related to methotrexate intake. The patient received treatment with intravenous fluids and sodium bicarbonate as promoters of urine excretion of the toxin, and oral calcium folinate following the institutional protocol. The patient was discharged with recovery of kidney function and improved creatinine and urea nitrogen levels. Conclusion: The treatment given to the patient in this case report shows that although methotrexate nephrotoxicity is a potentially serious entity, it can have a good prognosis if treated promptly.
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