Contexto: la lesión renal aguda inducida por contraste se ha convertido en un tema de gran interés en la comunidad médica a nivel mundial, siendo la tercera causa de lesión renal aguda adquirida en el hospital. Objetivo: el presente artículo presenta una revisión de la literatura con el fin de actualizar los conceptos de esta patología en el personal de la salud que está en contacto con la población pediátrica y que es sometida a procedimientos con medios de contraste. Metodología: en esta revisión narrativa de la literatura, presentamos la definición, los factores de riesgo, el enfoque clínico y las medidas preventivas de la nefropatía inducida por contraste en pediatría. Resultados: se define que hay un deterioro en la función renal aguda después de la administración del medio de contraste en donde se excluyen otras posibles etiologías y se establece una verdadera relación causal con la sustancia. Los factores de riesgo son múltiples, sin embargo, factores estrictamente relacionados en los niños no han sido establecidos en su totalidad. El abordaje de los pacientes que van a ser sometidos a estudios con medios de contraste inicia desde una historia clínica, un examen físico y unas medidas de laboratorio que permiten evaluar el estado basal de cada paciente para instaurar medidas preventivas. Por su parte, las estrategias de prevención de esta condición son múltiples, sin embargo, no existen guías basadas en la evidencia acerca de esta condición en el paciente pediátrico. Conclusiones: el artículo presenta una revisión de la literatura sobre lesión renal aguda para actualizar los conceptos de esta patología en el personal de la salud que está en contacto con la población pediátrica que se somete a procedimientos con medios de contraste.
Background Transplant-associated thrombotic microangiopathy (TA-TMA) presents with thrombocytopenia, nonimmune hemolytic anemia, peripheral blood schistocytes and end-organ damage to the kidney. TA-TMA is associated with a significant increased morbidity and mortality, especially when treatment is not initiated early. We present a pediatric clinical case of a 35-month child with history of hepatic transplantation, who develop the clinical spectrum of TA-TMA and acquired nephrotic syndrome. Case presentation: A 35-month-old boy with history of hepatic transplantation secondary of atresia of biliary ducts who received immunosuppressive therapy with tacrolimus, mycophenolate and steroids. He presents with 4 days of fever, vomiting, and non-dysenteric diarrhea. He received an initial course of antibiotics without response. After 3 days he continues with fever, low urine output and edema. Vital signs showed high blood pressure and physical exam revealed facial and extremity edema. Laboratory results showed proteinuria and hematuria, low albumin, and high triglycerides. All possible etiologies of nephrotic syndrome were ruled out. Kidney biopsy showed TMA changes. Plasma exchange and Eculizumab were started with clinical improvement. Discussion TMA can be classified as a primary or secondary. Primary TMA can be hereditary or acquired. Acquired TMA included the ones triggered by medications. This clinical syndrome has been described as an endothelial dysfunction secondary of an immune reaction over the endothelium and/or a direct cytotoxic effect over endothelium and platelets. In this case report the use of calcineurin inhibitors (tacrolimus) one of the most common drugs associated with TMA was one the triggers factors. Recent publications have described how these patients that are exposed to any triggers has also a genetically predisposing to develop TMA. There is a lack in diagnostics and prognostic markers. The earliest treatment is stared, the better prognosis and outcomes.
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