<p><strong>Introducción.</strong> La función retardada del injerto renal se presenta en 20 a 50 % de los trasplantes renales.<br /><strong>Objetivo.</strong> Describir el comportamiento de la lipocalina urinaria asociada a la gelatinasa de neutrófilos en receptores de trasplante renal de donante fallecido y compararlo con el porcentaje de descenso de la creatinina sérica para detectar tempranamente la función retardada del injerto renal.<br /><strong>Materiales y métodos.</strong> Se evaluaron los niveles de lipocalina urinaria asociada a la gelatinasa de neutrófilos en una cohorte prospectiva 1, 12, 24 y 48 horas después del trasplante renal, y se compararon diariamente con los de la creatinina sérica hasta el quinto día del trasplante.<br /><strong>Resultados.</strong> Se incluyeron en el estudio 79 pacientes con trasplante renal de donante fallecido. La función retardada del injerto renal se presentó en 13 pacientes (16,5 %) y cinco de ellos (6,3 %) necesitaron diálisis en la primera semana. Los valores de lipocalina urinaria asociada a la gelatinasa de neutrófilos en todos los puntos de corte fueron mayores en los pacientes con función retardada del injerto renal (p=0,526, p=0,049, p=0,032 y p=0,001, respectivamente). Se estableció un valor de más de 120 ng/ml a las 48 horas como factor de predicción de la función retardada del injerto, con una sensibilidad de 75 % y una especificidad de 71 %; el valor de creatinina sérica que mejor discriminó la función retardada se presentó a las 48 horas (59,5 %), con una sensibilidad de 92 % y una especificidad de 83 %. En la regresión logística los únicos valores significativos para predecir la función retardada del injerto renal fueron los de la creatinina serica.<br /><strong>Conclusión.</strong> Los niveles de lipocalina urinaria asociada a la gelatinasa de neutrófilos a las 48 horas del trasplante renal predijeron la función retardada, incluida la necesidad de diálisis, pero no fueron superiores a los de la creatinina sérica para la detección temprana.</p>
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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