ABSTRACT
Se presenta el caso de una adolescente sana que, como consecuencia de una deshidratación secundaria a un episodio de gastroenteritis aguda, manifiesta un cuadro compatible con necrosis tubular aguda (NTA), con buena evolución posterior. En la población infantil, esta entidad es, mayoritariamente, postisquémica, debido a hipoperfusión y fallo prerrenal prolongado que, al no ser corregido con prontitud, evoluciona de forma insidiosa a fracaso renal intrínseco. A pesar de estar descrito en la bibliografia, lo infrecuente del caso en la actualidad, debido a las pautas establecidas de rehidratación oral, obliga a reflexionar sobre la necesidad de una mayor atención en los pacientes de riesgo (diarrea o vómitos cuantiosos), para diagnosticar de forma precoz las lesiones prerrenales y corregirlas adecuadamente, evitando así un daño mayor. Se resumen las causas de fracaso renal agudo (FRA) en la población infantil; realizándose un diagnóstico diferencial entre las más frecuentes. Asimismo, se describe brevemente la fisiopatología de la NTA. (AU)
Subject(s)
Adolescent , Female , Humans , Kidney Tubular Necrosis, Acute/diagnosis , Diagnosis, Differential , Kidney Tubular Necrosis, Acute/etiology , Gastrointestinal Diseases/complicationsSubject(s)
Calciphylaxis/etiology , Protein S Deficiency/etiology , Renal Dialysis/adverse effects , Calciphylaxis/drug therapy , Calciphylaxis/pathology , Female , Heparin, Low-Molecular-Weight/therapeutic use , Humans , Hyperparathyroidism, Secondary/etiology , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/therapy , Middle Aged , Protein S Deficiency/metabolism , Protein S Deficiency/pathology , Skin/pathologyABSTRACT
Vascular calcifications are frequent in hemodialysis patients. Its incidence ranges from 25 to 67% depending of different series. Thirty hemodialysis patients were selected from a dialysis population of 150 patients. These 30 patients were divided into two groups: group I included 15 hemodialysis patients with severe secondary hyperparathyroidism and severe, roentgenographically visible diffuse vascular calcifications, and group II included 15 other hemodialysis patients with moderate hyperparathyroidism without radiographic evidence of arterial calcifications. The control group comprised 20 normal volunteers. In all patients, measurements of protein C activity, free protein S and intact parathyroid hormone (PTH) were performed. Statistical analysis showed that free protein S in the patients of group I had a tendency to be lower than in the patients of group II (p < 0.01) and the control group (p < 0.001). We did not find significant differences in free protein S between group II and control group patients nor a significant correlation between intact PTH and free protein S in groups I and II. Protein C activity was found to be in the normal range in both groups. Free protein S deficiency in patients of group I would suggest a synthesis defect by impaired endothelial cells-due to vascular calcifications (?). Free protein S deficiency could increase the risk of thrombotic complications in these patients.
