Jaramillo-Juárez Fernando, Rodríguez-Vázquez María Luisa, Rincón-Sánchez Ana Rosa, Consolación Martínez María, Ortiz Genaro G, Llamas Javier, Anibal Posadas Francisco, Reyes José L
Universidad Autónoma de Aguascalientes, Aguascalientes, México.
Ann Hepatol. 2008 Oct-Dec;7(4):331-8.
Relationship between cirrhosis and renal dysfunction is not yet fully understood. A model of cirrhosis with acute hepatic and renal damage (RF), produced by CCl4 in rats, with hemodynamic and renal functional alterations, similar to those observed in decompensated cirrhosis (DC) in man, was used to study chemical nephrotoxicity in animals. We performed in male Wistar rats hepatic and renal functional and hemodynamic studies in control, cirrhotic and decompensated cirrhotic (DC) groups. Cirrhosis was induced with carbon tetrachloride by chronic administration. Association between liver and renal functional alterations was detected in rats with decompensated cirrhosis, showing fall in mean arterial pressure and reduction of glomerular filtration rate and filtration fraction. Renal hemodynamics did not change in cirrhotic rats, similarly to what occurs in compensated cirrhotic patients. However, DC rats exhibited increased sodium, glucose and phosphate urinary excretions and decreased ATP in renal cortex. DC animals had severe hypoglycemia. There was an extensive liver fibrosis. Glomeruli had hypercellularity and tubules showed extensive vacuolization in cirrhotic and DC rats. The present study suggests that in this model, damage typical of acute tubular necrosis ensues in cirrhotic rats. We describe functional and morphological damage in liver and kidney in a model of cirrhosis that might predispose to the development of acute renal failure when an individual with hepatic damage is exposed in acute way to chemical toxicants.
肝硬化与肾功能不全之间的关系尚未完全明确。采用四氯化碳诱导大鼠产生急性肝损伤和肾损伤的肝硬化模型（RF），该模型具有血流动力学和肾功能改变，与人失代偿期肝硬化（DC）中观察到的情况相似，用于研究动物的化学性肾毒性。我们对雄性Wistar大鼠对照组、肝硬化组和失代偿期肝硬化（DC）组进行了肝脏和肾脏功能及血流动力学研究。通过慢性给予四氯化碳诱导肝硬化。在失代偿期肝硬化大鼠中检测到肝脏和肾脏功能改变之间的关联，表现为平均动脉压下降、肾小球滤过率和滤过分数降低。肝硬化大鼠的肾血流动力学未发生变化，这与代偿期肝硬化患者的情况类似。然而，DC大鼠的尿钠、葡萄糖和磷酸盐排泄增加，肾皮质中的ATP减少。DC动物出现严重低血糖。存在广泛的肝纤维化。在肝硬化和DC大鼠中，肾小球细胞增多，肾小管出现广泛空泡化。本研究表明，在该模型中，肝硬化大鼠会出现典型的急性肾小管坏死损伤。我们描述了肝硬化模型中肝脏和肾脏的功能及形态学损伤，当肝损伤个体急性接触化学毒物时，这种损伤可能易导致急性肾衰竭的发生。
