Wilkinson S P
Z Gastroenterol. 1977 Nov;15(11):663-9.
In cirrhosis and fulminant hepatic failure acute renal failure may occur both without ("functional renal failure") and with tubular necrosis, the two probably being the ends of a spectrum. The underlying pathophysiological change is an intense renal and intra-renal vasoconstriction. Evidence is presented that this is due to systemic endotoxaemia resulting from failure of the liver to filter endotoxins absorbed from the gastrointestinal tract. Acute renal failure complicating obstructive jaundic has also been related to endotoxaemia, but in contrast to cirrhosis and fulminant hepatic failure this is usually due to an associated gram-negative infection and the renal failure almost invariably has the features of acute tubular necrosis. Endotoxins have two major effects on the kidney: (i) renal vasoconstriction, and (ii) glomerular and peritubular fibrin deposition. The nature of the renal failure depends on the balance between these variables which may be profoundly altered by the underlying liver disease.
在肝硬化和暴发性肝衰竭中,急性肾衰竭可能在无肾小管坏死(“功能性肾衰竭”)的情况下发生,也可能伴有肾小管坏死,两者可能是同一病理过程的不同结局。潜在的病理生理变化是强烈的肾内和肾血管收缩。有证据表明,这是由于肝脏无法过滤从胃肠道吸收的内毒素而导致的全身性内毒素血症。并发梗阻性黄疸的急性肾衰竭也与内毒素血症有关,但与肝硬化和暴发性肝衰竭不同的是,这通常是由于合并革兰氏阴性菌感染,并且肾衰竭几乎总是具有急性肾小管坏死 的特征。内毒素对肾脏有两个主要影响:(i)肾血管收缩,以及(ii)肾小球和肾小管周围纤维蛋白沉积。肾衰竭的性质取决于这些变量之间的平衡,而这种平衡可能会因潜在的肝脏疾病而发生深刻改变。