involvement of several organs in patients with chronic active hepatitis probably due to diffuse immunological damage. Weil's disease and renal damage due to septicaemia-common in cirrhotic patients on immunosuppressive or corticosteroid therapy5 -are also causes of combined renal and liver failure. A rather important relationship is to be noted between obstructive jaundice and renal failure, for in this situation damage to the kidneys may be preventable. Jaundiced patients are more susceptible than the average to hypotension and renal damage after operations.6 The danger is directly proportional to the level of the serum bilirubin.7 It has been suggested that infusions of mannitol8 before operation may prevent this complication, because experimental evidence shows that the kidneys of animals in which the bile duct is ligated resist change if mannitol is given. This suggests that renal ischaemia is secondary to a primary change in the kidneys. An experimental study, published at page 229 of the B.M.7. this week by Mr. J. L. Dawson and his colleagues, who have done much of the work in Britain on this important association, shows that the susceptibility of the jaundiced kidney to postoperative ischaemic damage may be related to the nature of the retained bile pigment. They compared two strains of rats. The Gunn rat can produce only unconjugated bilirubin because of a congenital deficiency of an enzyme (glucuronyl transferase). It is not nearly so susceptible to renal change as is the normal, Wistar, strain, and these workers found there was no more evidence of renal damage in the operated Gunn rats after ligation of the bile duct than in the control group of Gunn rats. The villain of the piece therefore seems to be conjugated bilirubin, for it is the only component of bile that is known to differ between the two strains of rats. Moreover, bilirubin glucuronide is the only form found in the fluid in renal tubules, and it may be toxic even in the absence of ischaemia.9 It seems likely, however, that bilirubin glucuronide is deconjugated in the kidney to produce bilirubin. Can these results be applied to man ? If so, how can the toxic effects of conjugated bilirubin on renal tubules be modified ? Mannitol merely prevents the secondary ischaemic change. These problems are clearly of importance to the management of the jaundiced patient before operation.
慢性活动性肝炎患者多个器官受累可能是由于弥漫性免疫损伤。韦尔病以及败血症导致的肾损伤——在接受免疫抑制或皮质类固醇治疗的肝硬化患者中很常见——也是肝肾联合衰竭的原因。梗阻性黄疸和肾衰竭之间存在一种相当重要的关系,因为在这种情况下,肾脏损伤可能是可以预防的。黄疸患者在手术后比一般人更容易发生低血压和肾损伤。这种危险与血清胆红素水平成正比。有人建议在手术前输注甘露醇可能预防这种并发症,因为实验证据表明,胆管结扎的动物如果给予甘露醇,其肾脏能抵抗变化。这表明肾缺血是肾脏原发性变化的继发结果。本周《英国医学杂志》第229页发表了J.L.道森先生及其同事的一项实验研究,他们在英国对这一重要关联进行了大量研究,研究表明黄疸肾脏对术后缺血性损伤的易感性可能与潴留的胆色素的性质有关。他们比较了两种大鼠品系。冈恩大鼠由于一种酶(葡萄糖醛酸转移酶)先天性缺乏,只能产生未结合胆红素。它对肾脏变化的易感性远不如正常的维斯塔大鼠品系,这些研究人员发现,胆管结扎后的手术冈恩大鼠与对照组冈恩大鼠相比,没有更多肾损伤的证据。因此,罪魁祸首似乎是结合胆红素,因为它是已知在两种大鼠品系之间存在差异的胆汁的唯一成分。此外,胆红素葡萄糖醛酸苷是在肾小管液中发现的唯一形式,即使在没有缺血的情况下它也可能有毒性。然而,胆红素葡萄糖醛酸苷似乎在肾脏中被去结合产生胆红素。这些结果能应用于人类吗?如果可以,如何改变结合胆红素对肾小管的毒性作用呢?甘露醇仅仅是预防继发性缺血变化。这些问题对于黄疸患者手术前的处理显然很重要。