Guevara M, Ginès P, Fernández-Esparrach G, Sort P, Salmerón J M, Jiménez W, Arroyo V, Rodés J
Liver Unit, Hospital Clínic i Provincial, University of Barcelona, Catalunya, Spain.
Hepatology. 1998 Jan;27(1):35-41. doi: 10.1002/hep.510270107.
Hepatorenal syndrome is caused by a marked vasoconstriction of the renal circulation. It is suggested that the renal vasoconstriction is related to an overactivity of vasoconstrictor systems secondary to a vasodilation of the arterial circulation that causes a reduction in effective arterial blood volume. To test this hypothesis, 16 cirrhotic patients with hepatorenal syndrome were treated with a combination of ornipressin, a potent vasoconstrictor agent, and plasma volume expansion with albumin to improve effective arterial blood volume. The combined treatment was administered either for 3 or 15 days (8 patients each), and the effects on renal function, vasoactive systems, and systemic hemodynamics were assessed. The 3-day treatment with ornipressin and albumin was associated with a normalization of the overactivity of renin-angiotensin and sympathetic nervous systems, a marked increase in atrial-natriuretic peptide levels, and only a slight improvement in renal function. However, when ornipressin and albumin were administered for 15 days, a remarkable improvement in renal function was observed, with normalization of serum-creatinine concentration, a marked increase in renal plasma flow and glomerular filtration rate, and a persistent suppression in the activity of vasoconstrictor systems. However, 3 of 8 patients on 15-day therapy treatment had to be discontinued because of ischemic complications. In conclusion, the decrease in effective arterial blood volume and the activation of vasoconstrictor systems play a crucial role in the pathogenesis of hepatorenal syndrome. Although the prolonged administration of ornipressin combined with plasma volume expansion reverses hepatorenal syndrome, this treatment should be used with great caution in clinical practice because of the risk of ischemic complications.
肝肾综合征是由肾循环显著血管收缩引起的。有人认为，肾血管收缩与血管收缩系统过度活跃有关，这种过度活跃继发于动脉循环血管舒张，导致有效动脉血容量减少。为了验证这一假设，对16例肝肾综合征肝硬化患者联合使用强力血管收缩剂鸟氨加压素和白蛋白进行血浆容量扩充，以改善有效动脉血容量。联合治疗分别持续3天或15天（各8例患者），并评估其对肾功能、血管活性系统和全身血流动力学的影响。使用鸟氨加压素和白蛋白进行3天治疗后，肾素 - 血管紧张素和交感神经系统的过度活跃恢复正常，心房利钠肽水平显著升高，而肾功能仅略有改善。然而，当使用鸟氨加压素和白蛋白治疗15天时，肾功能有显著改善，血清肌酐浓度恢复正常，肾血浆流量和肾小球滤过率显著增加，血管收缩系统的活性持续受到抑制。然而，接受15天治疗的8例患者中有3例因缺血性并发症不得不停止治疗。总之，有效动脉血容量减少和血管收缩系统激活在肝肾综合征的发病机制中起关键作用。虽然长期联合使用鸟氨加压素和血浆容量扩充可逆转肝肾综合征，但由于存在缺血性并发症的风险，在临床实践中应谨慎使用这种治疗方法。
