Hepatology and Liver Intensive Care Unit, Hospital Beaujon, Clichy, France.
INSERM U1149, University Paris Diderot, Paris, France; and.
Clin J Am Soc Nephrol. 2019 May 7;14(5):774-781. doi: 10.2215/CJN.12451018. Epub 2019 Apr 17.
Hepatorenal syndrome is a severe complication of end-stage cirrhosis characterized by increased splanchnic blood flow, hyperdynamic state, a state of decreased central volume, activation of vasoconstrictor systems, and extreme kidney vasoconstriction leading to decreased GFR. The contribution of systemic inflammation, a key feature of cirrhosis, in the development of hepatorenal syndrome has been highlighted in recent years. The mechanisms by which systemic inflammation precipitates kidney circulatory changes during hepatorenal syndrome need to be clarified. Early diagnosis is central in the management and recent changes in the definition of hepatorenal syndrome help identify patients at an earlier stage. Vasoconstrictive agents (terlipressin in particular) and albumin are the first-line treatment option. Several controlled studies proved that terlipressin is effective at reversing hepatorenal syndrome and may improve short-term survival. Not all patients are responders, and even in responders, early mortality rates are very high in the absence of liver transplantation. Liver transplantation is the only curative treatment of hepatorenal syndrome. In the long term, patients transplanted with hepatorenal syndrome tend to have lower GFR compared with patients without hepatorenal syndrome. Differentiating hepatorenal syndrome from acute tubular necrosis (ATN) is often a challenging yet important step because vasoconstrictors are not justified for the treatment of ATN. Hepatorenal syndrome and ATN may be considered as a continuum rather than distinct entities. Emerging biomarkers may help differentiate these two conditions and provide prognostic information on kidney recovery after liver transplantation, and potentially affect the decision for simultaneous liver-kidney transplantation.
肝肾综合征是终末期肝硬化的严重并发症，其特征为内脏血流增加、高动力状态、中心血容量减少、血管收缩系统激活以及肾脏极度收缩导致肾小球滤过率降低。近年来，系统性炎症作为肝硬化的一个关键特征，在肝肾综合征的发生发展中的作用得到了强调。需要阐明系统性炎症如何在肝肾综合征期间引发肾脏循环变化的机制。早期诊断是治疗的关键，最近对肝肾综合征定义的改变有助于更早地识别患者。血管收缩剂（特别是特利加压素）和白蛋白是一线治疗选择。几项对照研究证明，特利加压素可有效逆转肝肾综合征，并可能改善短期生存率。并非所有患者都是应答者，即使是应答者，在没有肝移植的情况下，早期死亡率也非常高。肝移植是肝肾综合征唯一的治愈性治疗方法。从长远来看，与没有肝肾综合征的患者相比，移植后患有肝肾综合征的患者肾小球滤过率往往较低。将肝肾综合征与急性肾小管坏死（ATN）区分开来通常是一个具有挑战性但又很重要的步骤，因为血管收缩剂不应作为 ATN 的治疗方法。肝肾综合征和 ATN 可以被认为是一个连续体，而不是两个截然不同的实体。新兴的生物标志物可能有助于区分这两种情况，并提供关于肝移植后肾脏恢复的预后信息，并且可能会影响同时进行肝-肾移植的决策。
