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肝硬化时发生的肾功能不全称为肝肾综合征(HRS)。HRS 在肝硬化腹水住院患者中的发生率为10%左右,肝硬化腹水患者1年HRS的发生率约20%,而5年发生率可高达40%。HRS的发病机制包括肾外和肾内因素,其中最主要的是肾血管收缩导致肾脏血液循环严重障碍。其机制复杂,包括系统动脉循环的改变、门静脉压力的升高、血管收缩因子的激活以及肾脏血管扩张因素的抑制。造成这种失衡最常见原因是血管扩张因子增多,主要是一氧化氮,导致内脏血管扩张,由此诱发代偿性反应,包括血管收缩因子以及抗利尿系统的激活,如肾素-血管紧张素-醛固酮系统(RASS)、交感神经系统(SNS)以及精氨酸抗利尿激素等,从而导致肾脏血管收缩、水钠潴留。近年,有人提出HRS发病机制的二次打击学说。
Renal insufficiency, which occurs during cirrhosis, is called hepatorenal syndrome (HRS). The incidence of HRS in hospitalized patients with cirrhosis and ascites is about 10%. The incidence of 1-year HRS in patients with cirrhosis and ascites is about 20%, while the 5-year incidence can be as high as 40%. The pathogenesis of HRS includes extra-renal and intra-renal factors, the most important of which is the renal blood vessels causing severe renal blood circulation disorders. The mechanism is complex, including changes in systemic arterial circulation, portal pressure, vasoconstriction factor activation and renal vasodilator inhibition. The most common cause of this imbalance is the increase in vasodilators, predominantly nitric oxide, which leads to visceral vasodilatation, thereby inducing compensatory responses, including vasoconstriction factors and activation of the antidiuretic system such as renin-angiotensin - aldosterone system (RASS), the sympathetic nervous system (SNS) and arginine vasopressin, etc., resulting in renal vasoconstriction Shuinazhuliu. In recent years, some people put forward the second strike theory of the pathogenesis of HRS.