Badalamenti S, Graziani G, Salerno F, Ponticelli C
Division of Nephrology and Dialysis, IRCCS Ospedale Maggiore, Milan, Italy.
Arch Intern Med. 1993 Sep 13;153(17):1957-67. doi: 10.1001/archinte.153.17.1957.
Hepatorenal syndrome is a life-threatening complication of severe liver disease. It is generally accepted that the syndrome is the final stage of complex hemodynamic derangements associated with portal hypertension, ie, peripheral arterial vasodilation, effective hypovolemia, and hyperkinetic status. In spite of reduced systemic resistances, intrarenal vascular resistances are increased. This is probably the consequence of the activation of systemic vasoactive factors, such as the renin-angiotensin system, the sympathetic nervous system, and vasopressin aimed at restoring arterial filling pressure. Recently, it has been shown that intrarenal vasoconstrictors, such as leukotrienes and endothelins, are activated with the progression of liver disease. The renal vasoconstriction is counterbalanced by the intrarenal hyperproduction of vasodilating prostaglandins and kallikreins. When this balance is lost, for whatever mechanism, the renal vascular resistances dramatically increase and the hepatorenal syndrome develops. In spite of increased knowledge about pathogenesis, the treatment of hepatorenal syndrome remains unresolved. Low-dose dopamine or ornipressin are currently employed in many liver units to avoid further deterioration of renal function in patients with severe liver disease who are waiting for liver transplantation that remains, at present, the only effective treatment for hepatorenal syndrome.
肝肾综合征是严重肝病的一种危及生命的并发症。人们普遍认为，该综合征是与门静脉高压相关的复杂血流动力学紊乱的终末期，即外周动脉血管扩张、有效血容量不足和高动力状态。尽管全身血管阻力降低，但肾内血管阻力增加。这可能是全身血管活性因子（如肾素 - 血管紧张素系统、交感神经系统和血管加压素）激活的结果，其目的是恢复动脉充盈压。最近研究表明，随着肝病进展，肾内血管收缩剂（如白三烯和内皮素）被激活。肾血管收缩被肾内血管扩张性前列腺素和激肽释放酶的过度产生所抵消。无论通过何种机制，当这种平衡丧失时，肾血管阻力会急剧增加，肝肾综合征就会发展。尽管对发病机制的认识有所增加，但肝肾综合征的治疗仍然没有解决。目前许多肝病治疗单位使用小剂量多巴胺或鸟氨加压素，以避免等待肝移植的严重肝病患者肾功能进一步恶化，而肝移植目前仍然是肝肾综合征唯一有效的治疗方法。
