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肝肾综合征(He[atp Renal Syndrome,HRS)是进行性肝病最严重的关发症 因此,类患者并无器质性改变.其发病机制有”未满”理论、“泛溢”理论及外周血管扩张理沦,HRSS是其极端的表现 目前认为进行性肝病患者均存在着全身高动力循环状态,肾脏对血压及血流量的变化最为敏感肩动力循环对肾影响较大.肾对高动力循环的最新反应是水、钠潴留,可致血容量增加.属代偿性反应;但同时引起腹水及水肿,活化肾素一血管紧张素一醛固酮系统及交感神经系统,使缩血管物质生成增多 这样一方面扩血管物质引起血压下降,肾血流不足持续进行.另一方面又出现缩血管物质引起肾血管收缩的恶性循环.从而诱导HRS.近年来发现参与HRS发病的体液因子有肾素-血管紧张素一醛固酮系统、交感神经系统、抗利尿激素、利纳因子、花生四烯酸衍生物、肾激肽释放酶一激肽系统、内毒素、内皮素等.
Hepatic-renal syndrome (Hepatrenal Syndrome, HRS) is the most serious complication of progressive liver disease Therefore, the class of patients and no organic changes.The pathogenesis of “under the” theory, “overflow” theory and Peripheral vasodilator management, HRSS is its extreme performance At present, patients with progressive liver disease are the existence of the whole body hyperdynamic circulation, the kidney is most sensitive to changes in blood pressure and blood flow Shoulder circulation has a greater impact on the kidney. Kidney high power The latest response to the cycle is water, sodium retention, can lead to increased blood volume. Is a compensatory response; but at the same time cause ascites and edema, activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system, the vasoconstrictor substances increased Such vasodilator substances on the one hand caused by blood pressure, renal blood flow continued inadequate.On the other hand there vasoconstrictor vasoconstriction caused by a vicious cycle to induce HRS.In recent years, the body was found to participate in the pathogenesis of HRS with renin - Angiotensin-aldosterone system, sympathetic nervous system, anti-diuretic hormone, linina factor, arachidonic acid derivative, renal kallikrein-kallikrein system, endotoxin, Endothelin and so on.