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The natural history and management of hepatorenal disorders: from pre-ascites to hepatorenal syndrome

机译:肝肾疾病的自然病史和处理:从腹水到肝肾综合征

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摘要

In cirrhosis, the natural history of hepatorenal disorders starts with a pre-ascitic stage and is followed by the development of ascites; hepatorenal syndrome (HRS) begins with compensated renal sodium retention, or preascites. In pre-ascites, the renal sodium retaining tendency leads to ‘overfilling’ of total blood volume, with increased glomerular filtration rates (GFR), overcoming the renal sodium retaining tendency possibly due to renal accumulation of angiotensin II. As peripheral vasodilatation increases, the vascular capacity (in effect the arterial blood volume) becomes inadequately filled, GFR falls, compensatory vasoconstrictors rise, and the resulting renal sodium retention results in diuretic-responsive ascites formation. Increasing proximal reabsorption of sodium results in ascites refractory to diuretic therapy. Repeated abdominal paracentesis will not prevent insidious progression to HRS type II, nor to the precipitation of HRS type I. In contrast, liver transplantation, or transjugular intrahepatic hepatoportal stent shunt (TIPS) in refractory ascites, may prevent the onset of, or reverse, HRS. However, recent non-controlled studies indicate exciting possibilities of medical therapy reversing HRS.
机译:在肝硬化中,肝肾疾病的自然病史始于腹水前期,随后是腹水的发展。肝肾综合征(HRS)始于补偿性肾钠retention留或腹水。在腹水前期,肾钠保留趋势导致总血量“充盈”,肾小球滤过率(GFR)增加,克服了可能由于血管紧张素II的肾脏蓄积而导致的肾钠保留趋势。随着周围血管舒张增加,血管容量(实际上是动脉血容量)变得不足,GFR下降,代偿性血管收缩剂升高,并且最终的肾钠retention留导致利尿剂反应性腹水形成。钠的近端重吸收增加会导致利尿剂难以治疗的腹水。反复的腹腔穿刺术不会阻止隐匿性进展为II型HRS,也不会阻止I型HRS沉淀。相反,难治性腹水中的肝移植或经颈静脉肝内肝门支架分流术(TIPS)可能会阻止肝硬化的发作或逆转。 HRS。然而,最近的非对照研究表明,药物治疗逆转HRS的令人兴奋的可能性。

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