Zipser R D, Kerlin P, Hoefs J C, Zia P, Barg A
Am J Gastroenterol. 1981 Mar;75(3):183-7.
Severe liver disease is often associated with renal hemodynamic changes, and these changes may involve vasoactive hormones. The vasodilatory renal kallikrein-kinin system has received little previous study in these patients. We measured urinary kallikrein in nine patients with alcoholic cirrhosis under rigid metabolic conditions and simultaneously evaluated renin, aldosterone and urinary prostaglandins. Plasma renin and aldosterone were generally increased as expected but urinary kallikrein was surprisingly diminished (13.3 +/- 3.7 vs. 38.8 +/- 11.1 SE, E.U./day, P less than 0.05), despite adequate creatinine clearance (81 +/- 9 ml./min.). Administration of prostaglandin inhibitors reduced urinary prostaglandin E by 72% and creatinine clearance by 56% but did not alter urinary kallikrein. Mineralocorticoid inhibition by spironolactone induced a natriuresis in four patients with ascites (from 1.4-140 mEq.Na+/day) but also failed to alter kallikrein. Thus, kallikrein excretion is paradoxically reduced and seemingly unresponsive to alterations in the prostaglandin and renin-aldosterone systems. If urinary kallikrein quantitatively reflects intrarenal kallikrein-kinin activity, the impairment in this vasodilatory system may mediate the altered renal hemodynamics of severe liver disease.
严重肝病常伴有肾血流动力学改变，且这些改变可能涉及血管活性激素。血管舒张性肾激肽释放酶-激肽系统此前在这些患者中鲜有研究。我们在严格的代谢条件下测量了9例酒精性肝硬化患者的尿激肽释放酶，并同时评估了肾素、醛固酮和尿前列腺素。血浆肾素和醛固酮通常如预期那样升高，但尿激肽释放酶却出人意料地减少（13.3±3.7对38.8±11.1 SE，欧洲单位/天，P<0.05），尽管肌酐清除率足够（81±9毫升/分钟）。给予前列腺素抑制剂可使尿前列腺素E减少72%，肌酐清除率减少56%，但并未改变尿激肽释放酶。螺内酯对盐皮质激素的抑制作用在4例腹水患者中诱导了利钠作用（从1.4 - 140毫当量钠/天），但也未能改变激肽释放酶。因此，激肽释放酶排泄反常减少，且似乎对前列腺素和肾素-醛固酮系统的改变无反应。如果尿激肽释放酶定量反映肾内激肽释放酶-激肽活性，那么这个血管舒张系统的损害可能介导了严重肝病时肾血流动力学的改变。
