Caregaro L, Lauro S, Ricci G, Merkel C, Milani L, Gatta A
Clin Nephrol. 1981 Mar;15(3):143-7.
The mechanism of the renal tubular acidosis (RTA) occurring in patients with hepatic cirrhosis remains uncertain although it has been suggested that renal and intrarenal hemodynamic alterations could play a role in its pathogenesis. To verify this hypothesis, renal acidification was studied with an intravenous acid load of arginine hydrochloride in 51 patients with cirrhosis due to various causes. In 22 patients renal and intrarenal blood flow was also measured using the 133-Xe washout technique. RTA was found in 17 of 51 patients (33%) with the greatest incidence in alcoholic cirrhosis. The tubular defect did not appear related either to the degree of liver functional impairment or to the renal and intrarenal hemodynamic alterations.
尽管有观点认为肾脏及肾内血流动力学改变可能在肝硬化患者肾小管酸中毒（RTA）的发病机制中起作用，但该机制仍不明确。为验证这一假说，我们对51例因各种原因导致肝硬化的患者静脉注射盐酸精氨酸进行酸负荷试验，研究其肾脏酸化功能。其中22例患者还采用133-Xe洗脱技术测量了肾脏及肾内血流。51例患者中有17例（33%）发现有RTA，其中酒精性肝硬化患者发病率最高。肾小管缺陷似乎与肝功能损害程度以及肾脏和肾内血流动力学改变均无关。
