Caregaro L, Lauro S, Ricci G, Gatta A, Zuin R, Ruol A
Digestion. 1983;26(4):179-86. doi: 10.1159/000198887.
5 cirrhotic patients with latent distal renal tubular acidosis (RTA) and 5 cirrhotic patients with normal distal acidification ability were studied. All the patients were maintained on a 80 mEq/day sodium diet for at least 5 days before the study. Only 2 of the 5 patients with RTA showed a reduced daily sodium excretion while the 3 other patients with RTA had a normal natriuresis. Acidification ability was retested in all the patients after increasing sodium distal delivery by intravenous administration of ethacrynic acid. Some hours after the maximal natriuretic effect induced by ethacrynic acid, a normalization of the acidification test was seen in all patients with RTA. These findings support the concept that although sodium metabolism alterations are not the only factor in the pathogenesis of RTA in liver cirrhosis, reduced availability of sodium at the distal tubule may impair tubular acidification, probably by influencing the distal transtubular potential difference.
对5例患有潜在性远端肾小管酸中毒（RTA）的肝硬化患者和5例远端酸化能力正常的肝硬化患者进行了研究。在研究前，所有患者均维持80 mEq/天的钠饮食至少5天。5例RTA患者中只有2例每日钠排泄减少，而其他3例RTA患者钠利尿正常。在通过静脉注射依他尼酸增加远端钠输送后，对所有患者的酸化能力进行了重新测试。在依他尼酸诱导的最大利尿作用后的数小时内，所有RTA患者的酸化试验均恢复正常。这些发现支持了这样一种观点，即尽管钠代谢改变不是肝硬化患者RTA发病机制中的唯一因素，但远端小管钠的可用性降低可能会损害肾小管酸化，可能是通过影响远端跨小管电位差。
