Caregaro L, Lauro S, Angeli P, Merkel C, Gatta A
Eur J Clin Invest. 1985 Dec;15(6):360-4. doi: 10.1111/j.1365-2362.1985.tb00285.x.
The present study was attempted to evaluate sodium and water balance in compensated liver cirrhosis. Renal sodium and water handling was studied in six cirrhotic patients without ascites and/or oedema and in six controls before and after saline loading. Fractional sodium reabsorption at the various nephron sites (proximal, diluting and distal) was evaluated by means of clearance techniques during maximal water diuresis and hypotonic saline infusion. Compensated cirrhotic patients showed a normal baseline sodium and water balance but a blunted natriuretic response when saline loaded (urinary sodium excretion after saline load = 338 +/- 290 compared to 933 +/- 504 mumol min-1 of controls; P less than 0.05). The impaired natriuresis was found to be related to an increased reabsorption of sodium in the proximal tubule (proximal fractional sodium reabsorption = 88.4 +/- 3.8 compared to 81.7 +/- 4.3% of controls; P less than 0.05). These findings confirm the hypothesis that renal sodium handling abnormalities might precede ascites formation. Additional studies, however, are necessary to further define renal factors mediating the increased reabsorption of sodium in compensated liver cirrhosis.
本研究旨在评估代偿期肝硬化患者的钠和水平衡。在六位无腹水和/或水肿的肝硬化患者以及六位对照者中,研究了生理盐水负荷前后的肾脏钠和水代谢情况。通过清除技术,在最大水利尿和低渗盐水输注期间,评估了各个肾单位部位(近端、稀释段和远端)的钠重吸收分数。代偿期肝硬化患者的基线钠和水平衡正常,但在生理盐水负荷时利钠反应减弱(生理盐水负荷后尿钠排泄量为338±290,而对照组为933±504μmol·min⁻¹;P<0.05)。发现利钠功能受损与近端小管钠重吸收增加有关(近端钠重吸收分数为88.4±3.8,而对照组为81.7±4.3%;P<0.05)。这些发现证实了肾脏钠代谢异常可能先于腹水形成的假说。然而,需要进一步的研究来进一步明确介导代偿期肝硬化患者钠重吸收增加的肾脏因素。