Castellano G, Solis-Herruzo J A, Morillas J D, Larrodera L, Coca C, Gonzalez-Gamarra A, Muñoz-Yagüe T
Dept. of Medicine, University Hospital Doce de Octubre, Complutense University, Madrid, Spain.
Scand J Gastroenterol. 1991 Jan;26(1):49-57. doi: 10.3109/00365529108996483.
Renal function and plasma antidiuretic hormone (ADH) levels were studied basally and after oral water load in four groups of subjects: 15 healthy controls (group I), 15 cirrhotics without ascites (group II), 15 cirrhotics with ascites (group III), and 10 decompensated cirrhotics with hyponatremia (group IV). Renal function and ADH levels were normal in group II. In groups III and IV water diuresis and fractional proximal sodium excretion were significantly decreased, whereas fractional distal sodium resorption and fractional excretion of potassium did not differ from those of controls. Basal ADH was significantly increased only in patients of group IV. In these patients ADH remained abnormally high after water loading. ADH did not correlate with water diuresis, plasma osmolality, mean arterial pressure, and plasma renin activity. We conclude that impaired water excretion in decompensated cirrhotics without hyponatremia cannot be ascribed to high serum levels of ADH. On the contrary, it seems to be related mainly to a reduced delivery of filtrate to the diluting segment of the nephron. In cirrhotic patients with hyponatremia high levels of ADH may play an additional role.
对四组受试者进行基础状态下以及口服水负荷后的肾功能和血浆抗利尿激素(ADH)水平研究:15名健康对照者(第一组)、15名无腹水的肝硬化患者(第二组)、15名有腹水的肝硬化患者(第三组)以及10名失代偿期伴有低钠血症的肝硬化患者(第四组)。第二组患者的肾功能和ADH水平正常。第三组和第四组患者的水利尿和近端钠排泄分数显著降低,而远端钠重吸收分数和钾排泄分数与对照组无差异。仅第四组患者的基础ADH显著升高。在这些患者中,水负荷后ADH仍异常升高。ADH与水利尿、血浆渗透压、平均动脉压和血浆肾素活性无关。我们得出结论,无低钠血症的失代偿期肝硬化患者水排泄受损不能归因于血清ADH水平升高。相反,这似乎主要与到达肾单位稀释段的滤液输送减少有关。在伴有低钠血症的肝硬化患者中,高水平的ADH可能起额外作用。