Farber M O, Roberts L R, Weinberger M H, Robertson G L, Fineberg N S, Manfredi F
Arch Intern Med. 1982 Jul;142(7):1326-30.
The pathogenesis of edema and hyponatremia in chronic obstructive lung disease (COLD), is poorly understood. Previously, in nonedematous patients with hypercapnia, small increases in plasma renin activity occurred, which prompted this study. In 25 hypercapnic, edematous, often hyponatremic patients with COLD, we measured renal hemodynamics, H2O, and sodium (Na+) excretion, plasma levels of renin activity (PRA), plasma levels of aldosterone (PA), and the plasma arginine vasopressin (AVP)-osmolality relationship. A high prevalence of elevated PRA, PA, and AVP levels excessively high for plasma osmolality was observed. Elevated PRA and Pa correlated with the inability to excrete Na+; an elevated AVP level correlated with the inability to excrete H2). These data suggest that, in conjunction with the hypercapnia-hypoxia-mediated disturbance in renal function, stimulation of the renin-aldosterone level and of the AVP systems contributes, respectively, to edema formation and to hyponatremia in advanced COLD.
慢性阻塞性肺疾病(COLD)中水肿和低钠血症的发病机制尚不清楚。此前,在无水肿的高碳酸血症患者中,血浆肾素活性出现小幅升高,这促使了本研究。在25例患有COLD的高碳酸血症、水肿且常伴有低钠血症的患者中,我们测量了肾血流动力学、水和钠(Na+)排泄、血浆肾素活性(PRA)水平、血浆醛固酮(PA)水平以及血浆精氨酸加压素(AVP)与渗透压的关系。观察到PRA、PA和AVP水平升高的发生率很高,且相对于血浆渗透压过高。PRA和PA升高与无法排泄Na+相关;AVP水平升高与无法排泄水相关。这些数据表明,在高碳酸血症-低氧介导的肾功能紊乱的同时,肾素-醛固酮水平和AVP系统的刺激分别导致了晚期COLD中的水肿形成和低钠血症。