Ghose R R
Postgrad Med J. 1985 Dec;61(722):1043-6. doi: 10.1136/pgmj.61.722.1043.
Random estimations of plasma arginine vasopressin concentration were undertaken in 6 non-oedematous patients receiving diuretic therapy for hypertension, who were admitted to hospital with severe hyponatraemia. Hyponatraemia resolved within 2 weeks of discontinuing the diuretic. Measurable amounts of plasma arginine vasopressin were detected in all 6 patients. Sequential biochemical measurements in one patient, performed when plasma sodium concentration and osmolality were returning to the normal range, disclosed that urine osmolality remained higher than plasma osmolality during the first 5 days, when urine volume and sodium excretion were low. Thus the rise in plasma sodium was not initially related to water diuresis. The ability to excrete a water load was severely limited on the fifth day, but improved progressively by the tenth and seventeenth days. Diuretic-induced hyponatraemia is associated with incomplete suppression of anti-diuretic hormone secretion arising from non-osmotic stimulation, in conjunction with transient impairment of renal diluting ability which could be due to net sodium deficit.
对6例因高血压接受利尿治疗且因严重低钠血症入院的非水肿患者进行了血浆精氨酸加压素浓度的随机测定。停用利尿剂后2周内低钠血症得到缓解。所有6例患者均检测到可测量的血浆精氨酸加压素。对1例患者进行的连续生化测量显示,当血浆钠浓度和渗透压恢复到正常范围时,在前5天尿量和钠排泄量较低时,尿渗透压仍高于血浆渗透压。因此,血浆钠的升高最初与水利尿无关。第5天排出水负荷的能力严重受限,但到第10天和第17天逐渐改善。利尿剂引起的低钠血症与非渗透性刺激引起的抗利尿激素分泌不完全抑制有关,同时伴有可能由于净钠缺乏导致的肾稀释能力短暂受损。