Morgan D B, Ball S R, Thomas T H, Lee M R
Q J Med. 1978 Jan;47(185):21-34.
Two patients with sodium-losing renal disease were studied in detail. Both presented with shock and hypotension which was attributed at first to other causes, as was the recurrent hyponatraemia in one of them. In both patients the cause of the sodium loss was probably unrelieved urinary obstruction which has been reported previously to cause water loss but not sodium loss. Both patients had severe hyponatraemia when they were sodium depleted, which has previously been attributed to water retention from excessive secretion of antidiuretic hormone. Plasma arginine vasopressin concentrations were raised in one patient but not in the other. The cause of the water retention in the other patient is not known. One of the patients, like others described in the literature, was only able to vary his sodium excretion within narrow limits. He became sodium depleted on a normal intake and oedematous when he was given saline intravenously. We suggest that the term sodium-losing renal disease should be replaced by the term 'fixed sodium' excretion renal disease.
对两名失钠性肾病患者进行了详细研究。两人均出现休克和低血压，起初这些症状被归因于其他原因，其中一人反复出现的低钠血症亦是如此。在这两名患者中，失钠的原因可能是尿路梗阻未解除，此前曾有报道称尿路梗阻会导致水分流失，但不会导致钠流失。两名患者在钠缺乏时均出现严重低钠血症，此前这被归因于抗利尿激素分泌过多导致的水潴留。一名患者的血浆精氨酸加压素浓度升高，而另一名患者则未升高。另一名患者水潴留的原因尚不清楚。其中一名患者，与文献中描述的其他患者一样，只能在很窄的范围内改变其钠排泄量。他在正常摄入量时出现钠缺乏，静脉输注生理盐水时则出现水肿。我们建议用“固定钠排泄”性肾病这一术语取代失钠性肾病这一术语。
