Hayslett J P, Katz D L, Knudson J M
Departments of Internal Medicine and Obstetrics and Gynecology, Yale University, School of Medicine, New Haven, Connecticut, USA.
Am J Obstet Gynecol. 1998 Nov;179(5):1312-6. doi: 10.1016/s0002-9378(98)70153-x.
The objective of this report is to describe a defect in water metabolism, characterized by hyponatremia, in patients with pre-eclampsia-induced nephrotic syndrom.
This was an observational study of 3 women.
Hyponatremia was observed in 3 women with pre-eclampsia characterized by various extrarenal manifestations, as well as by nephrotic syndrome with normal or nearly normal renal function. Restriction in water intake partially corrected hyponatremia before delivery in each case, and no complications were observed in the neonates. The mechanism of impaired excretion of water in these patients is proposed to involve persistent and inappropriate production of vasopressin through stimulation of the nonosmotic mechanism for vasopressin secretion in response to a reduction in effective plasma volume.
These results indicate for the first time that women with pre-eclampsia are, at least when nephrotic, at risk for development of dilutional hyponatremia, which can cause neurologic complications that simulate those of eclampsia.
本报告旨在描述先兆子痫所致肾病综合征患者水代谢缺陷，其特征为低钠血症。
这是一项对3名女性的观察性研究。
在3名患有先兆子痫的女性中观察到低钠血症，其特征为各种肾外表现，以及肾功能正常或接近正常的肾病综合征。在每种情况下，限制水摄入在分娩前部分纠正了低钠血症，且未观察到新生儿出现并发症。这些患者水排泄受损的机制被认为涉及通过刺激抗利尿激素分泌的非渗透机制，持续且不恰当地产生抗利尿激素，以应对有效血浆量减少。
这些结果首次表明，先兆子痫女性至少在患有肾病时，有发生稀释性低钠血症的风险，这可能导致类似于子痫的神经系统并发症。
