Iwasaki Y, Oiso Y, Kondo K, Takagi S, Takatsuki K, Hasegawa H, Ishikawa K, Fujimura Y, Kazeto S, Tomita A
First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
N Engl J Med. 1991 Feb 21;324(8):522-6. doi: 10.1056/NEJM199102213240803.
Transient polyuria and polydipsia during pregnancy are rare, and their cause is not entirely clear. Possible explanations include the exacerbation of preexisting abnormalities in the secretion or action of vasopressin and abnormally large increases in plasma vasopressinase activity.
We studied two women in whom overt polyuria and polydipsia developed during the third trimester of pregnancy and disappeared after delivery. The secretion and action of vasopressin were studied both when the women had polyuria and polydipsia and later, when their water intake and urine volume were normal.
One patient had partial nephrogenic diabetes insipidus. She had little increase in urine osmolality in response to water deprivation, hypertonic-saline infusion, and vasopressin injection and no response to desmopressin acetate (1-deamino-8-D-arginine vasopressin) during the immediate postpartum period. Her basal and stimulated plasma vasopressin concentrations were high (16.5 to 203.4 pmol per liter) before and during hypertonic-saline infusion 30 months post partum. The other patient had partial neurogenic diabetes insipidus. She had subnormal basal plasma vasopressin concentrations, a subnormal increase in the plasma vasopressin level and a subnormal decrease in urine flow in response to the administration of vasopressin, and a normal response to desmopressin. After pregnancy, when her urine volume was normal, she had no increase in plasma vasopressin in response to hypertonic-saline infusion, but she had a normal rise in the plasma vasopressin level and a normal renal response to vasopressin administration.
Pregnancy may unmask subclinical forms of both nephrogenic and neurogenic diabetes insipidus. This exacerbation may result from both increased vasopressinase activity and diminished renal responsiveness to vasopressin.
孕期短暂性多尿和烦渴较为罕见，其病因尚不完全清楚。可能的解释包括血管加压素分泌或作用的原有异常加重以及血浆血管加压素酶活性异常大幅升高。
我们研究了两名在妊娠晚期出现明显多尿和烦渴且产后消失的女性。在她们出现多尿和烦渴时以及之后水摄入量和尿量正常时，均对血管加压素的分泌和作用进行了研究。
一名患者患有部分性肾性尿崩症。她在禁水、输注高渗盐水和注射血管加压素后尿渗透压升高不明显，产后即刻对醋酸去氨加压素（1 - 去氨基 - 8 - D - 精氨酸血管加压素）无反应。产后30个月，在输注高渗盐水前及过程中，她的基础和刺激后血浆血管加压素浓度均较高（16.5至203.4 pmol/升）。另一名患者患有部分性神经源性尿崩症。她的基础血浆血管加压素浓度低于正常，注射血管加压素后血浆血管加压素水平升高低于正常且尿流量减少低于正常，对去氨加压素反应正常。妊娠后，当她尿量正常时，输注高渗盐水后血浆血管加压素无升高，但血浆血管加压素水平正常升高且肾脏对血管加压素注射反应正常。
妊娠可能使肾性和神经源性尿崩症的亚临床形式显现出来。这种加重可能是血管加压素酶活性增加和肾脏对血管加压素反应性降低共同作用的结果。
