title: Aggravation of subclinical diabetes insipidus during pregnancy.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Iwasaki
authors.forename: Y
authors.initials: Y
authors.lastname: Oiso
authors.forename: K
authors.initials: K
authors.lastname: Kondo
authors.forename: S
authors.initials: S
authors.lastname: Takagi
authors.forename: K
authors.initials: K
authors.lastname: Takatsuki
authors.forename: H
authors.initials: H
authors.lastname: Hasegawa
authors.forename: K
authors.initials: K
authors.lastname: Ishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Fujimura
authors.forename: S
authors.initials: S
authors.lastname: Kazeto
authors.forename: A
authors.initials: A
authors.lastname: Tomita
mesh_terms: D000328:Adult; D003894:Deamino Arginine Vasopressin; D003919:Diabetes Insipidus / Q000175:diagnosis / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006982:Hypertonic Solutions; D009994:Osmolar Concentration; D011141:Polyuria / Q000175:diagnosis; D011247:Pregnancy; D011248:Pregnancy Complications / Q000175:diagnosis / Q000503:physiopathology*; D011263:Pregnancy Trimester, Third; D013894:Thirst; D014667:Vasopressins / Q000378:metabolism
chemical_list: D006982:Hypertonic Solutions; D014667:Vasopressins; D003894:Deamino Arginine Vasopressin