Aggravation of Subclinical Diabetes Insipidus During Pregnancy

Title: Aggravation of Subclinical Diabetes Insipidus During Pregnancy
Authors: Iwasaki, M.D., Yasumasa; Oiso, MD, PhD, Yutaka; Kondo, MD, PhD, Kunikaza; Takagi, Shinko; Takatsuki, Kensuke; Hasegawa, Haruhiko; Ishikawa, Kaoru; Fujimura, Yumi; Kazeto, Sadayuki; Tomita, Akio
Publisher: New England Journal of Medicine
Date Published: February 21, 1991
Reference Number: 328
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.

This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)

Though it is rare, some women experience transient polyuria (the passage of large volumes of urine) and polydipsia (chronic, excessive thirst) during pregnancy. The reasons for this are not always clear. In their paper, Iwasaki, et al., report on two pregnant women in which transient polydipsia and polyuria developed during the course of their pregnancies and subsided after their pregnancies.

The authors studied the secretion and action of the antidiuretic hormone, vasopressin (VP) in the women, both when they were experiencing polyuria and polydipsia and later, after their symptoms had disappeared. The tests showed that both women had a different form of diabetes insipidus (DI) that was not noticeable until the metabolic changes brought on by pregnancy caused their DI to surface.

The first woman had partial nephrogenic diabetes insipidus (NDI), a condition characterized by the kidney's inability to respond to VP's signal to concentrate urine and reabsorb the water flowing through the kidney collecting duct. The second woman had partial central diabetes insipidus (CDI), a disorder brought on by insufficient amounts of VP being synthesized and circulated in the body.

The authors suggest that the first woman's subclinical NDI became more manifest when her VP levels were lowered due to the action of vasopressinase, an enzyme that inactivates VP. Placental tissue produces vasopressinase. When the placenta is passed, the amount of vasopressinase in the body drops, so the woman's VP levels could rise and thus partially normalize her NDI.

The second woman's CDI could not be entirely explained by the breakdown of VP by vasopressinase. Other possible causal factors could be increases in the blood flow through the kidney, increases in the glomerular filtration rate, or an increased production of prostaglandins which could decrease sensitivity to low plasma levels of VP.

The authors conclude by stating that pregnancy may unmask subclinical forms of both CDI and NDI, and that pregnant women who experience polydipsia and polyuria should be examined for these disorders.