Aggravation of Subclinical Diabetes Insipidus during Pregnancy

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Abstract
Transient polyuria and polydip-sia during pregnancy are rare, and their cause is not en-tirely clear. Possible explanations include the exacerba-tion 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 poly-uria 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 re-sponse to water deprivation, hypertonic-saline infusion, and vasopressin injection and no response to desmopres-sin acetate (1-deamino-8-D-arginine vasopressin) during the immediate postpartum period. Her basal and stimulat-ed 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. (N Engl J Med 1991; 324:522–6.)

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