PATHOPHYSIOLOGY OF TRANSIENT CRANIAL DIABETES-INSIPIDUS DURING PREGNANCY

OBJECTIVE We investigated the possible mechanisms underlying transient cranial diabetes insipidus during pregnancy. DESIGN AND PATIENTS A wo man who developed clinical diabetes insipidus during the third trimest er of pregnancy was studied through a total of three pregnancies and p ostpartum. MEASUREMENTS Plasma AVP, urine and plasma osmolality, urine volume and specific gravity were measured during water deprivation te sts and hypertonic saline infusion. Plasma and urine osmolality were m easured after subcutaneous injection of AVP. The water deprivation and AVP test were repeated after proven inhibition of urinary PGE2 with a spirin. Serum vasopressinase activity was measured during one of the p regnancies affected with diabetes insipidus and compared with that obt ained between 26 and 38 weeks from 13 normal pregnancies. RESULTS The patient was found to have cranial diabetes insipidus which responded t o low dose intranasal 1-desamino-8-D-arginine vasopressin. Inhibition of PGE2 with aspirin did not enhance urine concentrating ability or th e response to a test dose of subcutaneous AVP. Plasma levels of vasopr essinase remained within the physiological range for normal pregnancy. CONCLUSIONS These studies indicate that subclinical cranial diabetes insipidus may be unmasked in late pregnancy. This effect is not relate d to AVP resistance resulting from PGE2 production or excessive vasopr essinase activity, but may be due to a combination of physiological va sopressinase secretion with reduced AVP secretory capacity and reducti on in the thirst threshold that accompanies normal pregnancy. We relat e these findings to a previously described group of women with transie nt diabetes insipidus during pregnancy who had impaired liver function .