1093 NEONATAL NEPHROGENIC DIABETES INSIPIDUS INDUCED BY MATERNAL LITHIUM (Li) CARBONATE USE

Abstract

There are few reports of transplacental Li intoxication none of which describe renal manifestations, although this is well documented in adults. We studied a 3510 gm male neonate born at 35 weeks gestation to a 38 year old woman who ingested 1.8 gm/day of Li carbonate throughout her pregnancy. Polyhydraminos was noted at delivery. At birth the serum Li concentration was 1.0 mEq/L. By the second day the urinary output exceeded 6.4 ml/kg/hr; polyuria persisted even after serum Li concentration fell to zero at four days of age. C_Cr was normal (4.8 ml/min). Serum and urinary osmolalities were 294 and 100 mOsm/kg respectively; urea provided 17% of the total urinary solute. At 5 days of age the child was subjected to a vasopressin test (50 mU/kg, I.V.). This resulted in an increase in Uosm from 87 to 156 mOsm/kg and a slight decrease in plasma osmolality from 293 to 287 mOsm/kg; urea accounted for 6.1% of the urinary solute. Cyclic AMP excretion rose from 0.25 before to 0.75 nM/min after vasopressin. A similar response was encountered at one month of age. By 2 months, Uosm rose to 597 mOsm/kg following 6 hours of water deprivation. These data indicate that Li intoxication results in similar but longer lasting effects on the kidney of the newborn than that of the adult. The duration of the concentrating defect may be due to enhanced sensitivity of the newborn tubule to Li or to interference with the development of the renal concentrating mechanisms.

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