Lithium-induced nephrogenic diabetes insipidus: Studies of tubular function and pathogenesis

J. Rapoport, C. Chaimovitz, G. G. Alroy, O. S. Better

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

We describe a patient with lithium-induced nephrogenic diabetes insipidus in whom detailed investigations of distal tubular function were performed. Clearance of free water during water diuresis was found to be augmented. This suggests proximal suppression of sodium reabsorption by lithium. Reabsorption of free water during high solute clearance was impaired. Acidification of the urine following ammonium chloride loading was abnormal, and this was corrected by sodium sulfate infusion. The cellular mechanism of lithium was investigated by means of indomethacin, an inhibitor of prostaglandin synthesis. Indomethacin caused a partial reversal of the nephrogenic diabetes insipidus, suggesting that the primary cellular action of lithium may be to inhibit the formation of cyclic AMP in the collecting duct cell, although a direct action of indomethacin in increasing solutes in the renal medulla could not be ruled out. It is possible that the lithium-induced polyuria is partially due to an enhancement by lithium of renal prostaglandin action.

Original languageEnglish
Pages (from-to)765-771
Number of pages7
JournalIsrael Journal of Medical Sciences
Volume15
Issue number9
StatePublished - 1 Dec 1979
Externally publishedYes

ASJC Scopus subject areas

  • Bioengineering

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