LITHIUM-INDUCED NEPHROGENIC DIABETES-INSIPIDUS - STUDIES OF TUBULAR FUNCTION AND PATHOGENESIS

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  • 1 January 1979
    • journal article
    • research article
    • Vol. 15  (9) , 765-771
Abstract
A patient with Li-induced nephrogenic diabetes insipidus is described in whom detailed investigations of distal tubular function were performed. Clearance of free water during water diuresis was augmented. This suggests proximal suppression of Na reabsorption by Li. Reabsorption of free H2O 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 Li was investigated by indomethacin, an inhibitor of prostaglandin synthesis. Indomethacin caused a partial reversal of the nephrogenic diabetes insipidus, suggesting that the primary cellular action of Li may be to inhibit the formation of cAMP in the collecting duct cell, although a direct action of indomethacin in increasing solutes in the renal medulla could not be ruled out. Li-induced polyuria may be partially due to an enhancement by Li or renal prostaglandin action.

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