Abstract
It is well known that lithium carbonate, which is frequently used in the treatment of psychiatric disorders,can induce a syndrome characterized by polyuria and polydipsia (1). According to the various investigators, these clinical findings appear in a range between 20% and 70% of the patients treated (2,3,4,5,6,7). Lithium-induced polyuria and polydipsia may be due to primary polydipsia with secondary polyuria or to primary polyuria with secondary polydipsia. In support of the above-mentioned alternatives, it has been reported that lithium may stimulate thirst or may interfere with the ADH-dependent mechanisms. Experimental studies on rats have demonstrated that lithium can stimulate thirst (8,9,10,11). Other experimental studies on rats have demonstrated that lithium can deplete the posterior pituitary gland and the supra-optic nuclei of their neuro-endocrine material (12,13), showing that lithium may interfere with the synthesis, deposit and/or release of the ADH hormone, causing central diabetes insipidus. On the other hand, another cause which has been suggested is an interference by the lithium with the tubular renal action of the ADH, causing nephrogenic diabetes insipidus (14,15,16,17). In contrast, however, some authors were unable, under somewhat different experimental conditions, to detect a lithium-induced inhibition of the ADH -stimulated water flow in toads’ urinary bladders (18).
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© 1989 Plenum Press, New York
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Passavanti, G., Buongiorno, E., De Fino, G., Rutigliano, G., Giannattasio, M., Coratelli, P. (1989). Lithium Induced Polyuria and Polydipsia. In: Amerio, A., Coratelli, P., Campese, V.M., Massry, S.G. (eds) Drugs, Systemic Diseases, and the Kidney. Advances in Experimental Medicine and Biology, vol 252. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8953-8_21
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