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Water Disturbances in Patients Treated with Oral Lithium Carbonate

P. H. BAYLIS, M.B., Ch.B., M.R.C.P.; and D. A. HEATH, M.B., Ch.B., M.R.C.P.
[+] Article, Author, and Disclosure Information

Financial support was provided by the University of Birmingham and the Endowment Fund, Queen Elizabeth Hospital, Birmingham, England.

▸Requests for reprints should be addressed to Peter H. Baylis, M.B.; Department of Medicine, Veterans Administration Hospitals, 1481 West Tenth St.; Indianapolis, IN 46202.

Birmingham, England

©1978 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1978;88(5):607-609. doi:10.7326/0003-4819-88-5-607
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Forty-eight patients treated with oral lithium carbonate and 20 control subjects were studied to define the causes of lithium-induced water disturbances. Measurement of plasma immunoreactive arginine vasopressin, plasma osmolality, and urine osmolality after a period of dehydration separated nephrogenic diabetes insipidus, cranial diabetes insipidus, and primary polydipsia, the three postulated mechanisms of lithium-induced polyuria. Seventeen patients had a urinary concentrating defect despite serum lithium concentrations in the therapeutic range. Ten of these patients had nephrogenic diabetes insipidus, one had results suggestive of cranial diabetes insipidus, but none had evidence of primary polydipsia. Symptoms of thirst and polyuria were poor indicators of the degree of hypo-osmolar urine. No patient had electrolyte abnormalities, and none had sufficiently severe polyuria to stop lithium treatment.





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