Abstract
It is intriguing that lithium exerts profound effects on physiologic systems at concentrations (5 X 10–3M) markedly lower than the dominant extracellular and intracellular alkali metal cations, sodium and potassium. The recent widespread use of lithium salts as treatment for affective disorders has drawn attention to two of its side effects — diabetes insipidus1 , 2 and thyroid hypofunction.3 Diabetes insipidus has been observed in 12 per cent of patients receiving lithium2 and most studies have indicated that the defect is nephrogenic in origin for a number of reasons. First of all, in contrast to patients with pituitary diabetes insipidus or . . .