“…Hyponatraemia most commonly occurs within 14 days of starting therapy (Sonnenblick et al, 1993), but may occur after prolonged periods of trouble-free treatment. Diuretic-induced hyponatraemia is multifactorial: excess natriuresis without adequate oral sodium replacement, and baroregulated vasopressin release in response to diuretic induced hypovolaemia are probably the most important mechanisms, but hypokalaemia, which promotes movement of sodium into cells, may also contribute to lowering extracellular sodium levels (Fichmann q 2000 Blackwell Science Ltd, Clinical Endocrinology, 52, 667±678 , 1971;Hamburger et al, 1981). Although the overwhelming majority of cases of thiazide-induced hyponatraemia are associated with natriuresis and hypovolaemia, thiazide diuretics have also been reported to potentiate the effect of small concentrations of vasopressin, permitting maximal reabsorption of water (Pitone et al, 1978;Sonnenblick et al, 1993), with occasional development of the syndrome of inappropriate antidiuretic hormone (SIADH), rather than hypovolaemic hyponatraemia (VanAssen & Mudde, 1999).…”