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Abstract
To the Editor: Thiazides, which have been the mainstay in the treatment of nephrogenic diabetes insipidus since 1959, decrease urine volume and increase urine osmolality by producing a mild sodium depletion.1 However, distal tubular exchange of sodium for potassium almost invariably results in hypokalemia, which is seldom corrected by potassium supplements or potassium-sparing diuretics.2 Kleeman and colleagues3 showed that hexamethonium produced a fall in glomerular filtration and a reduction in urine volume in patients with nephrogenic diabetes insipidus. Since the age of 21, the patient had received hydrochlorothiazide in combination with either amiloride, triamterene, or spironolactone. Another possible risk associated with hypokalemia is cardiac arrhythmia.4, 5 Potassium supplements, in the doses commonly given, may have little effect on serum potassium in patients taking diuretics with no correlation between serum potassium and the intake of potassium supplements in patients undergoing long-term therapy with diuretics.6 Up to 60 mM potassium chloride or more daily may be required to correct thiazide-induced hypokalemia.7 A combination of thiazide and hypotensive agents controlled the polyuria and nocturia in this man with nephrogenic diabetes insipidus.