Virtually all cases of severe diuretic-induced hyponatremia have been due to a thiazide-type diuretic6-12). In contrast, loop diuretics are implicated much less commonly7). This observation is probably derived from the different nephronal sites of action of these two classes of diuretics. Thiazide diuretics inhibit NaCl reabsorption in the distal convoluted tubule, the main diluting site of the nephron. Thus, thiazide diuretics interfere with maximum dilution of urine because sodium (Na+) excretion is increased along with diminished free-water excretion13, 14). On the other hand, loop diuretics inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle. The reabsorption of NaCl without water in the medullary thick ascending limb is normally the primary step in the generation of the hypertonicity in the medullary interstitium, and loop diuretics mainly impair urinary concentration and limit water retention and development of hyponatremia