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Background: Elderly women are at risk to develop severe hyponatremia after thiazide but not loop diuretic administration. In patients with previous thiazide-induced hyponatremia, the risk for recurrent hyponatremia after furosemide has not been established., Methods: In order to determine how both diuretics affect water metabolism, we here compare the effects of a rechallenge with either amiloride-hydrochlorothiazide fixed association (AmHTZ; amiloride chlorhydrate 5 mg+hydrochlorothiazide 50 mg; Moduretic) or furosemide (F; 40 mg; Lasix) on water excretion in a 79 year old woman who was previously admitted for severe symptomatic hyponatremia secondary to a 5 days course of AmHTZ for systolic hypertension. After correction of initial hydromineral disturbances, a standard oral water load (WL; 20 mL per kg body weight) was administered before, during and after AmHTZ or F challenges., Results: Hyponatremia developed after AmHTZ but not after F challenge. A negative free water clearance (CH(2)O) was only observed during AmHTZ (-0.39 mL/min), while maximal CH(2)O during F was 3.17 mL/min. Based on the results obtained during WL, the calculated maximal daily electrolyte free water clearance ability was only 888 mL after AmHTZ but 10,166 mL after F therapy. Taking into account a measured mean daily water intake of 1830 mL, severe hyponatremia could be predicted to occur after a few days treatment with AmHTZ. In comparison, F appears to be safer, without risk of hyponatremia, during an equivalent period of time., Conclusions: We here showed that F may be administered to a patient with previous AmHTZ induced hyponatremia without risk for recurrent hyponatremia.

Twenty-two patients with severe hyponatremia were divided into 12 patients with and ten without associated neurologic manifestations (groups 1 and 2, respectively). Marked hyperthyroxinemia was demonstrated in seven patients in group 1 but in none in group 2. The triiodothyronine concentration was also higher than normal in two patients in group 1. All serum iodothyronine concentrations in group 1 were significantly higher than in group 2. Thyrotropin and thyroxine-binding globulin levels were normal in both groups. The differences between groups were apparent only in the acute phase, and there were no clinical manifestations of hyperthyroidism. All iodothyronine concentrations returned to normal within two weeks after the correction of the hypo-osmolar disorder. Our results indicate that a transient asymptomatic increase in serum iodothyronine levels occurs during hyponatremia. Thus, thyroid test results should be interpreted cautiously in patients with acute, severe, symptomatic hyponatremia.