Background Tolvaptan and, recently, urea were both indicated for the treatment of hyponatraemia secondary to the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) in our country. The FDA also contemplated its use in patients with heart failure (HF). Regarding safety of these drugs, patients with very low baseline natraemia may be at risk for too-rapid correction of serum sodium (>12 mEq/L/24 hours).
Purpose To analyse the effectiveness and safety of tolvaptan and urea, and its use in relation to the diagnosis of hyponatraemia.
Material and methods Retrospective observational study of all cases of severe symptomatic hyponatraemia diagnosed during 2016 in a tertiary care hospital and patients who started treatment with oral urea or tolvaptan during hospitalisation. Variables collected: etiology of hyponatraemia, analytical parameters, dose and duration of treatment.
Results Seven patients treated with tolvaptan: four diagnosed with HF and three with SIADH. Dose ranged from 15 mg/day to 30 mg/day. Median duration: 7 days (2–28). Baseline and final mean natraemia: 119.8 mEq/L and 133 mEq/L respectively. Two patients with SIADH and one with HF had eunatraemia. Three patients were exitus. Six patients were treated with urea, five diagnosed with SIADH and one with adrenal insufficiency. Urea dose ranged from 15 g/day to 30 g/day. Median duration of treatment: 15 days (7–147), three patients continued at home. Baseline and final mean natraemia were 123.4 mEq/L and 133 mEq/L respectively. Three patients with SIADH achieved eunatraemia, two patients were exitus. Only three urea patients had all necessary data for a diagnosis of SIADH. The mean increase in natraemia at 24 hour was 4.57 mEq/L (0–8) in the urea group; 9.9 mEq/L (−3 to 21) in the tolvaptan group (>12 mEq/L in the three cases of SIADH and one case of HF). Deaths were due to complications related to their advanced disease.
Conclusion Off-label use of tolvaptan in HF has not been shown to be effective. Regarding hyponatraemia in SIADH, tolvaptan has shown to be moderately effective, but the correction was too rapid. This result can be related to an incorrect diagnosis of SIADH and/or a too low baseline natraemia. Urea proved to be an alternative of moderate efficacy but safer, allowing its ambulatory use. Therefore, the pharmacy service proposed to establish in our hospital a protocol for the management of severe hyponatraemia to improve the efficacy and safety of tolvaptan and urea.
References and/or acknowledgements No conflict of interest.