Urea como alternativa terap&eacute;utica a tolvapt&aacute;n en el tratamiento de la hiponatremia: reporte de caso  <span class="so-article-trans-title" dir="auto"> Translated title: Urea as a therapeutic alternative to tolvaptan in the treatment of hyponatremia: case report </span>

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

RESUMEN Los pacientes con secreción inadecuada de hormona antidiurética (SIADH) son propensos a sufrir hiponatremia. El tolvaptán está indicado en adultos para el tratamiento de hiponatremia secundaria al SIADH. Sin embargo la urea se propone como una buena opción terapéutica para el aumento de los niveles de sodio. En este documento informamos del caso de una paciente con hiponatremia asociada a SIAH que es tratado con tolvaptán consiguiendo una concentración plasmática de sodio muy variable. Parece ser que la urea puede contribuir a un mejor control de los niveles de sodio con un ascenso más lento, progresivo y estable, proporcionando mayor seguridad a nuestra paciente y logrando además reducción de costes.

Translated abstract

SUMMARY Patients with inadequate antidiuretic hormone secretion (SIADH) are prone to hyponatremia. Tolvaptan is indicated in adults for the treatment of hyponatremia secondary to SIADH. However, urea is proposed as a good therapeutic option for increasing sodium levels. In this document we report the case of a patient with hyponatremia associated with SIAH who is treated with tolvaptan, achieving a highly variable plasma sodium concentration. It seems that urea can contribute to a better control of sodium levels with a slower, progressive and stable rise, providing greater safety to our patient and also achieving cost reduction.

Related collections

Most cited references 6

Record: found
Abstract: found
Article: not found

Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia.

Frank S. Czerwiec, Robert W. Schrier, Mihai Gheorghiade … (2006)

Hyponatremia (serum sodium concentration, <135 mmol per liter) is a predictor of death among patients with chronic heart failure and cirrhosis. At present, therapy for acute and chronic hyponatremia is often ineffective and poorly tolerated. We investigated whether tolvaptan, an orally active vasopressin V(2)-receptor antagonist that promotes aquaresis--excretion of electrolyte-free water--might be of benefit in hyponatremia. In two multicenter, randomized, double-blind, placebo-controlled trials, the efficacy of tolvaptan was evaluated in patients with euvolemic or hypervolemic hyponatremia. Patients were randomly assigned to oral placebo (223 patients) or oral tolvaptan (225) at a dose of 15 mg daily. The dose of tolvaptan was increased to 30 mg daily and then to 60 mg daily, if necessary, on the basis of serum sodium concentrations. The two primary end points for all patients were the change in the average daily area under the curve for the serum sodium concentration from baseline to day 4 and the change from baseline to day 30. Serum sodium concentrations increased more in the tolvaptan group than in the placebo group during the first 4 days (P<0.001) and after the full 30 days of therapy (P<0.001). The condition of patients with mild or marked hyponatremia improved (P<0.001 for all comparisons). During the week after discontinuation of tolvaptan on day 30, hyponatremia recurred. Side effects associated with tolvaptan included increased thirst, dry mouth, and increased urination. A planned analysis that combined the two trials showed significant improvement from baseline to day 30 in the tolvaptan group according to scores on the Mental Component of the Medical Outcomes Study 12-item Short-Form General Health Survey. In patients with euvolemic or hypervolemic hyponatremia, tolvaptan, an oral vasopressin V2-receptor antagonist, was effective in increasing serum sodium concentrations at day 4 and day 30. (ClinicalTrials.gov numbers, NCT00072683 [ClinicalTrials.gov] [SALT-1] and NCT00201994 [ClinicalTrials.gov] [SALT-2].).