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Urine sodium excretion after tolvaptan administration is dependent upon baseline serum sodium levels: a possible explanation for the improvement of hyponatremia with scarce chance of hypernatremia by a vasopressin receptor antagonist
University of Tokyo, Japan .
University of Tokyo, Japan .
University of Tokyo, Japan .
University of Tokyo, Japan .
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2014 (English)In: International Heart Journal, ISSN 1349-2365, Vol. 55, no 2, 131-137 p.Article in journal (Refereed) Published
Abstract [en]

Several studies have demonstrated that tolvaptan (TLV) can improve hyponatremia in advanced heart failure (BF) patients with rare chance of hypernatremia. However, changes in serum sodium concentrations (S-Na) in patients with or without hyponatremia during TLV treatment have not been analyzed. Ninety-seven in-hospital patients with decompensated HF who had received TLV at 3.75-15 mg/day for 1 week were enrolled. Among 68 "responders", who had achieved any increases in urine volume (UV) during the first day, urinary sodium excretion during 24 hours (U-NaEx(24)) increased significantly during one week of TLV treatment along with higher baseline S-Na (P less than 0.05 and r = 0.325). Considering a cut-off value (S-Na, 132 mEq/L; AUC, 0.711) for any increases in U-NaEx(24), we defined "hyponatremia" as S-Na less than 132 mEq/L. In hyponatremic responders (n = 25), S-Na increased significantly, although 1 week was not sufficient for normalization (125.8 +/- 5.0 versus 128.9 +/- 4.3 mEq/L, P less than 0.05), along with unchanged U-NaEx(24) (2767 +/- 2703 versus 2972 +/- 2950 mg/day, NS). In contrast, in normonatremic responders (n = 43), S-Na remained unchanged (136.6 +/- 3.1 versus 137.4 +/- 2.9 mEq/L, NS) along with increased U-NaEx(24) (2201 +/- 1644 versus 4198 +/- 3550 mg/day, P less than 0.05). TLV increased S-Na only in hyponatemic responders by way of pure aquaresis, but increased U-NaEx(24) only in nonnonatremic responders, which explains the scarcity of hypernatremia. Epithelial Na-channels in the distal nephrons, whose repression by TLV increases urinary sodium excretion, may be attenuated by reduced ATP-supply in worse hemodynamics under hyponatremia.

Place, publisher, year, edition, pages
International Heart Journal Association , 2014. Vol. 55, no 2, 131-137 p.
Keyword [en]
Heart failure; Vasopressin; Urine osmolality
National Category
Health Sciences
URN: urn:nbn:se:liu:diva-111176DOI: 10.1536/ihj.13-221ISI: 000336465600008PubMedID: 24632953OAI: diva2:754554

Funding Agencies|Japan Society for the Promotion of Science [224943]; Japanese Heart Foundation; Japanese Association for Cerebro-Cardiovascular Disease Control and AstraZeneca; Pfizer Health Research Foundation

Available from: 2014-10-10 Created: 2014-10-10 Last updated: 2014-10-21Bibliographically approved

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Kato, Naoko
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