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

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Imamura, TeruhikoUniversity of Tokyo, Japan (author)

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

Article/chapterEnglish2014

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International Heart Journal Association,2014
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LIBRIS-ID:oai:DiVA.org:liu-111176
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-111176URI
https://doi.org/10.1536/ihj.13-221DOI

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Language:English
Summary in:English

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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
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.

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MEDICIN OCH HÄLSOVETENSKAP Hälsovetenskap hsv//swe
MEDICAL AND HEALTH SCIENCES Health Sciences hsv//eng
Heart failure; Vasopressin; Urine osmolality

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Kinugawa, KoichiroUniversity of Tokyo, Japan (author)
Minatsuki, ShunUniversity of Tokyo, Japan (author)
Muraoka, HironoriUniversity of Tokyo, Japan (author)
Kato, NaokoUniversity of Tokyo, Japan(Swepub:liu)naope77 (author)
Inaba, ToshiroUniversity of Tokyo, Japan (author)
Maki, HisatakaUniversity of Tokyo, Japan (author)
Hatano, MasaruUniversity of Tokyo, Japan (author)
Yao, AtsushiUniversity of Tokyo, Japan (author)
Komuro, IsseiUniversity of Tokyo, Japan (author)
University of Tokyo, Japan (creator_code:org_t)

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In:International Heart Journal: International Heart Journal Association55:2, s. 131-1371349-23651349-3299

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