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Urine sodium excret...
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, Teruhiko (författare)
- University of Tokyo, Japan
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- Kinugawa, Koichiro (författare)
- University of Tokyo, Japan
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- Minatsuki, Shun (författare)
- University of Tokyo, Japan
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- Muraoka, Hironori (författare)
- University of Tokyo, Japan
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- Kato, Naoko (författare)
- University of Tokyo, Japan
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- Inaba, Toshiro (författare)
- University of Tokyo, Japan
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- Maki, Hisataka (författare)
- University of Tokyo, Japan
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- Hatano, Masaru (författare)
- University of Tokyo, Japan
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- Yao, Atsushi (författare)
- University of Tokyo, Japan
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- Komuro, Issei (författare)
- University of Tokyo, Japan
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(creator_code:org_t)
- International Heart Journal Association, 2014
- 2014
- Engelska.
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Ingår i: International Heart Journal. - : International Heart Journal Association. - 1349-2365 .- 1349-3299. ; 55:2, s. 131-137
- Relaterad länk:
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https://www.jstage.j...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- 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.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Hälsovetenskap (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Health Sciences (hsv//eng)
Nyckelord
- Heart failure; Vasopressin; Urine osmolality
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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- Av författaren/redakt...
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Imamura, Teruhik ...
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Kinugawa, Koichi ...
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Minatsuki, Shun
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Muraoka, Hironor ...
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Kato, Naoko
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Inaba, Toshiro
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visa fler...
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Maki, Hisataka
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Hatano, Masaru
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Yao, Atsushi
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Komuro, Issei
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visa färre...
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- MEDICIN OCH HÄLSOVETENSKAP
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