{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T13:17:36Z","timestamp":1788268656824,"version":"build-2803163510"},"reference-count":24,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T00:00:00Z","timestamp":1785715200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T00:00:00Z","timestamp":1785715200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["APP2005300"],"award-info":[{"award-number":["APP2005300"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001114","name":"Endocrine Society of Australia","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001114","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007132","name":"Otsuka Pharmaceutical","doi-asserted-by":"publisher","award":["IIT 156\u2010419\u201000250"],"award-info":[{"award-number":["IIT 156\u2010419\u201000250"]}],"id":[{"id":"10.13039\/501100007132","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Hyponatraemia is a common electrolyte disorder often driven by excess arginine vasopressin (AVP). Copeptin is a stable surrogate marker co\u2010secreted with AVP. It is unclear whether treatment of hyponatraemia with tolvaptan, an AVP\u2010V2 receptor antagonist, impacts copeptin. We aimed to assess the effects of tolvaptan on serum copeptin, compared to fluid restriction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design<\/jats:title>\n                    <jats:p>Pre\u2010specified secondary analysis of an open\u2010label randomised trial comparing tolvaptan or fluid restriction for 3 days.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Patients<\/jats:title>\n                    <jats:p>Hospitalised patients with plasma sodium (pNa) 115\u2013130\u2009mmol\/L at a single\u2010centre tertiary hospital in Melbourne, Australia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements<\/jats:title>\n                    <jats:p>Copeptin measured at baseline and completion (Day 4, or discharge if sooner).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Copeptin results were available in 45\/54 participants, randomised to tolvaptan (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200925) or FR (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200920). Mean baseline copeptin was 10.4\u2009pmol\/L. pNa increased in both groups, significantly more with tolvaptan as previously reported. Copeptin remained stable after FR, but significantly increased after tolvaptan (mean adjusted difference between groups over 3 days 8.4\u2009pmol\/L, 95% CI 2.1\u201314.6,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.01). Baseline copeptin did not predict rapid sodium rise.\n                    <\/jats:p>\n                    <jats:p>The rise in copeptin after tolvaptan may represent an exaggerated response to osmolality rise in these patients (\u2018reset osmostat\u2019), or feedback mechanisms from AVP blockade.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Tolvaptan increased serum copeptin compared to fluid restriction. Further research is required to determine if there is clinical utility for measuring copeptin in hyponatraemia before it is adopted into practice.<\/jats:p>\n                    <jats:p>\n                      <jats:bold>Trial Registration:<\/jats:bold>\n                      ACTRN12619001683123.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/cen.70184","type":"journal-article","created":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T10:25:58Z","timestamp":1785752758000},"page":"514-518","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Serum Copeptin Rises After Tolvaptan for Hyponatraemia, but Does Not Predict Risk of Rapid Sodium Rise: Pre\u2010Specified Secondary Analysis of the TVFR Trial"],"prefix":"10.1111","volume":"105","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7287-6162","authenticated-orcid":false,"given":"Annabelle M.","family":"Warren","sequence":"first","affiliation":[{"name":"Department of Endocrinology Austin Health Heidelberg Victoria Australia"},{"name":"Department of Medicine, Austin Health University of Melbourne Heidelberg Victoria Australia"},{"name":"Department of Endocrinology and Diabetes Alfred Health Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kay Weng","family":"Choy","sequence":"additional","affiliation":[{"name":"Northern Pathology Victoria, Northern Health Epping Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rudolf","family":"Hoermann","sequence":"additional","affiliation":[{"name":"Department of Medicine, Austin Health University of Melbourne Heidelberg Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas","family":"Russell","sequence":"additional","affiliation":[{"name":"Department of Endocrinology Austin Health Heidelberg Victoria Australia"},{"name":"Department of Medicine, Austin Health University of Melbourne Heidelberg Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8261-3457","authenticated-orcid":false,"given":"Mathis","family":"Grossmann","sequence":"additional","affiliation":[{"name":"Department of Endocrinology Austin Health Heidelberg Victoria Australia"},{"name":"Department of Medicine, Austin Health University of Melbourne Heidelberg Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,3]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1210\/endrev\/bnad010"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-3011.1986.tb01827.x"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2008-1426"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1210\/clinem\/dgac070"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.beem.2025.102053"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.1530\/EC-19-0431"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2013.07.006"},{"key":"e_1_2_9_9_1","doi-asserted-by":"publisher","DOI":"10.1530\/EJE-13-1020"},{"key":"e_1_2_9_10_1","doi-asserted-by":"publisher","DOI":"10.1210\/jendso\/bvae106"},{"key":"e_1_2_9_11_1","doi-asserted-by":"publisher","DOI":"10.1093\/ejendo\/lvaf058"},{"key":"e_1_2_9_12_1","doi-asserted-by":"publisher","DOI":"10.1210\/clinem\/dgaf428"},{"key":"e_1_2_9_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.xkme.2025.101239"},{"key":"e_1_2_9_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.eprac.2025.04.012"},{"key":"e_1_2_9_15_1","doi-asserted-by":"publisher","DOI":"10.1186\/s13063-022-06237-5"},{"key":"e_1_2_9_16_1","unstructured":"R Core Team. 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