{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T09:28:29Z","timestamp":1781688509806,"version":"3.54.5"},"reference-count":33,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2007,1,1]],"date-time":"2007-01-01T00:00:00Z","timestamp":1167609600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["Journal of Investigative Medicine"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Diuretics are one of the most common causes of severe hyponatremia. The responsible pathogenetic mechanisms remain unclear. Serum uric acid concentration has been proposed as an index of differentiating between two pathophysiologic constructs of diuretic-induced hyponatremia-extracellular volume depletion and syndrome of inappropriate antidiuretic hormone secretion (SIADH)-like state-but its discriminating value has not been verified in large series of patients. Here we attempt to illuminate the pathophysiology of diuretic-induced hyponatremia by focusing on uric acid homeostasis. Additionally, we analyze the epidemiology and clinical characteristics of the disorder.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We studied prospectively 158 adult patients with hyponatremia on admission to our internal medicine clinic. Here we report on those with diuretic-induced hyponatremia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Forty patients (13 male and 27 female) had diuretic-induced hyponatremia, rendering it the most common cause of the disorder (25.3%). These patients had lower mean ([Na\n                      <jats:sup>+<\/jats:sup>\n                      ]) (121.2 \u00b1 7.2 vs 126.4 \u00b1 4.1 mEq\/L, p = .0001) than the remaining hyponatremic patients. Patients with serum uric acid levels &lt; 4 mg\/dL ( n = 14) exhibited a biochemical profile consistent with a SIADH-like state, whereas patients with serum uric acid levels \u2265 4 mg\/d ( n = 26) were consistent with extracellular volume depletion.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Diuretics are the most common cause of community-developed hyponatremia. The serum uric acid level effectively discriminates between two biochemical profiles of diuretic-induced hyponatremia, one consistent with extracellular volume depletion and another that simulates SIADH.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2310\/6650.2007.06027","type":"journal-article","created":{"date-parts":[[2007,8,13]],"date-time":"2007-08-13T16:16:59Z","timestamp":1187021819000},"page":"36-44","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":27,"title":["Uric Acid Homeostasis in the Evaluation of Diuretic-Induced Hyponatremia"],"prefix":"10.1177","volume":"55","author":[{"given":"George","family":"Liamis","sequence":"first","affiliation":[{"name":"Department of Internal Medicine (G.L., D.C., G.A., M.E.), Medical School, University of Ioannina, Ioannina, Greece;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dimitrios","family":"Christidis","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (G.L., D.C., G.A., M.E.), Medical School, University of Ioannina, Ioannina, Greece;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Alexandridis","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (G.L., D.C., G.A., M.E.), Medical School, University of Ioannina, Ioannina, Greece;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eleni","family":"Bairaktari","sequence":"additional","affiliation":[{"name":"Laboratory of Biochemistry (E.B.), University Hospital of Ioannina, Ioannina, Greece;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolaos E.","family":"Madias","sequence":"additional","affiliation":[{"name":"Laboratory of Biochemistry (E.B.), University Hospital of Ioannina, Ioannina, Greece;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moses","family":"Elisaf","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (G.L., D.C., G.A., M.E.), Medical School, University of Ioannina, Ioannina, Greece;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2023,5,10]]},"reference":[{"key":"bibr1-6650.2007.06027","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-110-1-24"},{"key":"bibr2-6650.2007.06027","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(81)90822-6"},{"key":"bibr3-6650.2007.06027","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1986.00360190131018"},{"key":"bibr4-6650.2007.06027","doi-asserted-by":"publisher","DOI":"10.1378\/chest.103.2.601"},{"key":"bibr5-6650.2007.06027","first-page":"1","volume":"13","author":"Abramow M","year":"1984","journal-title":"Adv Nephrol Necker 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