{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:51:51Z","timestamp":1787017911581,"version":"build-2736575974"},"reference-count":0,"publisher":"S. Karger AG","issue":"3","license":[{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nephron"],"published-print":{"date-parts":[[2015]]},"abstract":"<b><i>Background\/Aim:<\/i><\/b> Dietary phosphate intake and vitamin D receptor activator (VDRA) regulate fibroblast growth factor 23 (FGF23); iron may modulate FGF23 metabolism. We aimed to determine whether oral iron supplementation influences serum FGF23 concentration in hemodialysis (HD) patients, while excluding the effect of dietary phosphate intake. <b><i>Methods:<\/i><\/b> This prospective study enrolled 27 maintenance HD patients with iron deficiency and hyperphosphatemia treated with sevelamer-HCl. The phosphate binder was changed from sevelamer-HCl to ferric citrate hydrate (FCH) to maintain constant phosphate levels. VDRA, other phosphate binders, and cinacalcet HCl were not changed. Serum intact FGF23, C-terminal FGF23 (C-term FGF23), intact parathyroid hormone (PTH), 1,25(OH)<sub>2<\/sub>D and other parameters were monitored for 12 weeks. <b><i>Results:<\/i><\/b> Serum phosphate levels (5.89 \u00b1 1.45 mg\/dl at baseline, 5.54 \u00b1 1.35 mg\/dl at 12 weeks) and 1,25(OH)<sub>2<\/sub>D levels were unchanged. Serum ferritin levels increased from 25.6 \u00b1 24.3 ng\/ml at baseline to 55.8 \u00b1 33.5 ng\/ml at 12 weeks with FCH administration. Serum intact FGF23 and C-term FGF23 levels significantly decreased at 12 weeks compared with baseline (2,000 (1,300.0-3,471.4) to 1,771.4 (1,142.9-2,342.9) pg\/ml, p = 0.01, and 1,608.7 (634.8-2,308.7) to 1,165.2 (626.1-1,547.8) RU\/ml, p = 0.007, respectively); serum intact PTH levels significantly increased (96 (65-125) to 173 (114-283) pg\/ml, p < 0.001). <b><i>Conclusions:<\/i><\/b> Oral FCH administration decreased serum intact FGF23 and C-term FGF23 levels and increased intact PTH levels; phosphate and 1,25(OH)<sub>2<\/sub>D levels were unchanged. Oral FCH administration to treat iron deficiency is a possible strategy for reducing serum FGF23 levels independent of phosphate and VDRA.<\/jats:p>","DOI":"10.1159\/000440968","type":"journal-article","created":{"date-parts":[[2017,4,18]],"date-time":"2017-04-18T17:58:24Z","timestamp":1492538304000},"page":"161-166","source":"Crossref","is-referenced-by-count":36,"title":["Administration of Ferric Citrate Hydrate Decreases Circulating FGF23 Levels Independently of Serum Phosphate Levels in Hemodialysis Patients with Iron Deficiency"],"prefix":"10.1159","volume":"131","author":[{"given":"Akira","family":"Iguchi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junichiro J.","family":"Kazama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suguru","family":"Yamamoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuhiro","family":"Yoshita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuo","family":"Watanabe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noriaki","family":"Iino","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7692-3096","authenticated-orcid":false,"given":"Ichiei","family":"Narita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2015,11,6]]},"container-title":["Nephron"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/440968","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/440968","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/440968","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T13:55:23Z","timestamp":1745416523000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000440968"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2015]]},"references-count":0,"journal-issue":{"issue":"3","published-online":{"date-parts":[[2015,11,1]]},"published-print":{"date-parts":[[2015,11,26]]}},"URL":"https:\/\/doi.org\/10.1159\/000440968","archive":["Portico"],"relation":{},"ISSN":["1660-8151","2235-3186"],"issn-type":[{"value":"1660-8151","type":"print"},{"value":"2235-3186","type":"electronic"}],"subject":[],"published":{"date-parts":[[2015]]}}}