{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T21:28:57Z","timestamp":1790026137431,"version":"4.0.1"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CJASN"],"published-print":{"date-parts":[[2017,12]]},"abstract":"\n Background and objectives<\/jats:title>\n Epidemiologic studies suggest that higher serum phosphaturic hormone fibroblast growth factor 23 levels are associated with increase morbidity and mortality. The aim of the FGF23 Reduction Efficacy of a New Phosphate Binder in CKD Trial was to evaluate the effect of sevelamer carbonate on serum C-terminal fibroblast growth factor 23 levels in normophosphatemic patients with CKD stage 3b\/4.<\/jats:p>\n <\/jats:sec>\n \n Design, setting, participants, & measurements<\/jats:title>\n \n Patients with CKD, eGFR between 45 and 15 ml\/min per 1.73 m\n 2<\/jats:sup>\n , fasting serum phosphate concentration >3.1 mg\/dl, and serum C-terminal fibroblast growth factor 23 >80 relative units\/ml were included in our double-blind, placebo-controlled, randomized multicenter study. All patients received 100,000 IU cholecalciferol at time of randomization. Participants received either placebo or sevelamer carbonate 4.8 g daily during a 12-week period. Biologic parameters, including serum C-terminal fibroblast growth factor 23, intact fibroblast growth factor 23, and\n \u03b1<\/jats:italic>\n -klotho, were evaluated at baseline and 12 weeks after inclusion.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Of 96 screened patients, 78 (mean\u00b1SD age: 63\u00b113 years old; 70% men; mean eGFR: 27\u00b19 ml\/min per 1.73 m\n 2<\/jats:sup>\n ) met the inclusion criteria. At baseline, mean eGFR was 27\u00b19 ml\/min per 1.73 m\n 2<\/jats:sup>\n , mean serum phosphate level was 3.8\u00b10.5 mg\/dl, and median (interquartile range) serum C-terminal fibroblast growth factor 23 level was 157 (120\u2013241) relative units\/ml. After 12 weeks of treatment, urinary phosphate-to-creatinine ratio fell significantly in the sevelamer group. The sevelamer and placebo groups did not differ significantly in terms of median change in serum C-terminal fibroblast growth factor 23 levels: the median (interquartile range) change was 38 (\u221213\u2013114) relative units\/ml in the placebo group and 37 (\u22121\u2013101) relative units\/ml in the sevelamer group (\n P<\/jats:italic>\n =0.77). There was no significant difference in serum intact fibroblast growth factor 23,\n \u03b1<\/jats:italic>\n -klotho, or phosphate levels changes between the two groups. Serum total and LDL cholesterol levels fell significantly in the sevelamer group.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n In our double-blind, placebo-controlled, randomized study performed in normophosphatemic patients with CKD, a 12-week course of sevelamer carbonate significantly reduced phosphaturia without changing serum phosphorus but did not significantly modify serum C-terminal fibroblast growth factor 23 and intact fibroblast growth factor 23 or\n \u03b1<\/jats:italic>\n -klotho levels.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.2215\/cjn.03030317","type":"journal-article","created":{"date-parts":[[2017,10,26]],"date-time":"2017-10-26T20:20:11Z","timestamp":1509049211000},"page":"1930-1940","source":"Crossref","is-referenced-by-count":42,"title":["Randomized Clinical Trial of Sevelamer Carbonate on Serum Klotho and Fibroblast Growth Factor 23 in CKD"],"prefix":"10.2215","volume":"12","author":[{"given":"Sophie","family":"Liabeuf","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Philippe","family":"Ryckelynck","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Najeh","family":"El Esper","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pablo","family":"Ure\u00f1a","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Combe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bertrand","family":"Dussol","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denis","family":"Fouque","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philippe","family":"Vanhille","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luc","family":"Frimat","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Thervet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Romuald","family":"Mentaverri","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dominique","family":"Pri\u00e9","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriel","family":"Choukroun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"name":"for the FRENCH Study collaborators","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2017,10,26]]},"reference":[{"key":"B1-20230813","doi-asserted-by":"crossref","first-page":"339","DOI":"10.1016\/S0140-6736(13)60595-4","article-title":"Chronic kidney disease and cardiovascular risk: Epidemiology, mechanisms, and prevention.","volume":"382","author":"Gansevoort","year":"2013","journal-title":"Lancet"},{"key":"B2-20230813","doi-asserted-by":"crossref","first-page":"1119","DOI":"10.1001\/jama.2011.308","article-title":"Serum levels of phosphorus, parathyroid hormone, and calcium and risks of death and cardiovascular disease in individuals with chronic kidney disease: A systematic review and meta-analysis.","volume":"305","author":"Palmer","year":"2011","journal-title":"JAMA"},{"key":"B3-20230813","doi-asserted-by":"crossref","first-page":"1370","DOI":"10.1038\/ki.2011.47","article-title":"Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease.","volume":"79","author":"Isakova","year":"2011","journal-title":"Kidney Int"},{"key":"B4-20230813","doi-asserted-by":"crossref","first-page":"2600","DOI":"10.1681\/ASN.2006080936","article-title":"Fibroblast growth factor 23 (FGF23) predicts progression of chronic kidney disease: The Mild to Moderate Kidney Disease (MMKD) study.","volume":"18","author":"Fliser","year":"2007","journal-title":"J Am Soc Nephrol"},{"key":"B5-20230813","doi-asserted-by":"crossref","first-page":"2017","DOI":"10.1007\/s00198-011-1838-0","article-title":"FGF23 is independently associated with vascular calcification but not bone mineral density in patients at various CKD 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