{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T18:21:43Z","timestamp":1790878903805,"version":"4.1.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"10","license":[{"start":{"date-parts":[[2021,10,1]],"date-time":"2021-10-01T00:00:00Z","timestamp":1633046400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["ec.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,10,1]]},"abstract":"\n Low serum 1,25-dihydroxyvitamin D (1,25(OH)\n 2<\/jats:sub>\n D) in end-stage renal disease (ESRD) is considered a consequence of elevated fibroblast growth factor 23 (FGF23) and concomitant reduced activity of renal 1\u03b1-hydroxylase (\n CYP27B1<\/jats:italic>\n ). Current ESRD treatment strategies to increase serum calcium and suppress secondary hyperparathyroidism involve supplementation with vitamin D analogues that circumvent 1\u03b1-hydroxylase. This overlooks the potential importance of 25-hydroxyvitamin D (25(OH)D) deficiency as a contributor to low serum 1,25(OH)\n 2<\/jats:sub>\n D. We investigated the effects of vitamin D (cholecalciferol) supplementation (40,000 IU for 12 weeks and maintenance dose of 20,000 IU fortnightly), on multiple serum vitamin D metabolites (25(OH)D, 1,25(OH)\n 2<\/jats:sub>\n D\n 3<\/jats:sub>\n and 24,25(OH)\n 2<\/jats:sub>\n D\n 3<\/jats:sub>\n ) in 55 haemodialysis patients. Baseline and 12 month data were compared using related-samples Wilcoxon signed rank test. All patients remained on active vitamin D analogues as part of routine ESRD care. 1,25(OH)\n 2<\/jats:sub>\n D\n 3<\/jats:sub>\n levels were low at baseline (normal range: 60\u2013120 pmol\/L). Cholecalciferol supplementation normalised both serum 25(OH)D and 1,25(OH)\n 2<\/jats:sub>\n D\n 3<\/jats:sub>\n . Median serum 25(OH)D increased from 35.1 nmol\/L (IQR: 23.0\u201347.5 nmol\/L) to 119.9 nmol\/L (IQR: 99.5\u2013143.3 nmol\/L) (\n P<\/jats:italic>\n < 0.001). Median serum 1,25(OH)\n 2<\/jats:sub>\n D\n 3<\/jats:sub>\n and 24,25(OH)\n 2<\/jats:sub>\n D\n 3<\/jats:sub>\n increased from 48.3 pmol\/L (IQR: 35.9\u201357.9 pmol\/L) and 3.8 nmol\/L (IQR: 2.3\u20136.0 nmol\/L) to 96.2 pmol\/L (IQR: 77.1\u2013130.6 pmol\/L) and 12.3 nmol\/L (IQR: 9\u201316.4 nmol\/L), respectively (\n P<\/jats:italic>\n < 0.001). A non-significant reduction in daily active vitamin D analogue dose occurred, 0.94 \u00b5mcg at baseline to 0.77 \u00b5mcg at 12 months (\n P<\/jats:italic>\n = 0.73). The ability to synthesise 1,25(OH)\n 2<\/jats:sub>\n D\n 3<\/jats:sub>\n in ESRD is maintained but is substrate dependent, and serum 25(OH)D was a limiting factor at baseline. Therefore, 1,25(OH)\n 2<\/jats:sub>\n D\n 3<\/jats:sub>\n deficiency in ESRD is partly a consequence of 25(OH)D deficiency, rather than solely due to reduced 1\u03b1-hydroxylase activity as suggested by current treatment strategies.\n <\/jats:p>","DOI":"10.1530\/ec-21-0372","type":"journal-article","created":{"date-parts":[[2021,9,14]],"date-time":"2021-09-14T08:14:38Z","timestamp":1631607278000},"page":"1291-1298","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-10","source":"Crossref","is-referenced-by-count":11,"title":["Low serum 1,25(OH)2D3 in end-stage renal disease: is reduced 1\u03b1-hydroxylase the only problem?"],"prefix":"10.1530","volume":"10","author":[{"given":"Sharon A","family":"Huish","sequence":"first","affiliation":[{"name":"1University Hospitals of Coventry and Warwickshire NHS Trust, Coventry, UK"},{"name":"2The University of Warwick, Coventry, UK"},{"name":"3Royal Devon and Exeter NHS Foundation Trust, Exeter, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carl","family":"Jenkinson","sequence":"additional","affiliation":[{"name":"4The University of Birmingham, Birmingham, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janet A","family":"Dunn","sequence":"additional","affiliation":[{"name":"2The University of Warwick, Coventry, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David J","family":"Meredith","sequence":"additional","affiliation":[{"name":"3Royal Devon and Exeter NHS Foundation Trust, Exeter, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosemary","family":"Bland","sequence":"additional","affiliation":[{"name":"2The University of Warwick, Coventry, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Hewison","sequence":"additional","affiliation":[{"name":"4The University of Birmingham, Birmingham, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Endocrine Connections"],"original-title":[],"link":[{"URL":"https:\/\/ec.bioscientifica.com\/view\/journals\/ec\/10\/10\/EC-21-0372.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/ec.bioscientifica.com\/downloadpdf\/journals\/ec\/10\/10\/EC-21-0372.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:44:49Z","timestamp":1784555089000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/ec\/article\/10\/10\/1291-1298\/167"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,10,1]]},"references-count":0,"journal-issue":{"issue":"10"},"URL":"https:\/\/doi.org\/10.1530\/ec-21-0372","relation":{},"ISSN":["2049-3614"],"issn-type":[{"value":"2049-3614","type":"electronic"}],"subject":[],"published":{"date-parts":[[2021,10,1]]}}}