Effect of ferric citrate hydrate on fibroblast growth factor 23 and platelets in non-dialysis-dependent chronic kidney disease and non-chronic kidney disease patients with iron deficiency anemia.

IF 2.2 4区 医学 Q2 UROLOGY & NEPHROLOGY
Clinical and Experimental Nephrology Pub Date : 2024-07-01 Epub Date: 2024-02-25 DOI:10.1007/s10157-023-02455-6
Kyoko Ito, Tadao Akizawa, Kojo Arita, Yuko Mitobe, Norio Komatsu
{"title":"Effect of ferric citrate hydrate on fibroblast growth factor 23 and platelets in non-dialysis-dependent chronic kidney disease and non-chronic kidney disease patients with iron deficiency anemia.","authors":"Kyoko Ito, Tadao Akizawa, Kojo Arita, Yuko Mitobe, Norio Komatsu","doi":"10.1007/s10157-023-02455-6","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Iron deficiency anemia (IDA) increases levels of C-terminal fibroblast growth factor 23 (cFGF23) and platelet count (PLT), each of which is associated with cardiovascular events. Therefore, we hypothesized that iron replacement with ferric citrate hydrate (FC) would decrease cFGF23 levels and PLT in patients with IDA.</p><p><strong>Methods: </strong>In a randomized, open-label, multicenter, 24-week clinical trial, patients with non-dialysis-dependent chronic kidney disease (CKD) and non-CKD complicated by IDA (8.0 ≤ hemoglobin < 11.0 g/dL; and serum ferritin < 50 ng/mL [CKD]; < 12 ng/mL [non-CKD]) were randomized 1:1 to FC-low (500 mg: approximately 120 mg elemental iron/day) or FC-high (1000 mg: approximately 240 mg elemental iron/day). If sufficient iron replacement had been achieved after week 8, further treatment was discontinued.</p><p><strong>Results: </strong>Seventy-three patients were allocated to FC-low (CKD n = 21, non-CKD n = 15) and FC-high (CKD n = 21, non-CKD n = 16). Regardless of CKD status, FC increased serum ferritin and transferrin saturation, did not change intact FGF23 or serum phosphorus, but decreased cFGF23. In FC-low group, median changes in cFGF23 from baseline to week 8 were -58.00 RU/mL in CKD and -725.00 RU/mL in non-CKD; in FC-high group, the median changes were -66.00 RU/mL in CKD and -649.50 RU/mL in non-CKD. By week 8, FC treatment normalized PLT in all patients with high PLT at baseline (>35.2 × 10<sup>4</sup>/µL; FC-low: 1 CKD, 8 non-CKD; FC-high: 3 CKD, 8 non-CKD).</p><p><strong>Conclusion: </strong>Regardless of CKD status, iron replacement with FC decreased elevated cFGF23 levels and normalized elevated PLT in patients with IDA.</p><p><strong>Clinical trial registration number: </strong>jRCT2080223943.</p>","PeriodicalId":10349,"journal":{"name":"Clinical and Experimental Nephrology","volume":" ","pages":"636-646"},"PeriodicalIF":2.2000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11189996/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and Experimental Nephrology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10157-023-02455-6","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/25 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"UROLOGY & NEPHROLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Iron deficiency anemia (IDA) increases levels of C-terminal fibroblast growth factor 23 (cFGF23) and platelet count (PLT), each of which is associated with cardiovascular events. Therefore, we hypothesized that iron replacement with ferric citrate hydrate (FC) would decrease cFGF23 levels and PLT in patients with IDA.

Methods: In a randomized, open-label, multicenter, 24-week clinical trial, patients with non-dialysis-dependent chronic kidney disease (CKD) and non-CKD complicated by IDA (8.0 ≤ hemoglobin < 11.0 g/dL; and serum ferritin < 50 ng/mL [CKD]; < 12 ng/mL [non-CKD]) were randomized 1:1 to FC-low (500 mg: approximately 120 mg elemental iron/day) or FC-high (1000 mg: approximately 240 mg elemental iron/day). If sufficient iron replacement had been achieved after week 8, further treatment was discontinued.

Results: Seventy-three patients were allocated to FC-low (CKD n = 21, non-CKD n = 15) and FC-high (CKD n = 21, non-CKD n = 16). Regardless of CKD status, FC increased serum ferritin and transferrin saturation, did not change intact FGF23 or serum phosphorus, but decreased cFGF23. In FC-low group, median changes in cFGF23 from baseline to week 8 were -58.00 RU/mL in CKD and -725.00 RU/mL in non-CKD; in FC-high group, the median changes were -66.00 RU/mL in CKD and -649.50 RU/mL in non-CKD. By week 8, FC treatment normalized PLT in all patients with high PLT at baseline (>35.2 × 104/µL; FC-low: 1 CKD, 8 non-CKD; FC-high: 3 CKD, 8 non-CKD).

Conclusion: Regardless of CKD status, iron replacement with FC decreased elevated cFGF23 levels and normalized elevated PLT in patients with IDA.

Clinical trial registration number: jRCT2080223943.

Abstract Image

枸橼酸铁水合物对非透析依赖型慢性肾病和非慢性肾病缺铁性贫血患者成纤维细胞生长因子 23 和血小板的影响。
背景:缺铁性贫血(IDA)会增加 C 端成纤维细胞生长因子 23(cFGF23)和血小板计数(PLT)的水平,而这两者都与心血管事件有关。因此,我们假设用枸橼酸铁水合物(FC)替代铁能降低 IDA 患者的 cFGF23 水平和 PLT:在一项随机、开放标签、多中心、为期 24 周的临床试验中,非透析依赖型慢性肾脏病(CKD)和非 CKD 并发 IDA(血红蛋白 8.0≤ 结果:CKD 患者的血红蛋白水平为 8.0≤,而非 CKD 患者的血红蛋白水平为 8.0≤:73名患者被分配到FC-低(慢性肾脏病患者21人,非慢性肾脏病患者15人)和FC-高(慢性肾脏病患者21人,非慢性肾脏病患者16人)两组。无论CKD状态如何,FC都会增加血清铁蛋白和转铁蛋白饱和度,不会改变完整的FGF23或血清磷,但会降低cFGF23。在FC低浓度组中,从基线到第8周cFGF23的中位数变化为:CKD-58.00 RU/mL,非CKD-725.00 RU/mL;在FC高浓度组中,中位数变化为:CKD-66.00 RU/mL,非CKD-649.50 RU/mL。到第 8 周时,FC 治疗使所有基线 PLT 偏高(>35.2 × 104/μL;FC-低:1 名 CKD 患者,8 名非 CKD 患者;FC-高:3 名 CKD 患者,8 名非 CKD 患者)的患者的 PLT 恢复正常:结论:无论CKD状态如何,使用FC补铁都能降低IDA患者升高的cFGF23水平,并使升高的PLT恢复正常。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Clinical and Experimental Nephrology
Clinical and Experimental Nephrology UROLOGY & NEPHROLOGY-
CiteScore
4.10
自引率
4.30%
发文量
135
审稿时长
4-8 weeks
期刊介绍: Clinical and Experimental Nephrology is a peer-reviewed monthly journal, officially published by the Japanese Society of Nephrology (JSN) to provide an international forum for the discussion of research and issues relating to the study of nephrology. Out of respect for the founders of the JSN, the title of this journal uses the term “nephrology,” a word created and brought into use with the establishment of the JSN (Japanese Journal of Nephrology, Vol. 2, No. 1, 1960). The journal publishes articles on all aspects of nephrology, including basic, experimental, and clinical research, so as to share the latest research findings and ideas not only with members of the JSN, but with all researchers who wish to contribute to a better understanding of recent advances in nephrology. The journal is unique in that it introduces to an international readership original reports from Japan and also the clinical standards discussed and agreed by JSN.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信