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      Is Open Access

      Saccharated ferric oxide attenuates haematopoietic response induced by epoetin beta pegol in patients undergoing haemodialysis

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          Abstract

          Background

          Decreased erythropoietin levels and impaired iron metabolism due to excessive hepcidin levels are responsible for renal anaemia in patients undergoing haemodialysis. Recently, erythroferrone (ERFE) has been identified as a factor that regulates hepcidin. In addition, fibroblast growth factor 23 (FGF23), which has been recognized as a phosphorus-regulating hormone, appears to be involved in haematopoietic regulation. Clarification of the detailed mechanism of haematopoiesis could lead to the improvement of renal anaemia treatment.

          Methods

          Epoetin beta pegol (CERA) was administered to patients undergoing haemodialysis at week 0, and the same amount of CERA with saccharated ferric oxide (SFO) was administered at week 4. The changes in haematopoiesis-related biomarkers, including ERFE, intact FGF23 (iFGF23), C-terminal FGF23 (cFGF23), and inflammatory markers, were examined.

          Results

          Administration of CERA increased ERFE levels, decreased hepcidin levels, and stimulated iron usage for haematopoiesis, leading to an increase in reticulocytes (Ret) and haemoglobin (Hb). Simultaneous administration of SFO with CERA (CERA + SFO) significantly attenuated the responses of ERFE, Ret, and Hb compared with CERA alone. Although iFGF23 levels were not affected by either CERA or CERA + SFO, cFGF23 was significantly elevated from baseline after CERA. Since cFGF23 levels were not affected by CERA + SFO, cFGF23 levels after CERA + SFO were significantly lower than those after CERA alone. The ratio of iFGF23 to cFGF23 (i/cFGF23 ratio) was significantly higher after CERA + SFO than that after CERA alone. In addition, high-sensitivity C-reactive protein (hsCRP) levels were significantly higher after CERA + SFO than after CERA alone.

          Conclusion

          Administration of SFO suppressed haematopoietic responses induced by CERA. Elevation of i/cFGF23 ratio and hsCRP could account for the inhibitory effects of SFO on haematopoiesis.

          Trial registration

          This study was registered with the University Hospital Medical Information Network (ID UMIN000016552).

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12882-021-02320-2.

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          Most cited references17

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          A Red Carpet for Iron Metabolism.

          Martina U. Muckenthaler, Stefano Rivella, Matthias W Hentze … (2017)
          200 billion red blood cells (RBCs) are produced every day, requiring more than 2 × 1015 iron atoms every second to maintain adequate erythropoiesis. These numbers translate into 20 mL of blood being produced each day, containing 6 g of hemoglobin and 20 mg of iron. These impressive numbers illustrate why the making and breaking of RBCs is at the heart of iron physiology, providing an ideal context to discuss recent progress in understanding the systemic and cellular mechanisms that underlie the regulation of iron homeostasis and its disorders.
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            IDENTIFICATION OF ERYTHROFERRONE AS AN ERYTHROID REGULATOR OF IRON METABOLISM

            Léon Kautz, Grace Jung, Erika V. Valore … (2014)
            Recovery from blood loss requires a greatly enhanced supply of iron to support expanded erythropoiesis. After hemorrhage, suppression of the iron-regulatory hormone hepcidin allows increased iron absorption and mobilization from stores. We identified a new hormone, erythroferrone (ERFE), which mediates hepcidin suppression during stress erythropoiesis. ERFE is produced by erythroblasts in response to erythropoietin. ERFE-deficient mice fail to suppress hepcidin rapidly after hemorrhage and exhibit a delay in recovery from blood loss. ERFE expression is greatly increased in murine HbbTh3/+ thalassemia intermedia where it contributes to the suppression of hepcidin and systemic iron overload characteristic of this disease.
            Article 0 comments Cited 189 times – based on 0 reviews     Review now
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              Systemic iron homeostasis.

              Tomas Ganz (2013)
              The iron hormone hepcidin and its receptor and cellular iron exporter ferroportin control the major fluxes of iron into blood plasma: intestinal iron absorption, the delivery of recycled iron from macrophages, and the release of stored iron from hepatocytes. Because iron losses are comparatively very small, iron absorption and its regulation by hepcidin and ferroportin determine total body iron content. Hepcidin is in turn feedback-regulated by plasma iron concentration and iron stores, and negatively regulated by the activity of erythrocyte precursors, the dominant consumers of iron. Hepcidin and ferroportin also play a role in host defense and inflammation, and hepcidin synthesis is induced by inflammatory signals including interleukin-6 and activin B. This review summarizes and discusses recent progress in molecular characterization of systemic iron homeostasis and its disorders, and identifies areas for further investigation.
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                Author and article information

                Contributors
                Akira Fujimori: louie@kcc.zaq.ne.jp
                Journal
                Journal ID (nlm-ta): BMC Nephrol
                Journal ID (iso-abbrev): BMC Nephrol
                Title: BMC Nephrology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-2369
                Publication date (Electronic): 8 April 2021
                Publication date PMC-release: 8 April 2021
                Publication date Collection: 2021
                Volume: 22
                Electronic Location Identifier: 124
                Affiliations
                [1 ]GRID grid.272264.7, ISNI 0000 0000 9142 153X, Internal Medicine (Nephrology and Dialysis), Hyogo College of Medicine, ; Mukogawa-cho, Nishinomiya City, Hyogo 663-8501 Japan
                [2 ]Department of Nephrology, Konan Medical Centre, 1-5-16 Kamokogahara, Higashinada-ku, Kobe, 658-0064 Japan
                [3 ]Department of Internal Medicine (Nephrology), Sumiyoshigawa Hospital, 5-6-7 Konan-cho, Higashinada-ku, Kobe, 658-0084 Japan
                Article
                Publisher ID: 2320
                DOI: 10.1186/s12882-021-02320-2
                PMC ID: 8034147
                PubMed ID: 33832448
                SO-VID: 6ea916ed-ac82-4f63-aa35-b01929365324
                Copyright © © The Author(s) 2021
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 9 January 2021
                Date accepted : 17 March 2021
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                ScienceOpen disciplines: Nephrology
                Keywords: fibroblast growth factor 23,erythroferrone,hepcidin,epoetin beta pegol,saccharated ferric oxide
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: fibroblast growth factor 23, erythroferrone, hepcidin, epoetin beta pegol, saccharated ferric oxide

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