Evidence map›Paper›PMID 30007314›Full record

ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2019

Effects of erythropoietin on fibroblast growth factor 23 in mice and humans.

Mark R Hanudel, Michele F Eisenga, Maxime Rappaport, Kristine Chua, Bo Qiao, Grace Jung, Victoria Gabayan, Barbara Gales, Georgina Ramos, Maarten A de Jong and 7 more

Open access · greenAbstract read
In one paragraph

Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
9.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 95 citations in OpenAlex.

  1. Trial
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  7. Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024
    Review
  8. Associations between anemia and FGF23 in the CKiD study.Pediatric nephrology (Berlin, Germany) · 2024
    Article
  9. Article
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  18. Treatment of anemia associated with chronic kidney disease with the HIF prolyl hydroxylase inhibitor enarodustat: A review of the evidence.Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy · 2022
    Review
  19. Review
  20. Review

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 2 countries.

Mark R HanudelDepartment of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Michele F EisengaDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Maxime RappaportDepartment of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Kristine ChuaDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Bo QiaoDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Grace JungDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Victoria GabayanDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Barbara GalesDepartment of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Georgina RamosDepartment of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Maarten A de JongDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Jelmer J van ZandenCerte, Department of Clinical Chemistry, Martini Hospital, Groningen, The Netherlands.
Martin H de BorstDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Stephan J L BakkerDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Elizabeta NemethDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Isidro B SaluskyDepartment of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Carlo A J M GaillardDepartment of Internal Medicine and Dermatology, University of Utrecht, University Medical Center Utrecht, Utrecht, The Netherlands.
Tomas GanzDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
University of California, Los Angeles · USUniversity of Groningen · NLMartini Ziekenhuis · NLUniversity Medical Center Utrecht · NL

Funding

Regulation of Fibroblast Growth Factor 23 by Iron and Anemia in Chronic Kidney DiseaseK08DK111980 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HANUDEL, MARK ROBERT · 2016 to 2019
$758k
NIDDK NIH HHS K08 DK111980NIDDK NIH HHS L40 DK106813
6 · The paper itself

Abstract

backgroundErythropoietin (EPO) has been reported as a novel determinant of fibroblast growth factor 23 (FGF23) production; however, it is unknown whether FGF23 is stimulated by chronic exposure to EPO or by EPO administration in nonpolycystic chronic kidney disease (CKD) models.

methodsWe analyzed the effects of chronic EPO on FGF23 in murine models with chronically high EPO levels and normal kidney function. We studied the effects of exogenous EPO on FGF23 in wild-type mice, with and without CKD, injected with EPO. Also, in four independent human CKD cohorts, we evaluated associations between FGF23 and serum EPO levels or exogenous EPO dose.

resultsMice with high endogenous EPO have elevated circulating total FGF23, increased disproportionately to intact FGF23, suggesting coupling of increased FGF23 production with increased proteolytic cleavage. Similarly, in wild-type mice with and without CKD, a single exogenous EPO dose acutely increases circulating total FGF23 out of proportion to intact FGF23. In these murine models, the bone marrow is shown to be a novel source of EPO-stimulated FGF23 production. In humans, serum EPO levels and recombinant human EPO dose are positively and independently associated with total FGF23 levels across the spectrum of CKD and after kidney transplantation. In our largest cohort of 680 renal transplant recipients, serum EPO levels are associated with total FGF23, but not intact FGF23, consistent with the effects of EPO on FGF23 production and metabolism observed in our murine models.

conclusionEPO affects FGF23 production and metabolism, which may have important implications for CKD patients.

Indexed as

Gene Expression RegulationAnimalsbeta-ThalassemiaCohort StudiesErythropoietinFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsHumansKidney TransplantationMaleMiceMice, TransgenicMiddle AgedPrognosisRenal Insufficiency, ChronicEPO protein, humanEpo protein, mouseErythropoietinFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth Factorsanemiachronic kidney diseaseCKD-MBD, erythropoietinfibroblast growth factor 23

Identifiers

PMID30007314
PMCPMC6888066
OpenAlexW2830773612

What OpenQuestion holds

Textmetadata
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.