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Letters to the Editor
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Authors’ Reply

William G. Herrington, Killian Donovan and Borislava Mihaylova
JASN October 2018, 29 (10) 2602-2603; DOI: https://doi.org/10.1681/ASN.2018060612
William G. Herrington
1Clinical Trial Service Unit and Epidemiological Studies Unit,
2Medical Research Council Population Health Research Unit, and
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Killian Donovan
1Clinical Trial Service Unit and Epidemiological Studies Unit,
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Borislava Mihaylova
3Health Economics Research Centre, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom
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  • cardiovascular
  • Epidemiology and outcomes
  • FGF-23

The published observational data show similarly sized epidemiologic associations between increased fibroblast growth factor-23 (FGF-23) concentration and risk of a range of cardiovascular (atherosclerotic and nonatherosclerotic) and noncardiovascular outcomes. There is also an absence of any clear exposure-response relationship.1

Pelletier and Fouque2 have hypothesized that Klotho modifies FGF-23 associations with cardiovascular outcomes, and confirmation in large-scale studies is of interest. Such analyses, however, are unlikely to provide an explanation for the nonspecificity of FGF-23 associations. Instead, as recommended by Zhou et al.,3 further mechanistic experiments are needed. We suggest that such studies include the full range of noncardiovascular outcomes identified as associated with FGF-23. In the absence of good mechanistic evidence clearly supporting FGF-23’s role in a much wider range of disease processes, residual confounding is currently the most plausible explanation for the nonspecific associations. The epidemiology is suggesting the relationship between FGF-23 and cardiovascular disease risk may not be one of cause and effect.

Disclosures

None.

Acknowledgments

W.G.H. is supported by a Medical Research Council and Kidney Research UK Professor David Kerr Clinician Scientist Award.

Footnotes

  • Published online ahead of print. Publication date available at www.jasn.org.

  • See related Letters to the Editor, “Fibroblast Growth Factor-23 Is Not a Single Bystander in Chronic Kidney Disease Mortality,” and “Fibroblast Growth Factor-23 May Follow Cardiovascular Disease Rather than Causing It in Chronic Kidney Disease” on pages 2601 and 2602, respectively.

  • Copyright © 2018 by the American Society of Nephrology

References

  1. ↵
    1. Marthi A,
    2. Donovan K,
    3. Haynes R,
    4. Wheeler DC,
    5. Baigent C,
    6. Rooney CM, et al
    .: Fibroblast growth factor-23 and risks of cardiovascular and noncardiovascular diseases: A meta-analysis. J Am Soc Nephrol 29: 579–590, 2018
    OpenUrlAbstract/FREE Full Text
  2. ↵
    1. Pelletier S,
    2. Fouque D
    : Fibroblast growth factor-23 is not a single bystander in chronic kidney disease mortality. J Am Soc Nephrol 29: XXX–XXX, 2018
    OpenUrl
  3. ↵
    1. Zhou C,
    2. Mei C,
    3. Dai B,
    4. Xue C
    : Fibroblast growth factor-23 may follow cardiovascular disease rather than causing it in chronic kidney disease. J Am Soc Nephrol 29: 2602, 2018
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Journal of the American Society of Nephrology: 29 (10)
Journal of the American Society of Nephrology
Vol. 29, Issue 10
October 2018
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Authors’ Reply
William G. Herrington, Killian Donovan, Borislava Mihaylova
JASN Oct 2018, 29 (10) 2602-2603; DOI: 10.1681/ASN.2018060612

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Authors’ Reply
William G. Herrington, Killian Donovan, Borislava Mihaylova
JASN Oct 2018, 29 (10) 2602-2603; DOI: 10.1681/ASN.2018060612
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