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Letters to the Editor
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Fibroblast Growth Factor-23 May Follow Cardiovascular Disease Rather than Causing It in Chronic Kidney Disease

Chenchen Zhou, Changlin Mei, Bing Dai and Cheng Xue
JASN October 2018, 29 (10) 2602; DOI: https://doi.org/10.1681/ASN.2018050517
Chenchen Zhou
1Department of Nephrology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China; and
2Division of Nephrology, Changzheng Hospital, Second Military Medical University, Shanghai, China
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Changlin Mei
2Division of Nephrology, Changzheng Hospital, Second Military Medical University, Shanghai, China
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Bing Dai
2Division of Nephrology, Changzheng Hospital, Second Military Medical University, Shanghai, China
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Cheng Xue
2Division of Nephrology, Changzheng Hospital, Second Military Medical University, Shanghai, China
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  • cardiovascular disease
  • fibroblast
  • chronic kidney disease

We read the article “Fibroblast growth factor-23 and risks of cardiovascular and noncardiovascular diseases: A meta-analysis” by Marthi et al.1 with great interest. The study provided an important demonstration that serum higher fibroblast growth factor-23 (FGF-23) level was positively associated with cardiovascular and noncardiovascular outcomes in populations with or without CKD.1 In agreement with Marthi et al.,1 our previous meta-analysis also pointed out that there might be predictive effects of FGF-23 on cardiovascular diseases (CVDs; including myocardial infarction, atrial fibrillation, myocardial ischemia, heart failure, and stroke) and mortality in patients with CKD.2

However, the absence of an exposure-response relationship and similarly sized associations between FGF-23 and different outcomes may not be strong enough to suggest a noncausal relationship between FGF-23 and CVD. Indeed, interactions between FGF-23 and CVD are complicated and remain inconclusive. Experimental studies have revealed that FGF-23 could induce left ventricular hypertrophy.3 Both FGF-23 overexpression and Klotho deficiency showed cardiac remodeling effects in CKD.4 However, Slavic et al.5 found that genetic ablation of FGF-23 or Klotho did not modulate heart hypertrophy, indicating other mediators as the real culprits. Recently, left ventricular hypertrophy in transgenic mice was found to elevate myocardial and serum levels of FGF-23.3 Taken together, the mutual promotion between FGF-23 and CVD indicates a complex interaction between mineral metabolism and the cardiovascular system in CKD. FGF-23 may follow CVD rather than causing it in CKD.

In conclusion, the finding of this meta-analysis1 is very important, because it brings us a deep and broad view of FGF-23 in CVD and mortality in patients with or without kidney disease. More mechanisms between FGF-23 and CVD will need to be studied to better understand the effect of FGF-23 on cardiovascular health in patients with CKD.

Disclosures

None.

Acknowledgments

The work was supported by National Natural Science Foundation of China grant 81700579.

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 “Authors’ Reply,” on pages 2601 and 2602–2603, 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, 2018pmid:29764921
    OpenUrlAbstract/FREE Full Text
  2. ↵
    1. Xue C,
    2. Yang B,
    3. Zhou C,
    4. Dai B,
    5. Liu Y,
    6. Mao Z, et al
    .: Fibroblast growth factor 23 predicts all-cause mortality in a dose-response fashion in pre-dialysis patients with chronic kidney disease. Am J Nephrol 45: 149–159, 2017pmid:28006765
    OpenUrlPubMed
  3. ↵
    1. Matsui I,
    2. Oka T,
    3. Kusunoki Y,
    4. Mori D,
    5. Hashimoto N,
    6. Matsumoto A, et al
    .: Cardiac hypertrophy elevates serum levels of fibroblast growth factor 23. Kidney Int 94: 60–71, 2018pmid:29751971
    OpenUrlCrossRefPubMed
  4. ↵
    1. Hu MC,
    2. Shi M,
    3. Cho HJ,
    4. Adams-Huet B,
    5. Paek J,
    6. Hill K, et al
    .: Klotho and phosphate are modulators of pathologic uremic cardiac remodeling. J Am Soc Nephrol 26: 1290–1302, 2015pmid:25326585
    OpenUrlAbstract/FREE Full Text
  5. ↵
    1. Slavic S,
    2. Ford K,
    3. Modert M,
    4. Becirovic A,
    5. Handschuh S,
    6. Baierl A, et al
    .: Genetic ablation of Fgf23 or Klotho does not modulate experimental heart hypertrophy induced by pressure overload. Sci Rep 7: 11298, 2017pmid:28900153
    OpenUrlPubMed
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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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Fibroblast Growth Factor-23 May Follow Cardiovascular Disease Rather than Causing It in Chronic Kidney Disease
Chenchen Zhou, Changlin Mei, Bing Dai, Cheng Xue
JASN Oct 2018, 29 (10) 2602; DOI: 10.1681/ASN.2018050517

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Fibroblast Growth Factor-23 May Follow Cardiovascular Disease Rather than Causing It in Chronic Kidney Disease
Chenchen Zhou, Changlin Mei, Bing Dai, Cheng Xue
JASN Oct 2018, 29 (10) 2602; DOI: 10.1681/ASN.2018050517
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  • Calcium-Based Phosphate Binders and Plasma Oxalate Concentration in Dialysis Patients
  • Authors’ Reply: Calcium-Based Phosphate Binders and Plasma Oxalate Concentration in Dialysis Patients
  • Predicting Kidney Response to Plasma Exchange in ANCA-Associated Vasculitis: Need for Plausible Models
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