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FGF-23 and vascular dysfunction in patients with stage 3 and 4 chronic kidney disease
Kidney International
  • Mahmut I. Yilmaz, Gulhane Military Medical Academy
  • Alper Sonmez, Gulhane Military Medical Academy
  • Mutlu Saglam, Gulhane Military Medical Academy
  • Halil Yaman, Gulhane Military Medical Academy
  • Selim Kilic, Gulhane Military Medical Academy
  • Erkan Demirkaya, Gulhane Military Medical Academy
  • Tayfun Eyileten, Gulhane Military Medical Academy
  • Kayser Caglar, Gulhane Military Medical Academy
  • Yusuf Oguz, Gulhane Military Medical Academy
  • Abdulgaffar Vural, Gulhane Military Medical Academy
  • Mujdat Yenicesu, Gulhane Military Medical Academy
  • Carmine Zoccali, Azienda Ospedaliera Bianchi-Melacrino-Morelli
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Studies in animals show that fibroblast growth factor (FGF)-23 interferes with vascular reactivity induced by the nitric oxide (NO) system. To investigate the relationship between circulating FGF-23 levels and the response of forearm blood flow to ischemia (flow-mediated vasodilatation, FMD) and nitroglycerin, we tested 183 patients with stage 3-4 chronic kidney disease (CKD). None of them had cardiovascular complications or were taking drugs interfering with vascular function. Patients with FGF-23 levels above the median had significantly lower glomerular filtration rate, FMD, and fetuin-A levels (an anti-inflammatory molecule and potent inhibitor of calcification). They also had higher proteinuria and phosphate levels when compared to patients whose FGF-23 levels were below the median. The response to nitroglycerin was not different between the two groups. Multiple regression analysis showed that the relationship between FGF-23 and FMD was only modestly sensitive to adjustment for classical risk factors, biomarkers of bone mineral metabolism, high-sensitivity C-reactive protein, and homeostatic model assessment index. Adjustment for asymmetrical dimethyl arginine (ADMA) weakened the strength of this link; however, it remained highly significant. There was no independent association between FGF-23 and nitroglycerin. Thus, attenuation of FMD by ADMA suggests that this endogenous inhibitor of NO synthase may, in part, mediate the vascular effects of FGF-23 in patients with CKD. © 2010 International Society of Nephrology.

Citation Information
Mahmut I. Yilmaz, Alper Sonmez, Mutlu Saglam, Halil Yaman, et al.. "FGF-23 and vascular dysfunction in patients with stage 3 and 4 chronic kidney disease" Kidney International Vol. 78 Iss. 7 (2010) p. 679 - 685
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