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Abstract: TH-PO179

Fibroblast Growth Factor 23 and Arterial Stiffness in SPRINT

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical


  • Jovanovich, Anna Jeanette, Denver VA , Denver, Colorado, United States
  • You, Zhiying, UC Denver, Aurora, Colorado, United States
  • Ginsberg, Charles, UCSD, San Diego, California, United States
  • Ix, Joachim H., UCSD, San Diego, California, United States
  • Supiano, Mark A., University of Utah Geriatrics Division, Salt Lake City, Utah, United States
  • Shlipak, Michael, San Francisco VA Medical Center, San Francisco, California, United States
  • Cheung, Alfred K., University of Utah, Salt Lake City, Utah, United States
  • Chonchol, Michel, University of Colorado, Aurora, Colorado, United States
  • Nowak, Kristen L., University of Colorado Denver: Anschutz Medical Campus, Aurora, Colorado, United States

Fibroblast growth factor 23 (FGF23) and arterial stiffness are both associated with cardiovascular disease and mortality in chronic kidney disease (CKD). The relationship between FGF23 and arterial stiffness needs further investigation. We hypothesized that higher serum FGF23 levels would be associated with greater arterial stiffness in participants with CKD in the Systolic Blood Pressure Intervention Trial (SPRINT).


The SPRINT study was a randomized multicenter trial evaluating the effects of standard (SBP <140 mmHg) vs. intensive (SBP <120 mmHg) blood pressure lowering on cardiovascular outcomes among older adults without diabetes. Intact FGF23 (iFGF23) was measured at baseline among 2384 participants with an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73m2. Multivariable linear regression determined the association between baseline iFGF23 and pulse pressure (PP; a surrogate measure of arterial stiffness) (N = 2384) and aortic pulse wave velocity (aPWV) (N = 202), the latter of which was measured in an ancillary study. Models were adjusted for demographics, comorbidities, randomization group, baseline number of antihypertensives, eGFR, albuminuria, and serum calcium and phosphorus.


In the PP analysis, mean age was 73 ± 9 years, mean eGFR was 49 ± 11 mL/min/1.73m2, and median iFGF23 level was 71 [53-95] ng/mL. There was no significant association between baseline iFGF23 and PP (β: -0.08, 95% CI: -1.06 to 0.89). Notably, baseline serum phosphorus was significantly associated with PP (β: 1.33, 95% CI: 0.23 to 2.43) in the fully adjusted model. In the ancillary study, mean age was 73 ± 10 years, mean eGFR was 47 ± 12 mL/min/1.73m2, and median iFGF23 level was 71 [53-95] ng/mL. In the unadjusted model, higher iFGF23 was significantly associated with lower aPWV (β: -0.009, 95% CI: -0.02 to -0.003). However, in the fully adjusted model, this association was no longer significant (β: -0.003, 95% CI: -0.01 to 0.004).


Among SPRINT participants with baseline eGFR < 60 mL/min/1.73m2, iFGF23 was not associated with arterial stiffness as measured by PP and aPWV. However, higher serum phosphorus was associated with increased PP. The analysis of aPWV was limited due to a smaller sample size.


  • NIDDK Support