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Kidney Week

Abstract: PO0347

Intact and C-Terminal Fibroblast Growth Factor 23 Assays: Do Kidney Function, Inflammation, and Iron Deficiency Influence Relationships with Clinical Outcomes?

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Sharma, Shilpa, University of California Los Angeles, Los Angeles, California, United States
  • Katz, Ronit, University of Washington, Seattle, Washington, United States
  • Bullen, Alexander, University of California San Diego, La Jolla, California, United States
  • Houben, Alfons Jhm, Maastricht Universitair Medisch Centrum+ Interne Geneeskunde, Maastricht, Limburg, Netherlands
  • Shlipak, Michael, University of California San Francisco, San Francisco, California, United States
  • Ix, Joachim H., University of California San Diego, La Jolla, California, United States
Background

Higher fibroblast growth factor-23 (FGF23) concentrations are associated with heart failure (HF) and mortality, but strengths of associations differ depending upon FGF23 assay type. We investigated whether iron deficiency, inflammation, and kidney function account for these differences.

Methods

In 844 Cardiovascular Health Study participants, using a case-cohort design, we examined associations of intact and C-terminal FGF23 with risk of mortality and HF, using modified Cox models to account for case-cohort design, adjusting sequentially by iron status, inflammation, kidney function or their combinations.

Results

C-terminal FGF23 more strongly correlated with ferritin (r= -0.26) and CRP (r= 0.21) than intact FGF23 (r=0.04 & r=0.07, respectively). The two FGF23 assays moderately correlated with one another (r=0.47). During follow up, there were 658 deaths, and 220 incident HF events. FGF23 measured by either assay was associated with mortality in unadjusted analysis (intact FGF23 HR per two-fold higher 1.45; 1.25-1.68; C-terminal FGF23 1.38; 1.26-1.50). Adjustment for kidney function completely attenuated associations of intact FGF23 with mortality (HR 1.00; 0.85, 1.17; Figure 1), but had less influence on the C-terminal FGF23-mortality association (HR 1.15; 1.04, 1.28). Results were similar for HF where the HR for intact FGF23 went from 1.57 (1.25, 1.97) to 0.99 (0.76, 1.28) with eGFR and albuminuria adjustment, whereas C-FGF23 went from 1.45 (1.25, 1.68) to 1.16 (0.97, 1.38). Adjustment for iron deficiency and inflammation did not meaningfully influence the differential associations of the two assays with either endpoint.

Conclusion

The associations of biologically active FGF23 with clinical endpoints may be weaker than previously thought.

Effects of Adjustment for Iron Parameters, Inflammation, and Kidney Function on the Associations of C-terminal and intact FGF23 with Mortality

Funding

  • NIDDK Support