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Kidney Week

Abstract: SA-PO749

Single Measurements of Fibroblast Growth Factor 23 and Clinical Risk Prediction in CKD

Session Information

Category: CKD (Non-Dialysis)

  • 1901 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Edmonston, Daniel, Duke University, Durham, North Carolina, United States
  • Mehta, Rupal, Northwestern Univesrsity, Feinberg School of Medicine, Chicago, Illinois, United States
  • Wojdyla, Daniel, Duke Clinical Research Institute, Durham, North Carolina, United States
  • Cai, Xuan, Northwestern University, Chicago, Illinois, United States
  • Lora, Claudia M., University of Illinois at Chicago, Chicago, Illinois, United States
  • Weir, Matthew R., University of Maryland School of Medicine, Baltimore, Maryland, United States
  • Kusek, John W., NIDDK, Bethesda, Maryland, United States
  • Townsend, Raymond R., University of Pennsylvania School of Medicine, Villanova, Pennsylvania, United States
  • Cohen, Debbie L., University of Pennsylvania School of Medicine, Villanova, Pennsylvania, United States
  • He, Jiang, Tulane School of Public Health and Tropical Medicine, New Orleans, Louisiana, United States
  • Go, Alan S., Kaiser Permanente Northern California, Oakland, California, United States
  • Isakova, Tamara, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States
  • Wolf, Myles, Duke University, Durham, North Carolina, United States

Group or Team Name

  • for the CRIC Study Investigators
Background

Elevated fibroblast growth factor 23 (FGF23) levels are independently associated with a number of adverse outcomes in patients with chronic kidney disease (CKD) at the population level, but it is unknown if FGF23 testing can improve individual clinical risk prediction.

Methods

In 3879 participants in the Chronic Renal Insufficiency Cohort Study, we tested whether addition of a single baseline measurement of FGF23 testing to standard clinical risk predictors (Figure) significantly improves prediction of all-cause mortality, incident end-stage renal disease (ESRD), heart failure (HF) admission, and atherosclerotic events over periods of 3 (primary analysis), 5, and 8 years of follow-up. We assessed changes in C index, integrated discrimination improvement (IDI), relative IDI, and category-based net reclassification index (NRI). We also compared the incremental utility of FGF23 versus an analogous model using serum phosphate concentration.

Results

The base model best predicted incident ESRD and HF (Figure). The addition of FGF23 improved prediction of all-cause mortality and HF admissions by change in C index, IDI, and relative IDI (NRI trended towards significance), but not incident ESRD or atherosclerotic events (Figure). The years 5 and 8 results were qualitatively similar to the 3-year results. FGF23 outperformed phosphate for all outcomes.

Conclusion

In CKD, single measurements of FGF23 improves prediction of risks of all-cause mortality and HF admissions but not ESRD or atherosclerotic events. Future studies are needed to evaluate the predictive utility of repeated FGF23 testing.

Funding

  • NIDDK Support