Kidney Week

Abstract: PO0559

Longitudinal Changes in FGF-23 in Children with CKD

Session Information

• Bone and Mineral Metabolism: Clinical
  November 04, 2021 | Location: On-Demand, Virtual Only
  Abstract Time: 10:00 AM - 12:00 PM

Category: Bone and Mineral Metabolism

• 402 Bone and Mineral Metabolism: Clinical

Authors

• Perwad, Farzana, University of California San Francisco, San Francisco, California, United States

Farzana Perwad, MD

• Matheson, Matthew, Johns Hopkins University, Baltimore, Maryland, United States

Matthew Matheson,

• Salusky, Isidro B., University of California Los Angeles, Los Angeles, California, United States

Isidro B. Salusky,

• Jüppner, Harald, Massachusetts General Hospital, Boston, Massachusetts, United States

Harald Jüppner,

• Wolf, Myles, Duke University, Durham, North Carolina, United States

Myles Wolf,

• Warady, Bradley A., Children's Mercy Hospitals and Clinics, Kansas City, Missouri, United States

Bradley A. Warady,

• Furth, Susan L., The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States

Susan L. Furth,

• Ng, Derek, Johns Hopkins University, Baltimore, Maryland, United States

Derek Ng,

• Portale, Anthony A., University of California San Francisco, San Francisco, California, United States

Anthony A. Portale,

Background

Cross sectional studies show that plasma FGF23 is increased early in the course of chronic kidney disease (CKD) in children and adults and associates with disease progression and adverse cardiovascular outcomes. However, longitudinal changes in FGF23 have not been described in children with progressive CKD.

Methods

We measured C-terminal FGF23 and estimated GFR at baseline and every other year in 564 children with CKD stages 2-4 enrolled in the Chronic Kidney Disease in Children (CKiD) study. All subjects had 2 to 5 FGF23 measurements. We used linear mixed models to identify factors associated with baseline FGF23 level and longitudinal changes and latent group-based trajectory modeling to characterize distinct classes of FGF23 trajectories.

Results

Median age was 11 years and eGFR 55 ml/min/1.73m². In a univariate model with repeated measures, plasma FGF23 was 12% higher for every 10% lower eGFR (P<0.0001). In fully adjusted models, higher FGF23 at baseline was significantly associated with lower GFR, higher serum phosphorus, and glomerular diagnosis. Thereafter, FGF23 increased more rapidly in older subjects with lower GFR and higher proteinuria at baseline. We identified three distinct linear FGF23 trajectories: stable FGF23 in 62% of subjects (FGF23 slope 0% per yr); slowly rising in 32% (6% per yr) and rapidly rising in 6% (39% per yr). At baseline, median FGF23 in the trajectory groups were 90 [IQR:70,120], 166 [125, 242] and 461 [219, 924] RU/ml, respectively. Membership in the faster-rising trajectory groups was associated with lower eGFR, higher proteinuria and serum phosphorus, and glomerular diagnosis.

Conclusion

FGF23 was relatively stable in most children with CKD, but it increased more rapidly in those with traditional CKD risk factors. Further analyses of FGF23 trajectories will investigate whether FGF23 is a modifiable cause or a consequence of CKD progression and cardiovascular complications.

Funding

• NIDDK Support