Deviations from the expected relationship between serum FGF23 and other markers in children with CKD: a

Daisy Liu1, Ana Catalina Alvarez-Elías2,3,4, Brooke Wile2

  • 1Department of Pediatrics, McMaster University, Hamilton, ON, N6A 5W9, Canada.

BMC Nephrology
|June 30, 2017
PubMed

Insights

Fibroblast growth factor-23 (FGF23) levels in pediatric chronic kidney disease (CKD) are influenced by phosphate, vitamin D, and acidosis. Understanding these factors helps predict FGF23 levels in CKD patients.

Area of Science:

  • Pediatric Nephrology
  • Endocrinology
  • Biochemistry

Background:

  • Elevated fibroblast growth factor-23 (FGF23) is linked to mortality.
  • FGF23 levels increase with declining renal function in chronic kidney disease (CKD).
  • This study examines laboratory value contributions to FGF23 variance relative to estimated GFR (eGFR).

Purpose of the Study:

  • To analyze the relationship between various laboratory values and FGF23 levels in pediatric CKD patients.
  • To identify key determinants of FGF23 levels in relation to eGFR.
  • To establish a predictive model for FGF23 based on eGFR.

Main Methods:

  • Measured FGF23 and multiple laboratory parameters (including CysC eGFR, phosphate, vitamin D metabolites, PTH, and pH) in 141 pediatric CKD patients across stages.
  • Utilized statistical analysis to determine correlations between FGF23 and laboratory values.
  • Developed a formula to predict expected FGF23 levels based on eGFR.

Main Results:

  • FGF23 significantly correlated with CysC eGFR, PTH, 1.25(OH)2 vitamin D, phosphate, and pH.
  • Multivariate analysis confirmed PTH, 1.25(OH)2 vitamin D, and pH as significant independent predictors.
  • A formula was derived to estimate FGF23 based on eGFR (Y = 1295 * e-0.07247*X + 38.35), with deviations influenced by phosphate, vitamin D, and pH.

Conclusions:

  • Phosphate and 1.25(OH)2 vitamin D levels are crucial determinants of FGF23 in pediatric CKD.
  • The influence of acidosis on FGF23 requires further investigation.
  • These findings aid in understanding FGF23 regulation and its clinical implications in pediatric CKD.
Abstract

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