FGF23 metabolism, a new paradigm for chronic kidney disease

Piec, Isabelle, Nicholls, Holly, Tang, Jonathan, Washbourne, Christopher and Fraser, William (2015) FGF23 metabolism, a new paradigm for chronic kidney disease. In: American Society for Bone and Mineral Research, 2015-10-07 - 2015-10-12.

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Abstract

Introduction:  Fibroblast growth factor-23 (FGF23) is a major regulator of phosphate metabolism often elevated in genetic hypophosphataemic disorders and in chronic kidney disease. Recent studies have identified relationships between FGF23 and various markers of iron status including ferritin. New assays measuring the intact form of FGF23 have been released.  Objective:  To determine the relationship between ferritin and C-terminal and intact FGF23 concentrations in blood.  Method:  FGF23 concentrations were measured using the 2nd generation, two-site enzyme-linked immunosorbent assay for either C-terminal or intact FGF23 (Immutopics Inc., Ca, USA). Ferritin was measured on a COBAS 6000 (Roche Diagnostics). Assay accuracy and precision were monitored using kit controls supplied by the manufacturers.  Results:  We observe a weak negative correlation between measurements of C-terminal and intact FGF23 (Pearson’s rho=0.85 p<0.0001). We observed no statistically significant correlation of ferritin concentrations with either FGF23 C-terminal or intact. However high concentrations of ferritin were observed in samples showing low concentrations of C-terminal FGF23 (<140RU/mL) and intact FGF23 (<122pg/mL).  Conclusion:  Although not statistically significant, we observe a negative relationship between concentrations of ferritin and FGF23. High level of C-terminal FGF23 is found in patients with chronic kidney disease, especially in patients with end-stage renal disease usually regarded as a compensatory response to hyperphosphatemia or phosphate overload. We observed a cluster of patients with retention of both C-terminal and intact FGF23 associated with low levels of ferritin suggesting that metabolism and/or excretion of FGF23 in CDK patients might be an iron dependent mechanism.

Item Type: Conference or Workshop Item (Poster)
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
Depositing User: Pure Connector
Date Deposited: 01 Dec 2015 17:01
Last Modified: 18 Mar 2020 08:51
URI: https://ueaeprints.uea.ac.uk/id/eprint/55622
DOI:

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