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Clin Chim Acta. 2011 May 12;412(11-12):1008-11. doi: 10.1016/j.cca.2011.02.009. Epub 2011 Feb 12.

Instability of fibroblast growth factor-23 (FGF-23): implications for clinical studies.

Author information

1
Department of Clinical Biochemistry & Immunology, Brighton & Sussex University Hospitals NHS Trust, Brighton, BN2 5BE, UK. edward.smith@bsuh.nhs.uk

Abstract

BACKGROUND:

Fibroblast growth factor-23 (FGF-23) is a bone secreted hormone that regulates phosphate homeostasis and calcitriol levels. FGF-23 concentrations are elevated in chronic kidney disease (CKD), oncogenic osteomalcia and a number of rare hereditary disorders. Studies systematically evaluating the pre-analytical stability of intact FGF-23 are lacking.

METHODS:

The stability of FGF-23 was assessed in timed experiments using blood taken into K2-EDTA plasma specimen tubes from a group of healthy participants and from a group with mild-to-moderate CKD. We evaluated the use of aprotinin, a serine protease inhibitor, and a commercially available protease inhibitor cocktail to preserve intact FGF-23 after blood collection. FGF-23 measurements were made using both intact and C-terminal assays.

RESULTS:

Both whole blood and separated sample studies demonstrated a rapid loss of intact FGF-23 within 2 h, while concentrations increased using the C-terminal assay. The addition of protease inhibitor cocktail stabilised FGF-23 concentrations for 4 h after blood collection. Intact and C-terminal assay FGF-23 measurements showed poor correlation in both healthy and CKD cohorts.

CONCLUSION:

K2-EDTA plasma samples, even when promptly separated, are unsuitable for measurement of FGF-23 unless stabilised with a protease inhibitor cocktail.

PMID:
21324311
DOI:
10.1016/j.cca.2011.02.009
[Indexed for MEDLINE]

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