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Plasma fibroblast growth factor 23 concentration and iron status. Does the relationship exist in the elderly
Maria Bożentowicz-Wikarek1, Piotr Kocełak2, Aleksander Owczarek3
1Pathophysiology Unit, Department of Pathophysiology, Medical Faculty in Katowice, Medical University of Silesia, Katowice, Poland.
Objective:
Fibroblast growth factor 23 (FGF23) is a phosphaturic agent involved in calcium-phosphate homeostasis. Recent findings show that iron deficiency and inflammation regulate FGF23 release and/or biodegradation. Iron deficiency is frequently observed in the elderly, therefore the aim of this study was to find out if iron deficiency is independent from low grade inflammatory factors affecting both forms of FGF23 that are detectable in circulation in a large population-based study of elderly subjects.
Design And Methods:
The analysis included 3780 elderly (1798 females) PolSenior study participants and assessed levels of phosphorus, calcium, iron, ferritin, interleukin 6, C-reactive protein (hs-CRP), intact (iFGF23), and c-terminal FGF (cFGF23). The analysis was performed for all subjects and terciles of serum iron levels in relation to hs-CRP were calculated.
Results:
The highest plasma cFGF23 and iFGF23 concentrations were found in subjects with the lowest serum iron levels (p<0.001). The effect of low grade inflammation was markedly weaker and affected only iFGF23 levels. The adjusted serum levels of hs-CRP, iPTH, phosphorus, and 25-(OH)-D3 analysis revealed that plasma iFGF23 and cFGF23 levels were almost unchanged up to a serum iron level of 59.3 ng/mL and 57.3 ng/mL respectively and then were nearly linearly increasing by 0.285 pg/mL and 3.742 RU/mL for each unit of serum iron increase.
Conclusions:
Low iron levels are associated with increased levels of both cFGF23 and iFGF23, independent of low grade inflammation. A similar analysis of cFGF23 and iFGF23 does not suggest enhanced biodegradation of iFGF23 induced by iron deficiency.
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