Format

Send to

Choose Destination
Curr Osteoporos Rep. 2018 Dec;16(6):724-729. doi: 10.1007/s11914-018-0492-2.

Non-renal-Related Mechanisms of FGF23 Pathophysiology.

Author information

1
UCLA Department of Pediatrics, Division of Pediatric Nephrology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC A2-383, Los Angeles, CA, 90095-1752, USA. mhanudel@mednet.ucla.edu.
2
UCLA Department of Pediatrics, Division of Pediatric Nephrology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC A2-383, Los Angeles, CA, 90095-1752, USA.

Abstract

PURPOSE OF REVIEW:

We will review non-renal-related mechanisms of fibroblast growth factor 23 (FGF23) pathophysiology.

RECENT FINDINGS:

FGF23 production and metabolism may be affected by many bone, mineral, and kidney factors. However, it has recently been demonstrated that other factors, such as iron status, erythropoietin, and inflammation, also affect FGF23 production and metabolism. As these non-mineral factors are especially relevant in the setting of chronic kidney disease (CKD), they may represent emerging determinants of CKD-associated elevated FGF23 levels. Moreover, FGF23 itself may promote anemia and inflammation, thus contributing to the multifactorial etiologies of these CKD-associated comorbidities. CKD-relevant, non-mineral-related, bidirectional relationships exist between FGF23 and anemia, and between FGF23 and inflammation. Iron deficiency, anemia, and inflammation affect FGF23 production and metabolism, and FGF23 itself may contribute to anemia and inflammation, highlighting complex interactions that may affect aspects of CKD pathogenesis and treatment.

KEYWORDS:

Anemia; CKD-mineral and bone disorder; Chronic kidney disease; Fibroblast growth factor 23; Iron

PMID:
30353318
PMCID:
PMC6234055
DOI:
10.1007/s11914-018-0492-2
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Springer Icon for PubMed Central
Loading ...
Support Center