Journal
ANNUAL REVIEW OF PHYSIOLOGY, VOL 82
Volume 82, Issue -, Pages 365-390Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-021119-034650
Keywords
fibroblast growth factor 23; Klotho; chronic kidney disease; iron; inflammation; cardiovascular disease
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Funding
- US National Institutes of Health [R01DK076116, R01DK081374, U01DK099930, UG3DK118748]
- Strategically Focused Research Network Center Grant from the American Heart Association
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Chronic kidney disease (CKD) is a global health epidemic that accelerates cardiovascular disease, increases risk of infection, and causes anemia and bone disease, among other complications that collectively increase risk of premature death. Alterations in calcium and phosphate homeostasis have long been considered nontraditional risk factors for many of the most morbid outcomes of CKD. The discovery of fibroblast growth factor 23 (FGF23), which revolutionized the diagnosis and treatment of rare hereditary disorders of FGF23 excess that cause hypophosphatemic rickets, has also driven major paradigm shifts in our understanding of the pathophysiology and downstream end-organ complications of disordered mineral metabolism in CKD. As research of FGF23 in CKD has rapidly advanced, major new questions about its regulation and effects continuously emerge. These are promoting exciting innovations in laboratory, patient-oriented, and epidemiological research and stimulating clinical trials of new therapies and repurposing of existing ones to target FGF23.
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