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Published on: November 10, 2021
Regulation and Effects of FGF23 in Chronic Kidney Disease
John Musgrove1, Myles Wolf1,2
1Division of Nephrology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina 27710, USA;
Insights
Fibroblast growth factor 23 (FGF23) plays a key role in chronic kidney disease (CKD) complications. Research into FGF23 in CKD is driving new therapies for mineral metabolism disorders.
Area of Science:
- Nephrology
- Endocrinology
- Cardiovascular Disease
Background:
- Chronic kidney disease (CKD) is a global health issue with severe complications, including cardiovascular disease, infection, anemia, and bone disease.
- Disordered mineral metabolism, particularly calcium and phosphate homeostasis, is a significant risk factor in CKD progression and morbidity.
- Fibroblast growth factor 23 (FGF23) has emerged as a critical factor in understanding and managing rare genetic disorders and CKD-related mineral metabolism issues.
Purpose of the Study:
- To explore the evolving understanding of fibroblast growth factor 23 (FGF23) in the context of chronic kidney disease (CKD).
- To highlight the impact of FGF23 discovery on the pathophysiology and complications of disordered mineral metabolism in CKD.
- To discuss the emerging research questions and innovations in FGF23-targeted therapies for CKD.
Main Methods:
- Review of recent laboratory, patient-oriented, and epidemiological research on FGF23 in CKD.
- Analysis of the role of FGF23 in mineral metabolism and its downstream effects in CKD.
- Examination of ongoing clinical trials for FGF23-targeting therapies in CKD.
Main Results:
- FGF23 has revolutionized the understanding of rare FGF23-related disorders and significantly impacted CKD pathophysiology.
- Research on FGF23 in CKD is rapidly advancing, revealing new insights into its regulation and effects.
- The study of FGF23 is stimulating the development of novel therapeutic strategies for CKD complications.
Conclusions:
- FGF23 is central to understanding mineral metabolism disorders in CKD.
- Continued research into FGF23 is crucial for developing innovative treatments for CKD patients.
- Targeting FGF23 holds promise for mitigating major CKD morbidities and improving patient outcomes.
Abstract:
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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