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More trouble with FGF23: a novel role in systemic immunosuppression
Zeinab Abdullah1, Christian Kurts1
1Institute of Experimental Immunology, University of Bonn, Bonn, Germany.
Kidney International
|May 17, 2016
Summary
High levels of Fibroblast Growth Factor 23 (FGF23) in chronic kidney disease impair neutrophil function. This explains how chronic kidney disease contributes to widespread immune suppression.
Area of Science:
- Nephrology
- Immunology
- Biochemistry
Background:
- Chronic kidney disease (CKD) is associated with elevated circulating levels of Fibroblast Growth Factor 23 (FGF23).
- The role of FGF23 in immune dysfunction in CKD is not fully understood.
Purpose of the Study:
- To investigate the impact of excessive FGF23 on neutrophil function in patients with CKD.
- To elucidate the mechanisms linking CKD, FGF23, and systemic immunosuppression.
Main Methods:
- Analysis of neutrophil function markers in CKD patients with high FGF23 levels.
- In vitro studies assessing FGF23 effects on neutrophil behavior.
Main Results:
- Excessive FGF23 levels in CKD patients were correlated with impaired neutrophil function.
- Specific neutrophil functions, such as phagocytosis and oxidative burst, were found to be diminished.
Conclusions:
- Elevated FGF23 is a key factor contributing to neutrophil dysfunction in CKD.
- This impaired neutrophil function represents a significant mechanism underlying systemic immunosuppression in chronic kidney disease.
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