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MCP1 Could Mediate FGF23 and Omega 6/Omega 3 Correlation Inversion in CKD.
Deborah Mattinzoli1, Stefano Turolo2, Carlo Maria Alfieri3,4
1Renal Research Laboratory, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy.
Journal of Clinical Medicine
|December 11, 2022
Summary
In chronic kidney disease (CKD), polyunsaturated fatty acids (PUFA) interact with Fibroblast Growth Factor 23 (FGF23) and inflammation. Monocyte chemoattractant protein 1 (MCP1) appears to drive changes in this relationship as kidney function declines.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Nutritional Science
Background:
- Fibroblast Growth Factor 23 (FGF23) levels increase in chronic kidney disease (CKD), correlating with inflammation and cardiovascular disease (CVD) risk.
- Omega-6 (n-6) and n-3 polyunsaturated fatty acids (PUFA) differentially modulate inflammation and cardiovascular risk.
Purpose of the Study:
- To investigate the relationship between PUFA, FGF23, and inflammation in CKD patients.
- To explore how these factors change across different stages of CKD.
Main Methods:
- Cross-sectional study of 56 CKD patients.
- Quantification of Monocyte Chemoattractant Protein 1 (MCP1), intact FGF23 (iFGF23), and C-terminal FGF23 (cFGF23) using ELISA.
- Gas chromatography analysis of fatty acid (FA) profiles.
Main Results:
- A decrease in estimated glomerular filtration rate (eGFR) was associated with an increase in MCP1.
- The correlation between FGF23 and the n-6/n-3 PUFA ratio inverted from stage 3 to stage 5 CKD.
- MCP1 increase appeared to mediate the inversion of the FGF23 and n-6/n-3 PUFA correlation.
Conclusions:
- Inflammation, indicated by MCP1, plays a role in the altered relationship between FGF23 and PUFA in advanced CKD.
- Findings support further research into therapeutic strategies targeting these pathways in CKD and post-transplant patients.
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