Causal association pathways between fetuin-A and kidney function: a mediation analysis
Issued Date
2022-04-01
Resource Type
ISSN
03000605
eISSN
14732300
Scopus ID
2-s2.0-85128434943
Pubmed ID
35435033
Journal Title
Journal of International Medical Research
Volume
50
Issue
4
Rights Holder(s)
SCOPUS
Bibliographic Citation
Journal of International Medical Research Vol.50 No.4 (2022)
Suggested Citation
Bassey P.E., Numthavaj P., Rattanasiri S., Sritara P., McEvoy M., Ongphiphadhanakul B., Thakkinstian A. Causal association pathways between fetuin-A and kidney function: a mediation analysis. Journal of International Medical Research Vol.50 No.4 (2022). doi:10.1177/03000605221082874 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/83772
Title
Causal association pathways between fetuin-A and kidney function: a mediation analysis
Other Contributor(s)
Abstract
Objective: Body mass index (BMI), uric acid, diabetes mellitus, and hypertension are risk factors for reduced kidney function and are associated with fetuin-A levels, but their causal pathways remain unclear. The objective of this study was to investigate this knowledge gap. Methods: A repeated cross-sectional design was used to assess causal pathway effects of fetuin-A on the estimated glomerular filtration rate (eGFR), which is mediated through BMI, uric acid, diabetes mellitus, and hypertension. Results: Among 2305 participants, the mean eGFR at baseline decreased from 98.7 ± 23.6 mL/minute/1.73 m2 in 2009 to 92.4 ± 22.9 mL/minute/1.73 m2 in 2014. Fetuin-A was significantly associated with eGFR, suggesting that increasing fetuin-A levels predict a decrease in eGFR. Additionally, the indirect effect of fetuin-A on eGFR, as assessed through BMI, was also significant. The effects of fetuin-A on eGFR through other mediation pathways showed variable results. Conclusions: Our study revealed a possible role of fetuin-A in the etiology of declining renal function through mediating body mass index, uric acid, diabetes mellitus, and hypertension via complex causal pathways. Further studies to clarify these mediated effects are recommended.