- Title
- Causal association pathways between fetuin-A and kidney function: a mediation analysis
- Creator
- Bassey, Philip Etabee; Numthavaj, Pawin; Rattanasiri, Sasivimol; Sritara, Piyamitr; McEvoy, Mark; Ongphiphadhanakul, Boonsong; Thakkinstian, Ammarin
- Relation
- Journal of International Medical Research Vol. 50, Issue 4, p. 1-13
- Publisher Link
- http://dx.doi.org/10.1177/03000605221082874
- Publisher
- Sage
- Resource Type
- journal article
- Date
- 2022
- Description
- 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 fetuinA 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.
- Subject
- Fetuin-A,; renal function; mediation analysis; causal effect; chronic kidney disease
- Identifier
- http://hdl.handle.net/1959.13/1479449
- Identifier
- uon:50306
- Identifier
- ISSN:0300-0605
- Rights
- © The Author(s) 2022. Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
- Language
- eng
- Full Text
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