Open AccessCausal association pathways between fetuin-A and kidney function: a mediation analysis
Author(s) -
Philip Etabee Macdonald Bassey,
Pawin Numthavaj,
Sasivimol Rattanasiri,
Piyamitr Sritara,
Mark McEvoy,
Boonsong Ongphiphadhanakul,
Ammarin Thakkinstian
Publication year - 2022
Publication title -
journal of international medical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.421
H-Index - 57
eISSN - 1473-2300
pISSN - 0300-0605
DOI - 10.1177/03000605221082874
Subject(s) - medicine , mediation , association (psychology) , renal function , function (biology) , genetics , psychotherapist , psychology , political science , law , biology
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 m 2 in 2009 to 92.4 ± 22.9 mL/minute/1.73 m 2 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.