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Updated: Jun 13, 2026

Transdermal Measurement of Glomerular Filtration Rate in Mice
Published on: October 21, 2018
Serum C-reactive protein and thioredoxin levels in subjects with mildly reduced glomerular filtration rate
Shoko Tsuchikura1, Tetsuo Shoji, Naoko Shimomura
1Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.
Insights
Mildly reduced kidney function is linked to higher inflammation and oxidative stress markers. These changes may be influenced by blood pressure and lipid levels in individuals with early-stage chronic kidney disease.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Biochemistry
Background:
- Chronic kidney disease (CKD) is a significant risk factor for cardiovascular disease (CVD).
- Previous research focused on inflammation and oxidative stress in advanced CKD stages.
- This study investigates these markers in early-stage CKD with mildly reduced kidney function.
Purpose of the Study:
- To compare serum biomarker levels for inflammation and oxidative stress between individuals with normal and mildly reduced estimated glomerular filtration rate (eGFR).
- To explore the relationship between eGFR and these biomarkers in early CKD.
Main Methods:
- 182 health check-up participants were analyzed, categorized by eGFR (normal ≥90 mL/min/1.73 m2, mildly reduced 60-89 mL/min/1.73 m2).
- Individuals with eGFR <60 mL/min/1.73 m2 and proteinuria were excluded.
- Serum levels of C-reactive protein (CRP) and thioredoxin (TRX) were measured as markers of inflammation and oxidative stress, respectively.
Main Results:
- Subjects with mildly reduced eGFR exhibited elevated serum CRP and TRX levels compared to those with normal eGFR.
- A significant inverse correlation was observed between eGFR and both CRP and TRX levels.
- These associations remained significant after adjusting for age and sex, with further adjustments revealing links between CRP, blood pressure, and lipids, and TRX with sex and blood pressure.
Conclusions:
- Mildly reduced eGFR is associated with increased levels of inflammation (CRP) and oxidative stress (TRX).
- The relationship between eGFR and these biomarkers is partly mediated by changes in blood pressure and plasma lipids.
- These findings highlight the early systemic impact of declining kidney function on cardiovascular risk markers.
Background:
Chronic kidney disease (CKD) is a newly recognized high-risk condition for cardiovascular disease (CVD), and previous studies reported the changes in inflammation and oxidative stress in advanced stages of CKD. We compared the levels of serum biomarkers for inflammation and oxidative stress between subjects with normal and mildly reduced glomerular filtration rate (GFR).
Methods:
The subjects were 182 participants of a health check-up program including those with normal (>or= 90 mL/min/1.73 m2, N = 79) and mildly reduced eGFR (60-89 mL/min/1.73 m2, N = 103) which was calculated based on serum creatinine, age and sex. We excluded those with reduced eGFR < 60 mL/min/1.73 m2. No one had proteinuria. We measured serum levels of C-reactive protein (CRP) and thioredoxin (TRX) as the markers of inflammation and oxidative stress, respectively.
Results:
As compared with subjects with normal eGFR, those with mildly reduced eGFR had increased levels of both CRP and TRX. Also, eGFR was inversely correlated with these biomarkers. The associations of eGFR with these biomarkers remained significant after adjustment for age and sex. When adjustment was done for eight possible confounders, CRP showed significant association with systolic blood pressure, high density lipoprotein cholesterol (HDL-C) and non-HDL-C, whereas TRX was associated with sex significantly, and with eGFR and systolic blood pressure at borderline significance.
Conclusions:
We showed the increased levels of CRP and TRX in subjects with mildly reduced eGFR. The eGFR-CRP link and the eGFR-TRX link appeared to be mediated, at least partly, by the alterations in blood pressure and plasma lipids in these subjects.
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