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Published on: March 17, 2010
Association between cystatin C and inflammation in patients with essential hypertension
Takafumi Okura1, Masanori Jotoku, Jun Irita
1Department of Integrated Medicine and Informatics, Ehime University Graduate School of Medicine, Toon, Ehime 791-0295, Japan. okura@m.ehime-u.ac.jp
Insights
Serum cystatin C is a marker for both kidney function and inflammation. It correlates with inflammatory markers like IL-6 and TNF-α, suggesting a link between renal health and cardiovascular risk.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Inflammation Research
Background:
- Serum cystatin C is a recognized marker for renal function.
- It is also an independent risk factor for cardiovascular damage, heart failure, and mortality.
- Cardiovascular events and renal dysfunction are linked to chronic inflammation.
Purpose of the Study:
- To investigate the relationship between serum cystatin C and proinflammatory cytokines.
- To explore cystatin C as a potential marker of inflammation in patients with essential hypertension.
Main Methods:
- Eighty-eight patients with essential hypertension were enrolled.
- Measurements included serum cystatin C, serum creatinine, and estimated glomerular filtration rate (eGFR).
- Proinflammatory cytokines (TNF-α, IL-6, CRP) were quantified.
Main Results:
- Serum cystatin C showed significant correlations with eGFR, systolic blood pressure, and pulse pressure.
- Cystatin C also correlated with interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α).
- Tumor necrosis factor-alpha, eGFR, and pulse pressure were identified as independent determinants of serum cystatin C.
Conclusions:
- Serum cystatin C serves as a marker for both renal function and inflammation.
- These findings highlight the interconnectedness of renal health, inflammation, and cardiovascular risk.
Background:
Serum cystatin C is not only a marker of renal function but also acts as an independent risk factor for cardiovascular damage, heart failure, and death. It is known that the initiation and progression of these cardiovascular events contributes to renal dysfunction and chronic inflammation. In this study, we investigated the relationship between cystatin C and proinflammatory cytokines.
Methods:
Eighty-eight patients with essential hypertension participated in the study, which involved measuring proinflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and C reactive protein (CRP).
Results:
Positive correlations were detected between cystatin C and estimated glomerular filtration rate (eGFR) (r = -0.503, p < 0.001), systolic blood pressure (r = -0.246, p = 0.034), and pulse pressure (r = -0.295, p = 0.010). In contrast, serum creatinine correlated only with eGFR (r = -0.755, p < 0.001) and eGFR correlated only with age (r = -0.339, p = 0.001) and not with the other clinical parameters, whereas cystatin C also correlated with log natural (ln) IL-6 (r = -0.247, p = 0.033) and ln TNF-α (r = -0.405, p < 0.001) but not with CRP (r = -0.188, p = 0.108). In contrast, plasma creatinine and eGFR did not correlate with any of these proinflammatory cytokines. Stepwise regression analysis showed that ln TNF-α, eGFR and pulse pressure were independent determinants of serum cystatin C concentration.
Conclusion:
This study showed that cystatin C is a marker of inflammation as well as renal function.
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