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Cystatin C is associated with risk of venous thromboembolism in subjects with normal kidney function--the Tromsø
Ellen E Brodin1, Sigrid K Brækkan, Anders Vik
1Hematological Research Group (HERG), Department of Clinical Medicine, University of Tromsø, N-9037 Tromsø, Norway. ellen.brodin@uit.no
Insights
Serum cystatin C levels predict venous thromboembolism risk, even in individuals with normal kidney function. Higher cystatin C indicates a significantly increased risk of developing blood clots.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Thrombosis Research
Background:
- Previous research linked impaired kidney function (eGFR) to venous thromboembolism (VTE).
- Serum cystatin C is a marker for kidney function, but its independent association with VTE is less understood.
Purpose of the Study:
- To investigate the association between serum cystatin C and VTE risk in individuals with normal kidney function.
- To determine if cystatin C predicts VTE independently of kidney function.
Main Methods:
- Prospective population-based study of 3251 adults (25-84 years) with normal kidney function (eGFR > 90 mL/min/1.73 m²).
- Serum cystatin C levels measured; VTE events prospectively registered until September 1, 2007.
- Cox-regression models used to calculate hazard ratios (HR) and 95% confidence intervals (CI).
Main Results:
- A 1 SD increase in serum cystatin C correlated with a 43% increased VTE risk (HR 1.43; 95% CI 1.17-1.72).
- Top quartile of cystatin C showed a 2.5-fold higher VTE risk (HR 2.51; 95% CI 1.27-4.96) versus the bottom quartile.
- Risk was notably higher for provoked VTE (HR 3.11; 95% CI 1.23-7.86).
Conclusions:
- Elevated serum cystatin C is associated with increased VTE risk in individuals with normal kidney function.
- Findings suggest cystatin C may be a direct risk factor for venous thrombosis, not solely a marker of kidney impairment.
Background:
Previous studies have shown an association between impaired kidney function, assessed by cystatin C-based estimated glomerular filtration rate, and venous thromboembolism. The aim of this study was to investigate whether serum cystatin C was associated with a risk of venous thromboembolism among subjects with normal kidney function in a prospective population-based study.
Design And Methods:
Cystatin C was measured in serum from 3251 men and women with normal kidney function, aged 25-84 years, who participated in the Tromsø study in 1994-1995. Normal kidney function was defined as a creatinine-based estimated glomerular filtration rate greater than 90 mL/min/1.73 m(2) and absence of microalbuminuria. Incident venous thromboembolism was registered from the date of inclusion through to the end of follow-up, September 1, 2007. Cox-regression models were used to calculate hazard ratios with 95% confidence intervals for venous thromboembolism.
Results:
There were 83 incident venous thromboembolic events, of which 53 (63.9 %) were provoked, during a median of 12.3 years of follow-up. A one standard deviation (0.11 mg/L) increase in serum cystatin C levels was associated with a 43% (hazard ratio 1.43; 95% confidence interval 1.17-1.72) increased risk of total venous thromboembolism. Subjects with cystatin C levels in the top quartile (≥ 0.87 mg/L) had a 2.5-fold (hazard ratio 2.51; 95% confidence interval 1.27-4.96) increased risk of venous thromboembolism compared to those with levels in the bottom quartile (≤ 0.72 mg/L) in adjusted analysis. The risk estimates were even higher for provoked venous thromboembolism (hazard ratio 3.11; 95% confidence interval 1.23-7.86).
Conclusions:
Serum cystatin C levels were associated with the risk of venous thromboembolism in subjects with normal kidney function. Our findings suggest that elevated serum cystatin C levels may promote venous thrombosis beyond reflecting impaired kidney function.
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