Cystatin C—A marker of peripheral atherosclerotic disease?

Arpegård, J.; Östergren, J.; de Faire, U.; Hansson, L.-O.; Svensson, P.

doi:10.1016/j.atherosclerosis.2007.11.025

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Volume 199, Issue 2 , Pages 397-401, August 2008

Cystatin C—A marker of peripheral atherosclerotic disease?

J. Arpegård
- Department of Medicine, Division of Emergency Medicine, Karolinska University Hospital-Solna, Stockholm, Sweden
J. Östergren
- Department of Medicine, Division of Emergency Medicine, Karolinska University Hospital-Solna, Stockholm, Sweden
U. de Faire
- Department of Cardiology, Karolinska Institute Stockholm, Sweden
- Karolinska University Hospital-Solna, Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institute Stockholm, Sweden
L.-O. Hansson
- Department of Clinical Chemistry Akademiska University Hospital, Uppsala, Sweden
P. Svensson
- Department of Medicine, Division of Emergency Medicine, Karolinska University Hospital-Solna, Stockholm, Sweden
- Corresponding author at: Department of Emergency Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden. Tel.: +46 851775543; fax: +46 851775855.

Received 28 August 2007; received in revised form 24 October 2007; accepted 15 November 2007. published online 10 January 2008.

Abstract

It has been suggested that Cystatin C, besides its function as a marker of glomerular filtration, could be an independent marker of cardiovascular disease. However, studies on this topic are few and results have been indecisive. Our aim was to further investigate the subject of Cystatin C as an independent marker of peripheral atherosclerotic disease.

Method

Blood samples were analysed for serum Cystatin C, IL6, CRP and creatinine in 103 males with peripheral arterial disease (PAD) and 96 controls matched for age and sex. Creatinine clearance (CCr) was calculated according to Cockcroft's formula and estimated glomerular filtration rate (eGFR) was calculated according to MDRD formula.

Results

Cystatin C-concentration was higher in PAD-patients compared to controls; 1.09±0.40 vs. 0.95±0.17mg/L (p<0.01). There was no difference in CCr; 81±27 vs. 82±22mL/min or eGFR; 76±21 vs. 79±14mL/min. Cystatin C correlated to CCr, logIL-6 and logCRP in both patients (r=−0.60, p<0.001), (r=0.35, p<0.001) and (r=0.30, p<0.01) and controls (−0.44, p<0.001), (0.38, p<0.001) and (r=0.32, p<0.01), respectively. In an analysis of covariance, corrected for difference in eGFR, Cystatin C remained higher in PAD-patients compared to controls; 1.09 (C.I. 1.04–1.14) vs. 0.96 (C.I. 0.90–1.01).

Conclusion

Cystatin C-concentration, corrected for differences in eGFR, IL-6 and CRP values, is higher in PAD-patients compared to controls. Our finding suggests that Cystatin C may be an independent marker of atherosclerotic disease apart from its relation to kidney function.

Keywords: Peripheral vascular disease, Kidney, Inflammation, Atherosclerosis