European Heart Journal Advance Access originally published online on January 19, 2009
European Heart Journal 2009 30(3):314-320; doi:10.1093/eurheartj/ehn598
Cystatin C and cardiovascular mortality in patients with coronary artery disease and normal or mildly reduced kidney function: results from the AtheroGene study
1 Department of Medicine II, Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131 Mainz, Germany
2 Institute of Medical Biostatistics, Epidemiology, and Informatics, Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131 Mainz, Germany
3 INSERM, UMR S 525, Paris F-75634, France
4 Université Pierre et Marie Curie-Paris 6, UMR S 525, Paris F-75634, France
5 Department of Medicine II, GPR Klinikum Rüsselsheim, Germany
6 Innere Abteilung, Bundeswehrzentralkrankenhaus Koblenz, Germany
7 Institute of Clinical Chemistry and Laboratory Medicine, Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131 Mainz, Germany
Received 21 April 2008; revised 19 November 2008; accepted 17 December 2008; online publish-ahead-of-print 19 January 2009.
* Corresponding author. Tel: +49 6131 175992, Fax: +49 6131 175691, Email: schnabelr{at}gmx.de
Aims: Chronic kidney disease is associated with increased risk of cardiovascular disease. Cystatin C is a promising marker to reliably mirror renal function. The role of cystatin C in patients with coronary artery disease (CAD) and normal or mildly reduced kidney function is the subject of current investigation.
Methods and results: In 2162 patients, over the whole spectrum of CAD, baseline cystatin C concentrations were measured. Patients with an estimated glomerular filtration rate of 
60 mL/min per 1.73 m2 (n = 295) were excluded. In patients with complete follow-up information (n = 1827), 66 cardiovascular deaths were registered during a median follow-up of 3.65 years. Logarithmically transformed, standardized cystatin C was associated with cardiovascular death [hazard ratio: 1.94, 95% confidence interval (CI): 1.59–2.37, P < 0.001]. A potential threshold effect was observed; patients in the upper quartile had a 3.87-fold (95% CI: 2.33–6.42; P < 0.001) risk of mortality compared with the pooled lower quartiles. This risk association remained robust after adjustment for potential confounders including classical risk factors and N-terminal pro B-type natriuretic peptide. Serum creatinine was not associated with the outcome in this group of patients with normal renal function.
Conclusion: Results of this prospective study show that cystatin C is a potent predictor of cardiovascular mortality beyond classical risk factors in patients with CAD and normal or mildly reduced kidney function.
Key Words: Cystatin C • Risk stratification • Coronary artery disease • Cardiovascular mortality
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