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NDT Advance Access originally published online on July 22, 2006
Nephrology Dialysis Transplantation 2006 21(10):2718-2720; doi:10.1093/ndt/gfl317
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

C-reactive protein—does it promote vascular disease?*

Peter Stenvinkel

Division of Renal Medicine, Department of Clinical Science Intervention and Technology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden

Correspondence and offprint requests to: Peter Stenvinkel, MD, PhD, Department of Renal Medicine K56, Karolinska Institutet, Karolinska University Hospital at Huddinge.Email: peter.stenvinkel@ki.se

Keywords: atherosclerosis; chronic kidney disease; CRP; genetics; interleukin-6

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Although some in vitro data support a direct role for C-reactive protein (CRP) in atherogenesis, there is as yet no definite evidence that CRP per se mediates atherogenesis in vivo. Whereas a recent study demonstrates that a specific binder of human CRP has cardioprotective effects in rats, studies in non-renal patients, using the Mendelian approach, suggest that CRP is not a suitable target for direct intervention. Thus, additional studies evaluating genotype (or haplotype) and vascular events are needed to clarify whether the link between elevated CRP and vascular events in numerous observational studies of chronic kidney disease (CKD) patients is causal or confounded. The availability of a specific CRP binder may be yet another tool to determine whether CRP contributes directly to atherogenesis in humans or if this protein is just an . . . [Full Text of this Article]


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