NDT Advance Access originally published online on October 3, 2007
Nephrology Dialysis Transplantation 2008 23(1):7-10; doi:10.1093/ndt/gfm680
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Circulating endothelial cells in renal disease: markers and mediators of vascular damage
1Renal Unit, Lancashire Teaching Hospitals NHS Foundation Trust, Preston, Lancashire, UK and 2Division of Nephrology, Department of Medicine, Hannover Medical School, Hannover, Germany
Correspondence and offprint requests to: Alexander Woywodt, FASN, Consultant Renal Physician, Honorary Senior Lecturer, Renal Unit, Lancashire Teaching Hospitals NHS Trust, Royal Preston Hospital, Sharoe Green Lane, Preston, PR2 9HT, UK. Tel: +0044-1772524629; Fax: +0044-1772522162; E-mail: Alex.Woywodt@lthtr.nhs.uk
Keywords: circulating endothelial cells; endothelium; interactions; pathogenesis; vascular damage
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Introduction |
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During the last decade, circulating endothelial cells (CECs) have been used as a surrogate marker of endothelial damage in a variety of vascular disorders. The severely damaged phenotype of CECs in vasculitis led to the hypothesis that such circulating apoptotic and/or necrotic debris may itself be a mediator of disease. Very recently, first evidence has emerged to support this assumption [1]. The aim of this editorial comment is to provide a brief review of CECs, describe clinical applications with an emphasis on renal disease, and put the new pathogenetic findings into perspective. We also suggest further avenues of research.
CECs: promise and problems
The concept of circulating endothelial cells is not new. These cells were first described almost 40 years ago [2], although identification of these cells by light microscopy was rather primitive from today's point of view. Some studies on cardiovascular diseases followed until the next milestone in methodology,
CECs in renal disease
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Circulating endothelial cells as mediators of disease |
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Conclusion |
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