NDT Advance Access originally published online on September 27, 2006
Nephrology Dialysis Transplantation 2006 21(12):3354-3357; doi:10.1093/ndt/gfl446
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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
Beyond phosphaterole of uraemic toxins in cardiovascular calcification
1Inserm Unit 507 and Division of Nephrology, Necker Hospital, University Paris V, Paris and 2Inserm ERI-12, University of Picardie and Amiens University Hospital, Amiens, France
Correspondence and offprint requests to: Prof. Ziad Massy, MD, PhD, INSERM ERI-12, Division(s) of Clinical Pharmacology and Nephrology, Amiens University Hospital, Av. René Laennec, F-80054, Amiens, France. Email: massy@u-picardie.fr
Keywords: bone turnover; cardiovascular mortality; chronic kidney disease; uraemic toxins; vascular calcifications
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| Introduction |
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Vascular calcification (VC) is a hallmark of atherosclerosis and has been linked to increased cardiovascular disease and mortality. VC is highly prevalent in patients with chronic kidney disease (CKD), in whom it occurs more frequently and progresses more rapidly than in the general population [13]. In CKD patients, cardiovascular mortality increases exponentially with age and is up to 500 times higher than in the general population [4]. The presence of VC is independently predictive of subsequent cardiovascular disease and mortality, beyond established conventional risk factors [5, 6]. VC develops at two sites of the arterial wall: the intima and the media. The survival of CKD patients with arterial media calcification is longer than in patients with arterial intima calcification, whose survival in turn is significantly shorter than that of VC-free patients [7].
Metabolic disturbances in CKD involving calcium, phosphorus, parathyroid hormone
| Lessons from experimental studies in vitro and in vivo |
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| Role of uraemic toxicity |
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| Conclusion |
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