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NDT Advance Access originally published online on November 15, 2005
Nephrology Dialysis Transplantation 2006 21(1):33-35; doi:10.1093/ndt/gfi270
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Translational Nephrology

Calcification and the usual suspect phosphate: still guilty but there are other guys behind the scenes

Markus Ketteler and Jürgen Floege

Division of Nephrology, RWTH University Hospital Aachen, Germany

Correspondence and offprint requests to: M. Kettler. Email: mketteler@ukaachen.de

The first 10% of the full text of this article appears below.

In patients with renal failure, the high prevalence of vascular, valvular and soft-tissue calcifications and their consequences for cardiovascular outcomes have recently received much attention. Several studies documented that the calcification burden is associated with increased morbidity and mortality in uraemia. In vitro and in vivo research has demonstrated that tissue calcification is not just based on passive calcium and phosphate precipitation, but that active cellular processes such as osteogenic differentiation of vascular smooth muscle cells (VSMC) are involved and that a number of local and systemic calcium-regulatory factors control and prevent unwanted extra-osseous calcification. An important finding was the new understanding that calcium and phosphate are immediate inducers of osteogenic . . . [Full Text of this Article]


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