NDT Advance Access published online on November 26, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm801
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© 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
After Several Years of Witchhunting: Can Calcium-Based Phosphate Binding be Released on Probation?
Department of Nephrology, Klinikum Coburg, Coburg, Germany
Correspondence and offprint requests to: Prof. Markus Ketteler, III. Medizinische Klinik (Nephrologie), Klinikum Coburg, Ketschendorfer Str. 33, 96450 Coburg, Germany. Tel: +49-9561-249611; Fax: +49-9561-249612; E-mail: markus.ketteler@klinikum-coburg.de
Keywords: atherosclerosis; calcification; calcium; phosphate; sevelamer
| The first 10% of the full text of this article appears below. |
| Introduction |
|---|
The experimental model of uraemic ApoE-deficient mice has become increasingly used to investigate treatment options in the setting of chronic renal failure (CRF) created by 5/6-nephrectomy or other surgical methods, in combination with severe atherosclerotic plaque disease. Although the pathologic changes associated with this model are not immediately comparable to the development of CRF and atherosclerosis in humans, the phenotypic features of both vascular damage and biochemical abnormalities appear quite similar to what is observed in patients with progressive chronic kidney disease (CKD).
Phosphate binders and experimental atherosclerosis
In 2005, Phan et al. first published a study demonstrating that the phosphate binder sevelamer ameliorated not only vascular calcification, but also plaque progression in uraemic ApoE-deficient mice [1]. In addition to effective phosphate
Calcium-based phosphate binding: effective and an innocent bystander?
From bench to bedside: the good and the bad news
Support from clinical studies: calcium and calcification progression in pre-dialysis patients
What do we learn?
![]()
CiteULike
Connotea
Del.icio.us What's this?