Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (10)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Drüeke, T. B.
Right arrow Articles by Rostand, S. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Drüeke, T. B.
Right arrow Articles by Rostand, S. G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2002) 17: 1365-1368
© 2002 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Progression of vascular calcification in uraemic patients: can it be stopped?

Tilman B. Drüeke1, and Stephen G. Rostand2

1 Inserm U507 and Service de Néphrologie, Hôpital Necker, Paris, France and 2 Division of Nephrology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA

The first 150 words of the full text of this article appear below.

Introduction

Patients with advanced renal failure may develop several types of soft tissue calcification, including visceral, articular and vascular calcification. Among the latter, the most dramatic form is calciphylaxis, also called ‘calcific uraemic arteriolopathy’, which generally has an acute course and may be rapidly lethal. In general, more slowly progressive forms prevail which are characterized by either focal, patchy deposits of calcium and phosphate in atheromatous plaques, or by diffuse deposits in the medial layer of the arterial tree. Frequently, the two forms are combined.

Pathogenetic mechanisms

Disturbances of calcium and phosphate metabolism have been shown to play a major role in the pathogenesis of arterial calcification of either type, in association with either hyperparathyroidism or hypoparathyroidism and with vitamin D overload [1,2]. Atheromatous plaques of uraemic patients are more frequently and more intensively calcified than those of non-uraemic subjects [3]. The most marked difference compared with . . . [Full Text of this Article]

Beyond phosphate control: arrest of progressive vascular calcification?

Open questions

Future directions


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
M. S. Razzaque, R. St-Arnaud, T. Taguchi, and B. Lanske
FGF-23, vitamin D and calcification: the unholy triad
Nephrol. Dial. Transplant., October 1, 2005; 20(10): 2032 - 2035.
[Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
M. K. Sigrist, L. Devlin, M. W. Taal, R. J. Fluck, and C. W. McIntyre
Length of interdialytic interval influences serum calcium and phosphorus concentrations
Nephrol. Dial. Transplant., August 1, 2005; 20(8): 1643 - 1646.
[Abstract] [Full Text] [PDF]