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NDT Advance Access originally published online on January 23, 2006
Nephrology Dialysis Transplantation 2006 21(4):865-868; doi:10.1093/ndt/gfk039
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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

Editorial Review

Does obesity play a role in the pathogenesis of calcific uraemic arteriolopathy?

David T. Janigan1 and David J. Hirsch2

1 Departments of Pathology and Laboratory Medicine, Queen Elizabeth II Health Sciences Centre and 2 Dalhousie University School of Medicine, Halifax, Nova Scotia, Canada

Correspondence and offprint requests to: Dr David Hirsch, Dickson 5081, 5820 University Ave, QEII Health Sciences Centre, Halifax, Nova Scotia B3H 1V8, Canada. Email: David.Hirsch@cdha.nshealth.ca

Keywords: uraemia; calciphylaxis; obesity

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



   Introduction
 
Calcific uremic arteriolopathy (CUA) [1] refers to calcification of the media of small terminal arteries and arterioles and associated fibrotic intimal thickening and lumen narrowing, thereby increasing the risk of ischaemic necrosis. As the term suggests, CUA is reported in patients with chronic kidney disease (CKD) ‘nearly exclusively’ [2]. Identical clinical and pathologic features have developed with hyperphosphataemia from other causes [3–7].

CUA develops silently [1,5,8], sometime presenting only with subcutaneous plaques and/or nodules. But with ischaemic complications it presents acutely with foci with discoloured skin progressing to necrosis and deep ulcers; hereafter designated . . . [Full Text of this Article]



   The association of proximal lesions with obesity
 


   Relevance of the calcified septal–arteriolar tandem
 


   Subcutaneous plaques and nodules in CUA
 


   Limitations of the hypothesis
 


   Conclusion
 

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