Skip Navigation


NDT Advance Access originally published online on June 8, 2006
Nephrology Dialysis Transplantation 2006 21(8):2057-2060; doi:10.1093/ndt/gfl281
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
21/8/2057    most recent
gfl281v1
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 (2)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kotanko, P.
Right arrow Articles by Levin, N. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kotanko, P.
Right arrow Articles by Levin, N. W.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 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 Comment

Intestinal bacterial microflora—a potential source of chronic inflammation in patients with chronic kidney disease

Peter Kotanko, Mary Carter and Nathan W. Levin

Renal Research Institute, New York, NY, USA

Correspondence and offprint requests to: Nathan W. Levin, Renal Research Institute, 207 East 94th Street, Suite 303, New York, NY 10128, USA. Email: nlevin@rriny.com

Keywords: bacterial translocation; chronic inflammation; chronic kidney disease; gut; intestinal microflora

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



   Introduction
 
Inflammation is prevalent in a large proportion of dialysis patients, irrespective of the dialysis modality used. Central catheters, periodontal disease, exposure to endotoxins from non-ultrapure water dialysis and persistent chronic infections are well-established causes of chronic inflammation, but many infections go unrecognized [1].

Despite the fact that 10–100 trillion microorganisms populate the intestine in adult humans, the gastrointestinal tract has received little attention as a possible source contributing to the chronic inflammation noted in dialysis patients.

The mucosal surface is the physical interface of the immune system with the outside world, encompassing an extensive surface area of 300–400 m2, which constitutes the largest body interface between the host and microorganisms. The intestinal barrier is composed of different domains [2], the ecological barrier (the normal intestinal microflora), the mechanical barrier (single layer of polarized intestinal epithelial cells, the enterocytes, covered by mucus) and the . . . [Full Text of this Article]



   Bacterial translocation
 


   Intestinal microflora, intestinal barrier function and bacterial translocation in uraemia
 
Oral iron—a potential stimulus for intestinal bacterial growth


   Strategies to decrease intestinal permeability and bacterial translocation
 


   Conclusion
 

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