Skip Navigation


NDT Advance Access originally published online on May 3, 2007
Nephrology Dialysis Transplantation 2007 22(7):1840-1848; doi:10.1093/ndt/gfm205
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
22/7/1840    most recent
gfm205v1
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 arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Barsoum, R. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barsoum, R. S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Hepatitis C virus: from entry to renal injury—facts and potentials

Rashad S. Barsoum

Kasr-El-Aini Medical School, Cairo University, Egypt, Cairo, Egypt

Correspondence and offprint requests to: Rashad Barsoum, Cairo Kidney Center, POB 91 Bab-El-Louk, Cairo, 11513, Egypt. Email: Rashad.barsoum@gmail.com

Keywords: amyloidosis; glomerulonephritis; HCV; transplantation; vasculitis; viral nephropathy

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



   Introduction
 
In 1993, only 4 years after the discovery of HCV, three independent groups in Japan, Italy and the US reported the detection of relevant viral markers of infection in patients with Type I membranoproliferative glomerulonephritis. About half of those patients had circulating cryoglobulins, which were blamed in the pathogenesis of kidney disease. These observations were subsequently confirmed by hundreds of studies all over the world, thereby revealing that the majority of patients with type II mixed essential cryoglobulinaemia were, indeed, victims of HCV infection. The spectrum of renal pathology associated with this infection subsequently expanded to include many patterns in native as well as transplanted kidneys (Table 1, Figure 1) [1–12].


View this table:



  		Table 1. Renal lesions associated with HCV infection

 

Figure Removed (Available Only in the Full Text)
View larger version (123K):



  		Fig. 1. Histopathological lesions associated with HCV infection. (A) Cryoglobulinaemic membranoproliferative glomerulonephritis; (A1) H&E stain showing mesangial proliferation and matrix expansion with capillary thrombi (arrows); . . . [Full Text of this Article]

 


   The virus
 


   Infectivity
 


   Pathogenicity
 
Cytopathic effects
Immune response
Innate immune response
Adaptive response


   Mechanisms of renal injury in HCV disease
 
Cryoglobulins
Immune complexes
Endothelial injury
Podocyte injury
Mesangial inflammation
Amyloid deposition
Tubular injury


   Conclusion
 

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