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NDT Advance Access originally published online on March 19, 2007
Nephrology Dialysis Transplantation 2007 22(6):1518-1520; doi:10.1093/ndt/gfm003
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Mutant mice provide new insight into the role of (mis-)glycation in IgA nephropathy and other glomerular diseases*

Jürgen Floege1, Frank Eitner1, Jonathan Barratt2, Alice C Smith2 and John Feehally2

1Department of Nephrology and Clinical Immunology, RWTH University Hospital Aachen, Germany and 2Department of Nephrology, Leicester General Hospital, Leicester,UK

Correspondence and offprint requests to: Jürgen Floege, MD, Department of Nephrology and Clinical Immunology, University Hospital Aachen, Pauwelsstr. 30, D-52057 Aachen. Germany. Email: juergen.floege@rwth-aachen.de

Keywords: aminopeptidase N; glomerular; glomerulonephritis; glycosylation; IgA; podocalyxin

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

In the 24 October 2006 issue of PNAS, Alexander and colleagues [1] describe the results of a systematic search for thrombocytopenic mice generated by large-scale mutagenesis. Amongst 3523 mice, one pedigree indeed exhibited ~50% reduction in platelet counts. Apart from thrombocytopenia, the only other notable feature of these mice was prominent renal disease (albuminuria/proteinuria, glomerulosclerosis and tubulointerstitial inflammatory infiltration) leading to uraemia and death at around 200 days after birth. This renal disease was not immune mediated, since it persisted in mutant mice crossed to . . . [Full Text of this Article]



   Core1-ß1,3-galactosyltransferase and IgA nephropathy
 


   What are the potential clinical implications%
 


   Take-home-message
 

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