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NDT Advance Access published online on April 10, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn155
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Bacterial protease for the treatment of IgA nephropathy*

Frank Eitner and Jürgen Floege

Division of Nephrology and Immunology, Rheinisch-Westfälische Technische Hochschule Aachen, Aachen, Germany

Correspondence and offprint requests to: Prof. Frank Eitner, Klinikum der RWTH Aachen, Medizinische Klinik II (Nephrologie und Immunologie), Pauwelsstr 30, 52074 Aachen, Germany. Tel: +49-0-241-8089-532; Fax: +49-0-241-8082-446; E-mail: feitner@ukaachen.de

Keywords: glomerulonephritis; Haemophilus influenzae; IgA nephropathy; IgA protease

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

Mesangial IgA1 deposition accompanied by a mesangioproliferative glomerulonephritis is the key pathological finding in IgA nephropathy (IgAN) patients [1–3]. Although the pathogenesis of IgAN is still not completely understood, it is generally accepted that mesangial IgA1 deposits trigger local inflammatory mechanisms and thereby initiate and/or maintain the glomerulonephritis [2,3]. Consequently, the specific removal of mesangial IgA1 deposits might be a promising therapeutic approach for IgAN. Lamm et al. studied a bacterial IgA protease, isolated from Haemophilus influenzae, which exhibits substrate specificity for the hinge region of human IgA1. This protease cleaved human IgA1 and IgA1-containing immune complexes in vitro. They next studied the . . . [Full Text of this Article]


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