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NDT Advance Access originally published online on June 2, 2007
Nephrology Dialysis Transplantation 2007 22(11):3191-3195; doi:10.1093/ndt/gfm346
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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


Demonstration of secretory IgA in kidneys of patients with IgA nephropathy

Beatrijs D. Oortwijn1, Maria Pia Rastaldi3, Anja Roos1,2, Deborah Mattinzoli3, Mohamed R. Daha1 and Cees van Kooten1

1Department of Nephrology and 2Department of Clinical Chemistry, Leiden University Medical Center, Leiden, The Netherlands and 3Renal Immunopathology Laboratory. Fondazione D’Amico per la Ricerca sulle Malattie Renali, Associazione Nuova Nefrologia, c/o San Carlo Borromeo Hospital, Milano, Italy

Correspondence and offprint requests to: Cees van Kooten, LUMC, Department of Nephrology, C3-P, Albinusdreef 2 2333 ZA Leiden, The Netherlands. Email: kooten{at}lumc.nl



  Abstract

Background. Recently we reported a possible role for secretory IgA (SIgA) in IgA nephropathy (IgAN), as suggested by increased serum levels in patients with active disease and accumulation of SIgA in a glomerular eluate. Therefore, we attempted to find support for these findings by analysis of the presence of SIgA in biopsies of IgAN patients.

Methods. Renal biopsies of 26 patients with biopsy-proven IgAN were analysed for the presence of SIgA and complement proteins.

Results. In 15% mesangial deposition of SIgA was demonstrated, using a specific staining for secretory component (SC) and colocalization with IgA. The presence of SIgA in these biopsies showed a strong correlation with deposition of mannose-binding lectin (MBL) and C4d. Moreover, we observed a strong colocalization between SIgA and MBL or C4d. This local complement activation has previously been linked to more severe renal disease.

Conclusions. Therefore, these data provide additional evidence for a pathogenic role for SIgA in IgA nephropathy.

Keywords: IgA nephropathy; IgA; SIgA; MBL; C4d

Received for publication: 24.12.06
Accepted in revised form: 4. 5.07


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