Skip Navigation

This Article
Right arrow Full Text (PDF)
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 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 Montinaro, V.
Right arrow Articles by Rifai, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Montinaro, V.
Right arrow Articles by Rifai, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (1995) 10: 2035-2042
© 1995 European Renal Association-European Dialysis and Transplant Association

research-article

Evolution of renal injury in a chronic model of IgA immune-complex-associated nephropathy

V. Montinaro1,, L. Aventaggiato2, T. Cavallo2 and A. Rifai2

1Institute of Nephrology, University of Bari Italy 2Department of Pathology, Rhode Island Hospital and Brown University Providence, RI, USA

Correspondence and offprint requests to: Correspondence and offprint requests to: Dr Vincenzo Montinaro, Institute of Nephrology, University of Bari, Polyclinic, Piazza G. Cesare, 11, 70124 Bari, Italy

BACKGROUND.: IgA nephropathy (IgAN) is characterized by intense and diffuse IgA mesangial deposits, a variety of histopathological changes and unpredictable clinical course. To elucidate the cause of the discrepancy between the unvariable IgA deposition and the histological picture, we examined the short- and long-term influence of glomerular IgA immune complexes (IgA-IC) on the progression of renal lesions in experimental IgAN.

METHODS.: IgA-IC renal deposits were induced by sequential administration of IgA anti-phosphorylcholine and pneumococcal C polysaccharide. Mice treated every other day by three injections (groups A) or nine injections (groups B) were sacrificed 24 h and 1, 4, or 8 weeks (groups 1–4) after cessation of treatment.

RESULTS.: Group A1 showed segmental glomerular necrosis and thrombosis. Lesions then converted to segmental mesangial proliferation (A2), more pronounced in A3 and minimal in A4. Group B1 showed severe proliferative glomerulonephritis and segmental necrosis. The pattern altered to mesangial expansion with glomerular/interstitial infiltration in B2, milder features in B3 and residual mesangial proliferation in B4. Proteinuria increased progressively during treatment reaching its maximum in group B1, but it returned to near normal levels in group B4. The development of proteinuria paralleled glomerular/interstitial T cell infiltration.

CONCLUSIONS.: These findings demonstrate that renal histopathological alterations observed in experimental IgA nephropathy are sustainable only by continuous deposition of nephritogenic IgA-IC.

Keywords: antigen; glomerulonephritis; IgA; T cells


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




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.