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Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 1194523
Author(s) Bigler, Cornelia; Hopfer, Helmut; Danner, Doris; Schaller, Monica; Mihatsch, Michael J; Trendelenburg, Marten
Author(s) at UniBasel Mihatsch, Michael J.
Trendelenburg, Marten
Year 2011
Title Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis
Journal Nephrology, dialysis, transplantation
Volume 26
Number 4
Pages / Article-Number 1220-8
Keywords autoantibodies, complement, lupus nephritis
Abstract BACKGROUND: In systemic lupus erythematosus patients, a strong association between the occurrence of antibodies against complement C1q (anti-C1q) and lupus nephritis can be observed. However, the predictive value of anti-C1q titres for a renal flare remains to be determined. Increasing titres of anti-C1q before the occurrence of clinical apparent nephritis might not only serve as a clinical parameter but also indicate a direct pathogenic mechanism of anti-C1q. METHODS: The aim of this study was to analyse the occurrence of anti-C1q before the onset of experimental lupus nephritis in MRL/MpJ +/+ mice and to correlate anti-C1q titres with the type and severity of glomerulonephritis (GN) developing at advanced age. RESULTS: As judged by a number of morphological and immunological analyses, GN in MRL/MpJ +/+ mice resembled human lupus nephritis and occurred in variable degrees of severity. We also observed an abundant and early presence of anti-C1q. However, anti-C1q neither correlated with overall survival nor with any histological marker of severity of GN. CONCLUSIONS: The absence of a correlation between the presence of anti-C1q and the occurrence of experimental lupus nephritis contradicts the hypothesis that anti-C1q are pathogenic. However, different pathogenic mechanisms of experimental lupus nephritis and human proliferative lupus nephritis cannot be excluded.
Publisher Oxford University Press
ISSN/ISBN 0931-0509
edoc-URL http://edoc.unibas.ch/dok/A6004737
Full Text on edoc No
Digital Object Identifier DOI 10.1093/ndt/gfq558
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/20841491
ISI-Number WOS:000289309400017
Document type (ISI) Journal Article
 
   

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