Occurrence of anti-C1q antibodies in IgA nephropathy

Background: The pathogenic mechanisms and the antigensinvolved in the establishment and progress of IgA nephropathy are unknown.As antibodies against C1q have been reported to correlate with SLEnephritis, we analysed the occurrence of these antibodies in IgAnephropathy in order to investigate the possibility of pathogeneticsimilarities in these renal disorders. Methods: Theoccurrence of IgA- and IgG anti-C1q antibodies (anti-C1q) were determinedby ELISA in patients with IgA nephropathy (n=36) and SLE nephritis (n=37),diseases both known to be associated with circulating immune complexes.Levels of these antibodies were also determined in two other glomerulardiseases, i.e. idiopathic membranous glomerulo-nephritis (n=7) and minimalchange disease (n=2), in which circulating immune complexes are usually notpresent, and in 40 healthy controls. Results: IgAanti-C1q was observed in increased titres in 11/36 of the patients with IgAnephropathy, in 2/37 of the patients with SLE nephritis (both withproliferative disease) and in 1/9 of the patients with membranous andminimal change disease (P<0.001). Increased titres of IgG anti-C1qwere observed in 1/36 of the patients with IgA nephropathy, in 17/37 of thepatients with SLE nephritis and in 0/9 of the patients with membranous andminimal change disease (P<0.001). There were no correlations betweenthe levels of anti-C1q antibodies and clinical parameters such as degree ofproteinuria, haematuria, or renal function. Nor was there any correlationto the concentration of C3a and the terminal complement complex (TCC) inpatients with IgA nephropathy. Conclusions: Theoccurrence of anti-C1q antibodies in both IgA nephropathy and SLEnephritis, albeit of different predominating isotypes, indicates thepossibility of a similar pathogenic mechanism involved in these renaldisorders. The occurrence of IgA anti-C1q antibodies in patients with IgAnephropathy has to our knowledge not previously been reported.