title: Occurrence of anti-C1q antibodies in IgA nephropathy.
abstract: BACKGROUND
  The pathogenic mechanisms and the antigens involved in the establishment and progress of IgA nephropathy are unknown. As antibodies against C1q have been reported to correlate with SLE nephritis, we analysed the occurrence of these antibodies in IgA nephropathy in order to investigate the possibility of pathogenetic similarities in these renal disorders.
  
  
  METHODS
  The occurrence of IgA- and IgG anti-C1q antibodies (anti-C1q) were determined by 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 glomerular diseases, i.e. idiopathic membranous glomerulonephritis (n = 7) and minimal change disease (n = 2), in which circulating immune complexes are usually not present, and in 40 healthy controls.
  
  
  RESULTS
  IgA anti-C1q was observed in increased titres in 11/36 of the patients with IgA nephropathy, in 2/37 of the patients with SLE nephritis (both with proliferative disease) and in 1/9 of the patients with membranous and minimal change disease (P < 0.001). Increased titres of IgG anti-C1q were observed in 1/36 of the patients with IgA nephropathy, in 17/37 of the patients with SLE nephritis and in 0/9 of the patients with membranous and minimal change disease (P < 0.001). There were no correlations between the levels of anti-C1q antibodies and clinical parameters such as degree of proteinuria, haematuria, or renal function. Nor was there any correlation to the concentration of C3a and the terminal complement complex (TCC) in patients with IgA nephropathy.
  
  
  CONCLUSIONS
  The occurrence of anti-C1q antibodies in both IgA nephropathy and SLE nephritis, albeit of different predominating isotypes, indicates the possibility of a similar pathogenic mechanism involved in these renal disorders. The occurrence of IgA anti-C1q antibodies in patients with IgA nephropathy has to our knowledge not previously been reported.
authors.affiliation: Department of Rheumatology, Karolinska Hospital, Stockholm, Sweden.
authors.forename: I
authors.initials: I
authors.lastname: Gunnarsson
authors.forename: J
authors.initials: J
authors.lastname: Rönnelid
authors.forename: I
authors.initials: I
authors.lastname: Lundberg
authors.forename: S H
authors.initials: SH
authors.lastname: Jacobson
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000936:Antigen-Antibody Complex / Q000276:immunology; D001323:Autoantibodies / Q000097:blood*; D015922:Complement C1q / Q000276:immunology*; D004247:DNA / Q000276:immunology; D005260:Female; D005922:Glomerulonephritis, IGA / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000276:immunology; D008297:Male; D008875:Middle Aged
chemical_list: D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D015922:Complement C1q; D004247:DNA