title: High levels of antibodies against Clq are associated with disease activity and nephritis but not with other organ manifestations in SLE patients.
abstract: OBJECTIVE
  Serum concentration of antibodies to C1q (C1qAb) has been reported to be elevated in a high percentage of patients with systemic lupus erythematosus (SLE). The associations of high C1qAb levels with different clinical manifestations and the activity of the disease, however, are not definitely understood.
  
  
  METHODS
  We measured the levels of IgG type C1qAb in the sera of 137 patients with SLE using an ELISA method.
  
  
  RESULTS
  Serum concentrations of C1qAb were found to be higher (p < 0.0001) in SLE patients than in healthy controls. High titer (> 66 AU/ml) C1qAb was found in 40/137 (29.2%) SLE patients, and 4/192 (2.1%) healthy controls (p < 0.0001). A strong negative correlation (R = -0.4, p < 0.0001) between the age of the patients and the C1qAb titers could be detected. C1qAb levels in clinically active SLE patients significantly (p < 0.0001) exceeded those measured in the sera of patients in the inactive stage of the disease. A significant positive correlation was detected between C1qAb levels and the laboratory activity markers (anti-DNA, low C3 level) of the disease. We found a significant negative correlation between levels of C1qAb and a negative acute phase protein, alpha2-HS-glycoprotein. Renal involvement was present in 11/40 (27.5%) and 11/97 (11%) of the patients with high and low titers of C1qAb, respectively (p = 0.038). The prevalence of other organ manifestations was, however, the same in the patients with or without high titer C1qAb.
  
  
  CONCLUSIONS
  These findings indicate that C1qAb measurement is a useful method for detecting the activity of SLE and predicting renal manifestations, but not other organ involvement in the disease.
authors.affiliation: 3rd Department of Internal Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
authors.forename: L
authors.initials: L
authors.lastname: Horváth
authors.forename: L
authors.initials: L
authors.lastname: Czirják
authors.forename: B
authors.initials: B
authors.lastname: Fekete
authors.forename: L
authors.initials: L
authors.lastname: Jakab
authors.forename: T
authors.initials: T
authors.lastname: Pozsonyi
authors.forename: L
authors.initials: L
authors.lastname: Kalabay
authors.forename: L
authors.initials: L
authors.lastname: Romics
authors.forename: K
authors.initials: K
authors.lastname: Miklós
authors.forename: L
authors.initials: L
authors.lastname: Varga
authors.forename: Z
authors.initials: Z
authors.lastname: Prohászka
authors.forename: A
authors.initials: A
authors.lastname: Szakács
authors.forename: E
authors.initials: E
authors.lastname: Nagy
authors.forename: M R
authors.initials: MR
authors.lastname: Daha
authors.forename: G
authors.initials: G
authors.lastname: Füst
mesh_terms: D000328:Adult; D000367:Age Factors; D000974:Antibodies, Antinuclear / Q000097:blood; D001798:Blood Proteins / Q000032:analysis; D015922:Complement C1q / Q000276:immunology*; D003176:Complement C3 / Q000032:analysis; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008181:Lupus Nephritis / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D060749:alpha-2-HS-Glycoprotein
chemical_list: C556354:AHSG protein, human; D000974:Antibodies, Antinuclear; D001798:Blood Proteins; D003176:Complement C3; D060749:alpha-2-HS-Glycoprotein; D015922:Complement C1q