title: Anti-C1q antibodies have higher correlation with flares of lupus nephritis than other serum markers.
abstract: OBJECTIVE
  Autoantibodies are important in the diagnosis and classification of systemic lupus erythematosus (SLE), but whether they correlate with changes in disease activity within individual patients is controversial. We assessed the association between changes in SLE global and renal activity and changes in several autoantibodies and cell adhesion molecules in patients with SLE.
  
  
  METHODS
  Stored sera collected at two or three clinic visits from each of 49 SLE patients (91% female, 59% African-American, 31% Caucasian, 10% other ethnicity, 38% under 30 years, 41% between 30-44 years, and 21% 45-63 years) were analyzed. The visits were chosen to include one visit with proteinuria, and one or two without, for each patient. Global disease activity was measured by the Physician's Global Assessment (PGA), SELENA-SLEDAI (SLE Disease Activity Index modified to exclude anti-dsDNA and complement) and renal activity assessed by urine protein (by urine dipstick) and Renal Activity Score. Sera were assayed for anti-C1q, anti-chromatin, anti-dsDNA, anti-ribosomal P, monocyte chemotactic protein-1 (MCP-1), vascular cell adhesion molecule (VCAM) intercellular adhesion molecule (ICAM) and complement. The associations between changes in disease activity and changes in biomarker levels were assessed.
  
  
  RESULTS
  In terms of global disease activity, anti-C1q had the highest association with the PGA (p = 0.09) and was strongly associated with modified SELENA-SLEDAI (p = 0.009). In terms of renal activity, anti-C1q had the highest association with proteinuria (p = 0.079), and was strongly associated with Renal Activity Score (p = 0.006).
  
  
  CONCLUSIONS
  Anti-C1q performed the best of the potential biomarkers, being significantly associated with the modified SELENA-SLEDAI and with the Renal Activity Score. This study indicates the potential superior utility of anti-C1q over anti-dsDNA and other measures to track renal activity.
authors.affiliation: Johns Hopkins University School of Medicine, Baltimore, MD, USA.
authors.forename: E
authors.initials: E
authors.lastname: Akhter
authors.forename: R W
authors.initials: RW
authors.lastname: Burlingame
authors.forename: A L
authors.initials: AL
authors.lastname: Seaman
authors.forename: L
authors.initials: L
authors.lastname: Magder
authors.forename: M
authors.initials: M
authors.lastname: Petri
mesh_terms: D000328:Adult; D000974:Antibodies, Antinuclear / Q000097:blood; D001323:Autoantibodies / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood; D015331:Cohort Studies; D015922:Complement C1q / Q000037:antagonists & inhibitors / Q000276:immunology*; D003176:Complement C3 / Q000378:metabolism; D003181:Complement C4 / Q000378:metabolism; D005260:Female; D006801:Humans; D008181:Lupus Nephritis / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000097:blood / Q000276:immunology / Q000503:physiopathology
chemical_list: D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D015415:Biomarkers; C111835:CCL2 protein, human; D015815:Cell Adhesion Molecules; D018932:Chemokine CCL2; D003176:Complement C3; D003181:Complement C4; D015922:Complement C1q