title: A prospective study of anti-chromatin and anti-C1q autoantibodies in patients with proliferative lupus nephritis treated with cyclophosphamide pulses or azathioprine/methylprednisolone.
abstract: OBJECTIVE
  To study the prevalence and course of anti-chromatin (anti-nucleosome, anti-double-stranded (ds) DNA and anti-histone) and anti-C1q autoantibodies in patients with proliferative lupus nephritis (LN), treated in a randomised controlled trial with either cyclophosphamide or azathioprine plus methylprednisolone.
  
  
  METHODS
  Autoantibody levels were measured and analysed in 52 patients with proliferative LN, during their first year of treatment. Levels in both treatment arms were compared and associations with clinical, serological and outcome parameters were studied.
  
  
  RESULTS
  At study entry, prevalences for anti-nucleosome, anti-dsDNA, anti-histone and anti-C1q autoantibodies were 81%, 96%, 23% and 65%, respectively. Anti-chromatin autoantibodies correlated with each other, but not with anti-C1q levels. If patients were divided for their autoantibody titre at the start of treatment above or below the median, the only significant differences were higher SLE disease activity index with higher anti-nucleosome, and higher creatinine with higher anti-C1q autoantibodies. During the first year, a comparable rapid decline in the levels of anti-nucleosome, anti-dsDNA and anti-C1q autoantibodies was seen in both treatment arms. Anti-histone autoantibody levels were low and did not change. Renal flares were not preceded by rises in autoantibody titres.
  
  
  CONCLUSIONS
  These results indicate that measurement of anti-chromatin and anti-C1q autoantibodies is useful for diagnosing LN, but not for monitoring disease course.
authors.affiliation: Division of Nephrology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
authors.forename: Cecile
authors.initials: C
authors.lastname: Grootscholten
authors.forename: Jürgen W C
authors.initials: JW
authors.lastname: Dieker
authors.forename: Fabian D
authors.initials: FD
authors.lastname: McGrath
authors.forename: Anja
authors.initials: A
authors.lastname: Roos
authors.forename: Ronald H W M
authors.initials: RH
authors.lastname: Derksen
authors.forename: Johan
authors.initials: J
authors.lastname: van der Vlag
authors.forename: Mohamed R
authors.initials: MR
authors.lastname: Daha
authors.forename: Jo H M
authors.initials: JH
authors.lastname: Berden
mesh_terms: D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D001323:Autoantibodies / Q000276:immunology*; D001379:Azathioprine / Q000008:administration & dosage; D015415:Biomarkers / Q000097:blood; D002843:Chromatin / Q000276:immunology*; D015922:Complement C1q / Q000276:immunology*; D003520:Cyclophosphamide / Q000008:administration & dosage; D004247:DNA / Q000276:immunology; D004359:Drug Therapy, Combination; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage*; D008181:Lupus Nephritis / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D008775:Methylprednisolone / Q000008:administration & dosage; D009707:Nucleosomes / Q000276:immunology; D011446:Prospective Studies
chemical_list: D000893:Anti-Inflammatory Agents; D001323:Autoantibodies; D015415:Biomarkers; D002843:Chromatin; D007166:Immunosuppressive Agents; D009707:Nucleosomes; D015922:Complement C1q; D003520:Cyclophosphamide; D004247:DNA; D001379:Azathioprine; D008775:Methylprednisolone