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A prospective study of anti-chromatin and anti-C1q autoantibodies in patients with proliferative lupus nephritis treated with cyclophosphamide pulses or azathioprine/methylprednisolone
  1. Cecile Grootscholten1,*,
  2. Jürgen W C Dieker1,*,
  3. Fabian D McGrath2,
  4. Anja Roos3,
  5. Ronald H W M Derksen4,
  6. Johan van der Vlag1,
  7. Mohamed R Daha2,
  8. Jo H M Berden1,
  9. on behalf of the Dutch Working Party on SLE
  1. 1Division of Nephrology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
  2. 2Department of Nephrology, Leiden University Medical Centre, Leiden, The Netherlands
  3. 3Department of Nephrology and Clinical Chemistry, Leiden University Medical Centre, Leiden, The Netherlands
  4. 4Department of Rheumatology and Clinical Immunology, University Medical Centre Utrecht, Utrecht, The Netherlands
  1. Correspondence to:
    Dr Jo H M Berden
    Division of Nephrology (464), Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands; j.berden{at}nier.umcn.nl

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.

  • AU, arbitrary units
  • AZA, azathioprine plus methylprednisolone
  • CR, complete remission
  • CY, cyclophosphamide pulses
  • ds DNA, double-stranded DNA
  • LN, lupus nephritis
  • IQR, interquartile range
  • SLE, systemic lupus erythematosus
  • SLEDAI, SLE disease activity index

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Footnotes

  • * These authors contributed equally to the work.

  • Competing interests: None.

  • Published Online First 29 November 2006

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