Relationship between anti-dsDNA, anti-nucleosome and anti-alpha-actinin antibodies and markers of renal disease in patients with lupus nephritis: a prospective longitudinal study |
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| Authors: | Jessica J Manson Alexander Ma Pauline Rogers Lesley J Mason Jo H Berden Johan van der Vlag David P D'Cruz David A Isenberg Anisur Rahman |
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| Affiliation: | (1) Centre for Rheumatology Research, Windeyer Institute, University College London, 46 Cleveland Street, London, W1T 4JF, UK;(2) Joint University College London Hospital/University College London and Royal Free Biomedical Research Unit, Research and Development(1st Floor Maple House), Rosenheim Wing, 25 Grafton Way, London, WC1E 6DB, UK;(3) Nephrology Research Laboratory, Nijmegen Centre for Molecular Life Sciences, Department of Nephrology, Radboud University Nijmegen Medical Centre, PO Box 9101, Nijmegen, 6500, HB, The Netherlands;(4) Lupus Research Unit, The Rayne Institute, St Thomas' Hospital, Lambeth Palace Road, SE1 7EH London, UK |
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| Abstract: | Introduction Glomerulonephritis is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Deposition of autoantibodies in the glomeruli plays a key role in the development of lupus nephritis (LN). Different groups have proposed that either anti-nucleosome antibodies or antibodies that bind the intrinsic renal antigen, α-actinin, are central to the pathogenesis of LN. These theories have been based mainly on cross-sectional studies in patients and on experiments in animal models. No previous longitudinal studies have compared the relationships between levels of these antibodies and markers of renal function. We assessed how well anti-α-actinin, anti-nucleosome and anti-double-stranded DNA (anti-dsDNA) antibodies reflected renal outcome measures in patients with new-onset LN followed for up to 2 years. |
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