Open AccessHigher anti‐heparan sulphate reactivity during systemic lupus erythematosus (SLE) disease exacerbations with renal manifestations; a long term prospective analysis
Author(s) -
KRAMERS C.,
TERMAAT R. M.,
BORG E. J.,
BRUGGEN M. C. J.,
KALLENBERG C. G. M.,
BERDEN J. H. M.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb06493.x
Subject(s) - immunology , antibody , medicine , autoantibody , reactivity (psychology) , prospective cohort study , histone , kidney disease , lupus erythematosus , autoimmune disease , dna , anti dsdna antibodies , pathology , biology , genetics , alternative medicine
SUMMARY Cross‐reactive antibodies against heparan sulphate (HS) have been suggested to play a role in initiating renal disease in SLE. Recently, we found that HS‐reactivity is mediated by anti‐DNA antibodies complexed with DNA and histones. To evaluate the clinical significance of anti‐HS reactivity, we studied prospectively a cohort of 72 consecutive SLE patients, of whom 22 experienced 40 exacerbations. In 20 of these exacerbations renal symptoms were present. In these 20 exacerbations significantly higher anti‐DNA (median 1:160) and anti‐HS (median 1:30) titres were detected compared with exacerbations without renal manifestations (median 1:60 for anti‐DNA and negative for anti‐HS). There were no correlations with other symptoms of SLE. Anti‐HS titres showed a significant correlation with anti‐DNA antibody titres ( r s = 0·57, P < 0·05). Anti‐HS without anti‐DNA reactivity was never detected. Some SLE patients showed a high anti‐DNA titre without anti‐HS reactivity, suggesting that not all anti‐DNA antibodies are able to bind to histone/DNA complexes and thus to exhibit anti‐HS reactivity. Our findings indicate that anti‐HS reactivity is correlated with renal disease in SLE.