Abnormal IgA glycosylation in Henoch-Schonlein purpura restricted to patients with clinical nephritis |
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Authors: | Allen A; Willis F; Beattie T; Feehally J |
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Institution: | Department of Nephrology, Leicester General Hospital, Gwendolen Road, Leicester LE5 4PW, UK; Renal Unit, Royal Hospital for Sick Children, Yorkhill, Glasgow G3 8SJ, UK |
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Abstract: | Background: Glomerular deposition of IgA1 is a common
feature of Henoch-Schonlein purpura, and is indistinguishable from that
seen in IgA nephropathy. Serum IgA1 is abnormally O-glycosylated in IgA
nephropathy, and this may contribute to mesangial IgA1 deposition and the
development of glomerular injury. This altered O-glycosylation of IgA1 can
be detected by its increased binding to the lectin Vicia
villosa. Methods: To investigate whether
IgA1 is abnormally glycosylated in Henoch-Schonlein purpura, the binding of
Vicia villosa lectin to serum IgA1 was studied in the
following subject groups: IgA nephropathy; adults and children with
Henoch-Schonlein purpura and nephritis; children with clinically diagnosed
Henoch-Schonlein purpura but no renal involvement; adults and children with
non-IgA associated glomerulonephritis; and matched controls.
Results: The abnormality of lectin binding seen in IgA
nephropathy was also found in both adults and children with
Henoch-Schonlein purpura with nephritis. However the lectin binding of
serum IgA1 from children with Henoch-Schonlein purpura lacking renal
involvement did not differ from controls, and similarly no abnormality of
lectin binding was seen in patients with non-IgA associated
glomerulonephritis. Conclusions: These data indicate
that the abnormality of IgA1 O-glycosylation seen in IgA nephropathy is
also found in Henoch Schonlein purpura, but only in those subjects with
renal involvement, while IgA1 O-glycosylation is normal in patients with
other forms of renal disease. These findings lend strong support to a role
for altered IgA1 O-glycosylation in the pathogenesis of IgA-associated
glomerular disease. |
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