Anti-α-galactosyl antibodies and immune complexes in children with Henoch-Schonlein purpura or IgA nephropathy

Abstract

Episodes of hematuria in IgA nephropathy or Henoch-Schonlein purpura are frequently associated with microbial infections. Some of those infectious agents bear α-galactosyl residues on their cell surface. These observations prompted us to determine, by passive hemagglutination, the titers of natural anti-galactosyl antibodies in the serum of children presenting with Henoch-Schonlein purpura (10 cases) or IgA nephropathy (7 cases). Antibody titers of normal subjects (103 cases), children with a pharyngitis of unknown etiology (7 cases), and children exhibiting mesangial IgA deposits but no hematuria at the time of testing (6 cases) ranged from 1:20 to 1:80. Elevated titers (> 1:80) were observed in nine of 11 patients with mesangial IgA deposits and micro- or macroscopic hematuria, in nine of 19 children with other evolutive glomerular diseases (5 cases of acute glomerulonephritis and 4 cases of minimal change disease), and in most subjects presenting with a M. pneumoniae (4/5 cases) or a E. coli (4/5 cases) infection. Antibody titers decreased after incubation of normal and pathological sera with D-galactose (10 mM) or with α-galactosyl-glucoside (10 mM), but not with D-glucose (10 mM). The anti-α-galactosyl antibodies purified, by affinity chromatography, from sera of 10 normal children, 10 pathological controls and four children with mesangial IgA deposits without hematuria belonged to IgG class. In contrast, both IgG and IgA anti-α-galactosyl antibodies were detected in six of six patients with mesangial IgA deposits and hematuria. The IgA content of immune complexes detected in those patients decreased after incubation of sera with α-galactosyl-glucoside, but not with D-glucose. We conclude that an IgA anti-α-galactosyl immune response is frequently observed during hematuria episodes in IgA-associated nephrites.