Increased concentration of serum IgA antibody to pneumococcal polysaccharides in patients with IgA nephropathy

It has been postulated that IgA nephropathy (IgAGN) is caused by deposition within the glomerular mesangium of IgA polymers and IgA containing immune complexes which are overproduced in response to antigens presented at mucosal surfaces. To test this, the concentrations of specific antibodies to capsular polysaccharides from pneumococci, which are common commensal and/or pathogenic bacteria in the respiratory tract, have been measured. Sera from 35 patients with IgAGN, six with systemic lupus erythematosus (SLE), eight with membranous glomerulonephritis (MGN) and six with Goodpasture's syndrome (GPS), and from 20 controls (C) were assayed. The concentrations of IgG and IgA antibodies specific for each of five pneumococcal polysaccharides (serotypes 2, 7F, 9N, 14 and 23F) were determined by ELISA. The results from the SLE, MGN and GPS patients were pooled and used as a control group of patients with forms of nephritis other than IgAGN (patient controls, PC). Groups were compared using the Wilcoxon test or the Chi square test. There were no significant differences in the concentrations of IgG antibody to any of the serotypes between the IgAGN and normals, but the PC sera had significantly lower concentrations than either the IgAGN or normals. By contrast, there were no differences between the PC and C in the proportion with detectable IgA antibody to four of the serotypes, but this was significantly increased in IgAGN. There was insufficient IgA antibody to serotype 2 to detect in the assay system used. It is concluded that IgAGN patients have greater concentrations of IgA antibodies, but not IgG, to these pneumococcal polysaccharides, compared with normal controls or patients with other forms of nephritis.