Background: Post-methicillin-resistant Staphylococcus aureus infection glomerulonephritis (post-MRSA infection GN) is seen after MRSA infection and is a similar disorder to IgA nephropathy (IgAN). We have found that immune complexes composed of staphylococcal cell membrane antigen and IgA are deposited in the glomerular mesangial areas in patients with post-MRSA infection GN and in more than 60% of patients with IgAN.
Aim: To examine the characteristics of serum IgA obtained from patients with IgAN.
Patients and methods: Experiment 1. Serum samples were obtained from patients with IgAN (n = 16) and post-MRSA infection GN (n = 19), and from healthy donors (n = 13). Serum IgA and IgG titers against Staphylococcus aureus (S. aureus) were measured using an ELISA. Experiment 2. Relative antibody avidities of serum IgA and IgG against S. aureus from patients and healthy donors were determined in a dissociation assay using an ELISA.
Results: Experiment 1. IgA class titers of anti-S. aureus antibodies in patients with IgAN and post-MRSA infection GN were significantly higher than in healthy controls, and IgG class titers of anti-S. aureus antibodies in patients with post-MRSA infection GN were significantly higher than those in IgAN patients and healthy donors. A significant correlation between IgG and IgA titers was found across all cases, and this was particularly evident in patients with IgAN. Experiment 2. No significant correlation was observed between avidity and titer of IgA class antibodies. The avidity of anti-S. aureus IgG did not differ significantly between IgAN patients, post-MRSA infection GN patients, and healthy donors, but the avidity of anti-S. aureus IgA from patients with IgAN was significantly lower than that from the other groups. There was a significant correlation between antibody titer and antibody avidity for the IgG class in patients with post-MRSA GN, but no significant correlation was observed for the IgA class.
Conclusion: These results suggest that patients with IgAN have a strong response through production of IgA with low avidity against S. aureus.