IgA nephropathy (IgAN), a common glomerular disease, is characterized by the presence of
IgA deposits, predominantly in the glomerular mesangium, and by mesangial proliferative
glomerulonephritis (GN). Concerning its pathogenesis, several investigators suggest that the deposited
IgA is an antibody to viral, bacterial, or dietary
antigens. Thus the antibody is probably produced as part of the specific host immune response to various environmental
antigens. Such reports strengthen the possibility of a relationship between mucosal immunity and the pathogenesis of IgAN. Nevertheless, attempts to isolate a specific
IgA-circulating
immune complex associated
antigen in patients with IgAN have been unsuccessful. We have showed that such mucosal
infections as
pharyngitis are often associated with the acute onset of IgAN. Then IgAN is an
immune complex disease that is caused by a poor mucosal immune response to environmental
antigens to which the patient has been chronically exposed. We observed that Haemophilus parainfluenzae (HP) is more commonly isolated from the pharynx of patients with IgAN than from those with other diseases. We have also identified the glomerular deposition of outer membranes of HP
antigens (OMHP) and an increased serum concentration of
IgA antibodies against OMHP in patients with IgAN. Further studies will be necessary to determine whether the association of OMHP
antigens in the glomeruli and
IgA antibody against OMHP
antigens in the sera of patients with IgAN can be confirmed in other parts of the world and whether this association is important in the pathogenesis of IgAN. Nevertheless, the demonstration of glomerular deposition of OMHP
antigens and of
IgA antibody against OMHP in sera indicates a potential new avenue of investigation into the elusive cause of IgAN.