Several different experimental animal models of IgA nephropathy contribute to our understanding of the clinical disease. These models collectively indicate that IgA immune complexes can deposit in glomeruli and elicit the characteristics of IgA nephropathy; they also establish the potential for an IgA immune response to generate, in the face of antigen exposure, IgA-containing immune complexes. Defective immunoregulation, mononuclear phagocyte function, and the role of antigen and complement on glomerular function emerge from the animal studies as issues ripe for clinical investigation.