The different models of experimental IgA nephropathy described so far have provided insight into pathogenesis; however, the evidence for a role of IgA immune complexes (IC) has only been gained in passive systems. In an active model of IgA nephropathy, induced in mice by repeated injections of dextran, some of the mechanisms that could explain the formation of glomerular IgA deposits are studied in this report. Serum total IgA and anti-dextran IgA antibody levels increased significantly over the period of immunization. Only 13-30% of mice had total and/or specific IgA IC, determined by Raji cell and PEG assay in ELISA. Analytical ultracentrifugation showed that IgA IC were of small (7-13 S) or intermediate (13-17 S) size. There was a close correlation between total serum IgA levels and the presence of IC-containing IgA anti-dextran antibodies, with the existence of IgA in the mesangium. The percentage of animals (n = 76) with IgA mesangial deposits increased over the immunization period (88% at 10 weeks). Forty-three per cent of mice had polymeric IgA in the mesangium; by contrast, only 12% had dextran deposits. On the whole, these data suggest that in the dextran-induced IgA nephropathy, the glomerular IgA could be the result of circulating IgA complexes and/or IgA polymers deposition.