Epimembranous glomerular deposition of circulating immune complexes in considered to be the pathogenesis of immune complex glomerulonephritis, based on experiments in serum sickness glomerulopathy. A subepithelial localization of immune aggregates, however, was never obtained after the intravenous injection of preformed immune complexes. Recent studies on heterologous immune complex glomerulonephritis provide evidence of in situ formation of subepithelial glomerular immune complex aggregates as a second pathogenetic mechanism. We investigated the existence of a comparable mechanism in a serum sickness model of glomerulonephritis. A passive immune complex glomerulopathy involving lysozyme/antilysozyme and bovine serum albumin (BSA)/anti-BSA was used to investigate this thesis. Alternating perfusion of a kidney with antigen and antibody resulted in a granular deposition of both components along the glomerular basement membrane (GBM). The deposits of immune aggregates were localized exclusively along the epithelial side of the GBM and were still present 3 days after the perfusion. Control perfusions with preformed immune complexes or with either BSA or anti-BSA alone did not result in subepithelial deposition. Conclusion. The alternating excess of antigen and antibody in the circulation might result in in situ formation of immune complexes localized at the epithelial side of the GBM.