An experimental model of glomerulonephritis was produced by the in situ formation of immune complexes directly in the glomerular capillary wall. Perfusing the lectin concanavalin A (Con A) into the left renal arteries of rats led to its binding diffusely to the glycoproteins of the glomerular capillary wall of only that kidney in each animal. The subsequent reaction with anti-Con A antibody (either administered systemically or actively induced) resulted in an exudative and proliferative glomerulonephritis confined to the Con A perfused kidney. Immunofluorescence disclosed the diffuse deposition of immunoglobulin, Con A, and C3 in the perfused, but not the unperfused kidney. The quantitative relationship between antigen and antibody binding and histologic outcome was determined. Since lectins have been found in mammalian tissues, as well as in infectious agents that are pathogenic in man, a series of events conceptually similar to this in situ model may occur in some cases of glomerulonephritis in man.