Previous studies have shown that a rat experimental model of membranous nephropathy (Heymann nephritis) is often associated with tubulointerstitial changes. Although antibody-dependent tubular injuries have been proposed in this model, precise mechanisms have been ill-defined. In the present report, we established a model of acute tubulointerstitial nephritis (TIN) by injecting puromycin aminonucleoside (PAN) to Wistar rats which had been immunized with tubular antigens (Tub-Ag). In this model, TIN developed 4 weeks after Tub-Ag immunization when rats had a high titer of circulating anti-Tub-Ag antibodies and began to excrete massive proteinuria. Deposits of immunoglobulins along tubular brush borders were also demonstrated. Rats receiving either Tub-Ag or PAN alone failed to develop TIN during this relatively acute phase. These results suggest that anti-Tub-Ag antibodies excreted into the urine play a role in developing TIN in this model.