Attempts were made to produce experimental IgA nephropathy by oral administration for 18 weeks of dextran having a molecular weight of 10,000, 70,000, and 500,000 to 6-week old female BALB/c mice. It was observed that in three out of eight cases belonging to the group given dextran having a molecular weight of 70,000 and in three out of seven cases belonging to the group given dextran having a molecular weight of 500,000, deposition of IgA on the mesangium was demonstrated by immunofluorescence direct method. Furthermore, deposition of IgG and IgM was observed in not only the groups given dextran but also in the control group, but no significant difference in deposition pattern could be demonstrated between the groups. C3 was observed only in one case belonging to the group given dextran having a molecular weight of 10,000. The serum IgA value showed a higher value in the cases with IgA deposition than in the control group. Serum C3 value was higher in the IgA deposition cases in the group given dextran having a molecular weight of 500,000 than in the control group. These results suggest that it is possible to produce experimental IgA nephropathy by continual oral administration of carbohydrate antigen of bacterial origin and that bacterial infection is involved in the development of IgA nephropathy.