Experimental IgA nephropathy in mice.

Based on a hint from an immunological abnormality found in human IgA nephropathy, we tried to make up an experimental IgA nephropathy in mice by administration of a food antigen for a long term with blockage of the reticuloendothelial system (RES). Mice were divided into three groups: group 1 had oral administration of lactalbumin (Lalb); group 2 was treated with colloidal carbon to block RES in addition to oral administration of lactalbumin; and group 3 was treated only with colloidal carbon for RES blockage. Renal biopsy was performed at 18 weeks after RES blockage and the animals were sacrified at 30 weeks for histopathological observation of renal tissue. The deposits of IgA in the mesangial area were not found in animals of groups 1 and 3 but 17.6% of group 2 at 18 weeks following RES blockage, also in no animal of group 1 but 91.7% of Group 2, and 15.4% of group 3 at 30 weeks. They were highly frequent in group 2 at 30 weeks (p less than 0.001). Observation under electron microscope also revealed a significant increase (p less than 0.001) of mesangial dense deposits in group 2 at 30 weeks, and formation of large dense deposits similar to those seen in human IgA nephropathy. Through observation over a period of time, an increase of mesangial IgA deposition and histopathological aggravation were confirmed. Serologically, serum level of IgA was significantly higher in group 2 (p less than 0.001) and was correlated with the intensity of mesangial IgA deposition. It was concluded that lesions very similar to human IgA nephropathy could be prepared in mice by inducing a dysfunction of RES as continuous oral immunization.