Diabetes was induced in Lewis rats with streptozotocin. Six to 9 mth later glomeruli showed significant mesangial matrix thickening; by immunofluorescent microscopy large quantities of IgG, β1C and in some instances, IgM were seen in a mesangial distribution. Sustained normoglycemia was then achieved in 9 of these animals by successful pancreatic islet isotransplantation. Three mth following transplantation 5 of these animals had decreased mesangial matrix while 4 had no further progression of glomerular lesions. All had a marked decrease in IgG, IgM and β1C in the mesangium. In contrast, untreated diabetic rats, over the same time period, demonstrated progressive mesangial thickening and focal tuft sclerosis. Immunoglobulins and complement were in the mesangium in quantities equal to or greater than seen in earlier biopsies. Thus, successful pancreatic islet transplantation in the rat results in regression or arrest of the diabetic glomerular lesion.