Considering our unexpected divergent results regarding an increase of glomerulosclerosis and IF/TA despite inhibition of TGF-β activation and inflammation via TSP-2 gene therapy in Fischer-Lewis CAN, we considered the antiangiogenic long-term properties of TSP-2 as a possible explanation and therefore investigated capillary density by immunohistological staining for CD31. Here, TGFB1 is linked to glomerulosclerosis.