Diabetic retinopathy is the leading cause of blind-ness in the Western world (1) and is character-ized by abnormal angiogenesis driven by several factors, including tissue ischemia and hyperglycemia. This abnormal angiogenesis results in new vessels that are often immature and play a pathological role in retinopathy, contributing to both vitreous hemorrhage and fibrosis (2). In addition, increased vascular permeability leading to plasma leakage accounts for the development of macula edema, disrupting visual function (2). These evidences have led to the development of several therapeutic strategies targeting angiogenesis in diabetic retinopathy (3).

Abnormal angiogenesis also occurs in diabetic nephropathy; therefore, the overriding question is whether new vessel formation in the kidney plays a pathological role in diabetic nephropathy similar to that observed in retinopathy. Intriguingly, the progression of both diabetic retinopathy and nephropathy is altered by vascular growth factor signaling through receptor tyrosine kinases, specifically involving the vascular endothelial growth factor (VEGF)-A and angiopoietin families. This review discusses abnormal angiogenesis and the role of both VEGF-A and angiopoietins in diabetic nephropathy.