Similarly, although SDF-1 may ameliorate kidney injury and promote repair after nondiabetic ischemia [26], potentiation of the chemokine can contribute to a proliferative response that leads to glomerulosclerosis, podocyte loss, and albuminuria [27, 28], thus implicating SDF-1 in the pathogenesis of diabetic nephropathy. This evidence concerns the gene CXCL12 and glomerulosclerosis.