Interestingly, hyperglycemia per se does not necessarily cause the typical morphological and functional changes associated with DN, but in combination with the functional impairment of eNOS rodents develop albuminuria, decline of glomerular filtration rate (GFR), and renal histological pathologies such as glomerular and tubularinterstial fibrosis, similar to human DN [10]–[12], [28]. Here, NOS3 is linked to fibrosis.