Additionally, as both obesity, diabetic nephropathy, and primary hypertension are associated with an enhanced activity of the RAS, it becomes plausible that the enhanced activity of this system in PRAT and in the adrenal gland participates in the pathogenesis of obesity-associated hypertension and diabetic nephropathy, particularly through Ang II-mediated PRAT dysfunction (101, 102). This evidence concerns the gene AGT and diabetic kidney disease.