The complex pro-inflammatory milieu of hyperglycaemia, reactive oxygen species (ROS), advanced glycation end products (AGE) and angiotensin-II contributes to activation of transcription factors, growth factors, inflammatory cytokines and chemokines that mediate glomerular, microvascular and tubulo-interstitial injury—eventually leading to progression to ESRD and to the increased cardiovascular mortality associated with DKD [2–4]. This evidence concerns the gene AGT and diabetic kidney disease.