TGFB1 and Hyperglycemia: It is well accepted that chronic hyperglycaemia activates various inflammatory pathways to induce oxidative stress, fibrotic cytokines including transforming growth factor β-1 (TGF-β1), the renin-angiotensin-aldosterone system, and increases advanced glycation end-products, leading collectively to tubular and podocyte injury, apoptosis, extracellular matrix deposition and associated albuminuria [4, 5].