While reducing obesity is effective in reducing inflammation and delaying disease onset and progression, including diabetes, CKD and metabolic syndrome, the metabolic effects of hyperglycemia also lead to production of AGE, TGF-β and protein kinase C. These toxic products have some role in nephropathy and clinical albuminuria with histological changes of thickening of glomerular basement membrane, mesangial matrix expansion and arteriolar hyalinosis. The gene discussed is TGFB1; the disease is obesity disorder.