Increased leptin secretion in MetS patients leads to kidney damage through the following two pathways, including (1) promoting the expression of TGF-β1 in renal parenchymal cells, increasing the production of type IV collagen, leading to tubular atrophy, interstitial fibrosis and glomerulosclerosis, (2) Leptin causes sodium reabsorption, leading to changes in renal hemodynamics (60, 61). The gene discussed is LEP; the disease is metabolic syndrome.