In concert with salt-sensitive hypertension, hyperglycemia, and hyperlipidemia, decreased OCTN2-mediated reabsorption of carnitine and downregulation of carnitine biosynthesis result in carnitine deficiency, and impairment of carnitine-induced FAO could contribute to tubular injury, kidney dysfunction, and fibrosis with enhanced lipid accumulation in the kidneys of DKD (Figure 12). This evidence concerns the gene SLC22A5 and hyperlipidemia.