Different studies [24, 25] have shown that fructose accelerates the progression of tubular and glomerular lesion by cell growth, apoptosis, increase of the chemotactic protein expression of monocytes type 1 (MCP-1), endothelial dysfunction due to an increment of intracellular adhesion molecule 1 (ICAM-1), and a nitric oxide decrease. This evidence concerns the gene CCL2 and endothelial dysfunction.