Many factors including high glucose (hyperglycemia), angiotensin II and advanced glycation end-products (AGEs) serve as potent inducers of TNFα, which upregulates the expression of cell adhesion molecules (ICAM-1 and VCAM-1), monocyte chemoattractant protein 1 and colony-stimulating factor-1 in various kidney compartments, thereby promoting the recruitment of monocytes and macrophages to sites of inflammation9. This evidence concerns the gene TNF and Hyperglycemia.