The early hyperuricemia caused renal vasoconstriction mediated by endothelial dysfunction resulting from a reduction in endothelial levels of nitric oxide and activation of the rennin-angiotensin system [5], [7], followed by progressive renal microvascular disease resulting from uric acid induced cellular proliferation after urate enters into the vascular smooth muscle, inflammation due to production of various inflammatory mediators including C-reactive protein and monocyte chemoattractant protein-1, oxidative stress and activation of the local rennin-angiotensin system [43]. Here, CCL2 is linked to hyperuricemia.