Serum uric acid gave rise to renal damage in an acute kidney injury model through renal vasoconstriction (via activation of the renin-angiotensin system and reduction in NO of endothelial cell), antiangiogenic properties (via blockage of endothelial cell proliferation/migration, stimulation of endothelial cell apoptosis), proinflammatory properties (via activation of monocyte chemoattractant protein-1, C-reactive protein, NF-kB, and p38 mitogen-activated protein kinase) and alteration of renal autoregulation [29]. This evidence concerns the gene CCL2 and acute kidney injury.