Significantly, pharmacolological inhibition of XOR with allopurinol concomittantly reduced both SUA and CRP in patients with either normal renal function or in patients expressing chronic kidney disease[13,97,98], and direct support for a functional role of UA in the production of CRP was obtained in vascular smooth muscle cells and endothelial cells where UA stimulated secretion of CRP as well as MCP-1[61,62]. This evidence concerns the gene CRP and chronic kidney disease.