In the brain death animals, increased serum Cr and pathological tubular injury were observed, accompanied by increased pro-inflammatory cytokine (IL-1β, IL-6 and TNF-α) and chemokine (MCP-1 and IP-10) mRNA expression, suggesting the animal model was successful established and a clear role for inflammation in brain-death induced kidney damage. This evidence concerns the gene CCL2 and Nephropathy.