Not only does AKI cause pulmonary edema secondary to volume overload, but also evidence from animal models of ischemic, nephrotoxic and bilateral nephrectomy shows that AKI induces a pro-inflammatory process highlighted by increased levels of neutrophils, tnf- α, interleukins, free radicals, endothelial growth factors and granulocyte colony stimulating factor [36–38]. This evidence concerns the gene TNF and acute kidney injury.