The occurrence of embolic occlusion can be attributed to various factors, such as the presence of fat emboli resulting from long bone fractures, the dissemination of pancreatic proteases in the systemic circulation observed in cases of acute pancreatitis, and the activation of C5 and complement factors associated with renal failure and other autoimmune diseases, which ultimately leads to leucocyte aggregation [11–13]. This evidence concerns the gene C5 and acute kidney injury.