A study using a rat myocardial infarction model to examine the potential mechanisms of renal damage after cardiac dysfunction found that the mRNA expression of inflammatory cytokines IL-6 and TNF-α in the kidneys of myocardial infarction rats, as well as microvascular endothelial permeability and renal tubular cell apoptosis, were significantly increased, confirming the important role of the inflammatory response in the occurrence and development of CRS (71). This evidence concerns the gene IL6 and myocardial infarction.