Reversely, AKI may also result in acute cardiac disorder via some mechanisms such as: (1) increased preload secondary to AKI-induced salt and water retention; (2) myocardial damage due to neutrophil trafficking, myocyte apoptosis, endothelial dysfunction, as well as elevated level of inflammatory cytokines (interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α) resulting from increased production and impaired clearance [21, 50–52]. This evidence concerns the gene TNF and endothelial dysfunction.