Table 3 Potential pathophysiological mechanisms of septic AKI

Pro-inflammatory state

 Complement and coagulation activation

 Protease activation (heparan sulfate, elastase)

 Free radical formation

 Pro-inflammatory cytokine production (IL-1, IL-6, IL-18, TNF-α)

 Cell activation (neutrophil, macrophage, platelet, endothelial cell)

Anti-inflammatory state

 Anti-inflammatory cytokine (IL-10)

 Reduced phagocytosis and chemotaxis

 Deranged immune function (lymphocyte apoptosis)

Dysregulation of microcirculation

 Vasodilation-induced glomerular hypoperfusion

 Abnormal blood flow within the peritubular capillary network