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Table 3 Potential pathophysiological mechanisms of septic AKI

From: Role of kidney injury in sepsis

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  
  1. TNF tumor necrosis factor