Fig. 4. Proposed mechanism of acute kidney injury (AKI)-induced liver dysfunction. AKI increases small intestinal expression of interleukin-17A (IL-17A) and causes small intestinal injury (impaired vascular permeability, villous endothelial apoptosis and epithelial necrosis, leukocyte infiltration with subsequent cytokine flow into the liver). These events result in hepatic injury (inflammation, apoptosis and necrosis) and increased generation and release of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) into systemic circulation causing further multiorgan injury.