Acute kidney injury (AKI) is a common complication of advanced cirrhosis with high mortality and high morbidity, often experience poor prognosis. It is characterized by a sudden drop in glomerular filtration rate, retention of metabolic waste products, water-electrolyte imbalance, and acid-base disturbance. The pathogenesis of advanced cirrhosis complicated by acute kidney injury is complicated and not completely understood, and the therapeutic approaches are limited.Therefore, to improve the understanding of the pathophysiological mechanisms involved in renal dysfunction occurring on a background of cirrhosis is the key to develop the effective treatment strategies, improve QOL and prognosis of patients, and reduce the economic burden of family. Traditionally, it is believed that the decreased effective circulating blood volume resulted in the renal artery hypoperfusion (vasomotor mechanism). The AKI is due to the combination of an impaired effective arterial blood volume secondary to arterial vasodilation and the effects of excessive activation of the rennin-angiotensin-aldosterone system, with increased intrarenal vasoconstriction and impaired renal autoregulation that predisposes to renal dysfunction. In recent years, more and more studies have found that the activation of different inflammatory factors, such as mediators of inflammation (tumor necrosis factor-α, Interleukin-6, Toll-like receptor 4, Interleukin-17A), increased the intra-abdominal pressure resulted by cirrhotic ascites, the increased the concentration of serum bilirubin and bile acids caused by the dysfunction of bilirubin uptake, combination and excretion, the relative adrenal insufficiency leaded by anomaly expression level of serum cortisol and the endotoxin play an important role in AKI in cirrhosis. This paper will summarize the recent advances in understanding the nonvasomotor mechanism of AKI in end-stage liver disease.
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