Acute kidney injury (AKI) occurs in about half of critically ill patients and is associated with high in-hospital mortality, increased long-term mortality postdischarge, and subsequent progression to chronic kidney disease. Numerous clinical studies have shown that AKI is often complicated by dysfunction of distant organs, which is a cause of the high mortality incidence associated with AKI. Experimental studies have elucidated many mechanisms of AKI-induced distant organ injury, which include inflammatory cytokines, oxidative stress, and immune responses. This review provides an update on evidence of organ crosstalk and potential therapeutics for AKI-induced organ injuries, and presents the new concept of a systemic organ network that balances homeostasis and involves multi-organ crosstalk beyond that of the kidney with a single distant organ.
Keywords: acute kidney injury; immune cells; inflammatory cytokines; oxidative stress.
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