**10. Conclusions**

The pathophysiology of AKI is remarkably complex, due to the involvement of multiple cells types in the endothelium, renal tubules, and the immune system. To add to this complexity, AKI occurs in the setting of other diseases such as sepsis, rhabdomyolysis, cancer, and cardiovascular disorders, wherein the underlying disease or related therapies trigger renal dysfunction through complex mechanisms that remain incompletely understood. The animal models described in the current chapter reflect and recapitulate the complexities associated with AKI and are essential tools for studying the pathophysiological mechanisms that drive acute kidney injury.
