**9.1 Methods**


#### **9.2 Key notes**

This model shows similar hemodynamic and physiological changes to those in human sepsis, is reproducible, and is operator-independent [76]. The development of S-AKI in this model is still understudied [77] and the induction of peritonitis by this model may not always induce kidney injury as shown recently by Shaver *et. al*78. However, since degree of early inflammation associated with this model is mild, it allows us to introduce other confounding like hemorrhage and investigate the finer mechanisms that can lead to S-AKI [78].

The principal reason for investigating different animal models of abdominal sepsis and its progression to S-AKI is eventually to develop therapies to treat sepsis and associated morbidities in a clinical setting. Therefore, the choice of animal model should incorporate and account for clinical caveats. Animal models of sepsis and S-AKI are essential for scientific understanding of human disease, but if they are not well characterized and understood, erroneous conclusions may be drawn, which can hinder scientific progress. A well-designed septic animal model requires a thorough understanding of the similarities and differences in the physiology of humans. To that end, the information presented in this chapter provides a systematic basis for the development of animal models for abdominal sepsis research. A perfect murine model of sepsis does not exist. While none of the current animal

models manifest and replicate the intricacies of human sepsis and S-AKI, they provide a platform for sophisticated testing that is far beyond that of cell and tissue culture.
