**1. Introduction**

Acute kidney injury (AKI) is a common clinical disorder characterized by a precipitous decline in renal function [1]. AKI is particularly prevalent in hospitalized patients and is associated with varied underlying etiologies, such as sepsis [2], cardiac surgery [3], rhabdomyolysis [4], and drug toxicity [5]. Patient outcomes are varied and depend partly on severity, with higher mortality seen in critically ill patients [1]. Importantly, patients who survive an episode of AKI are at increased risk for major adverse cardiovascular events, as well as for progression to chronic kidney disease (CKD) and end-stage renal disease (ESRD) [6]. Despite our growing understanding of the causes and mechanisms of AKI, as well as an effort to develop better diagnostic strategies, few preventive or therapeutic options exist.

Therefore, animal models of AKI are essential for identifying mechanisms of renal dysfunction and for development of therapeutic and diagnostic strategies [7]. To this end, mice have been the main experimental organisms for studying AKI. Since the underlying causes of AKI are varied, several murine animal models have been established. These animal models recapitulate several pathophysiological features of AKI, such as endothelial dysfunction [8], epithelial cell death [9], and immune cell infiltration [10] (**Figure 1**). In the current chapter, we provide an overview of the methods and highlight issues that are critical in establishing various murine models of AKI.

#### **Figure 1.**

*Complex pathophysiology of AKI: Involvement of endothelium, renal tubules (specifically proximal tubule (PT) segment) and immune cells. Compared to normal/healthy kidney, various AKI insults result in overall decrease in ATP, loss of PT brush border, increase in vascular permeability and inflammation ultimately resulting in apoptosis and necrosis.*
