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The kidney is one of the most energy-demanding organs in the human body, and the maintenance of mitochondrial homeostasis is central to kidney function.  Mitochondria dysfunction plays a pivotal role in the pathogenesis of acute kidney injury (AKI), including enhanced mitochondrial oxidative stress, decreased ATP production, and impaired activation of downstream processes such as the immune response, apoptosis and necrosis.  There is increasing interest in mitochondria as a therapeutic target for different causes of AKI.  Accumulating evidence demonstrate that sex-specific differences contribute to differential injury response in patients with AKI.  Recently, it has been shown that there are important sex-related differences in intrinsic mitochondrial respiration, and mitochondrial biogenesis and dynamics; sex hormones mediate many of these differences.  By understanding the influences of sexual dimorphism or sex hormones on mitochondrial homeostasis and disease manifestations, we may be able to identify novel therapeutic targets and improve existing treatment options for AKI.