Acute kidney injury (AKI) is a common clinical syndrome characterized by damage to the kidney structure and rapid impairment of renal function, which leads to the inability to maintain fluid-electrolyte and acid-base homeostasis. AKI is recognized as a growing public health problem due to its complex pathophysiology and limited treatment efficacy, leading to an increase in morbidity. This review describes the key causes of AKI, analyzes the cellular and molecular mechanisms involved in the pathogenesis of this disease, with particular attention paid to oxidative stress and the role of amphoterin. The need to search for new therapeutic targets, pharmacological methods, and develop correction methods that would contribute to the attenuation of inflammation in AKI is substantiated.