Acute kidney injury (AKI) is a leading cause of nephrology consultations and is associated with high mortality. It is primarily caused by ischemia, hypoxia, or nephrotoxicity, leading to a rapid decline in glomerular filtration rate (GFR). Inflammation plays a key role in the extension phase of injury, which may be resistant to vasodilator therapy. Sublethal injury is a significant component of AKI, affecting GFR and renal blood flow. Recovery depends on repair processes, which may be compromised in elderly or CKD patients. AKI may link to CKD in surviving patients, and early diagnosis is crucial for effective treatment. AKI is classified into three etiologies: prerrenal, renal, and postrenal. Prerenal azotemia results from decreased renal perfusion without parenchymal damage. Postrenal causes involve urinary tract obstruction, leading to decreased GFR. Renal etiologies include ischemic and nephrotoxic injury, which are common and associated with direct renal tissue injury. AKI pathophysiology involves multiple phases: initiation, extension, maintenance, and recovery. During initiation, renal blood flow decreases, leading to cellular ATP depletion and injury. Extension phase involves hypoxia and inflammation, with increased vascular resistance and leukocyte infiltration. Maintenance phase involves cellular repair and proliferation, while recovery phase restores normal function. Hemodynamic changes in AKI include increased renal vascular resistance, influenced by factors such as tubuloglomerular feedback, adenosine, sympathetic nervous system, angiotensin II, endothelin, prostaglandins, and platelet-activated factor. These factors contribute to reduced GFR and renal perfusion. Inflammation is a key component of AKI, with leukocyte infiltration and adhesion playing a significant role. T cells and macrophages are involved in the inflammatory response, with T cells contributing to injury through IFN-γ production. Macrophages can exacerbate injury by producing pro-inflammatory cytokines, but M2 macrophages may aid in tissue repair. Dendritic cells and inflammatory signals also play roles in AKI, with inflammatory mediators promoting a positive feedback loop that worsens kidney injury. Understanding these mechanisms is crucial for developing effective therapies for AKI.Acute kidney injury (AKI) is a leading cause of nephrology consultations and is associated with high mortality. It is primarily caused by ischemia, hypoxia, or nephrotoxicity, leading to a rapid decline in glomerular filtration rate (GFR). Inflammation plays a key role in the extension phase of injury, which may be resistant to vasodilator therapy. Sublethal injury is a significant component of AKI, affecting GFR and renal blood flow. Recovery depends on repair processes, which may be compromised in elderly or CKD patients. AKI may link to CKD in surviving patients, and early diagnosis is crucial for effective treatment. AKI is classified into three etiologies: prerrenal, renal, and postrenal. Prerenal azotemia results from decreased renal perfusion without parenchymal damage. Postrenal causes involve urinary tract obstruction, leading to decreased GFR. Renal etiologies include ischemic and nephrotoxic injury, which are common and associated with direct renal tissue injury. AKI pathophysiology involves multiple phases: initiation, extension, maintenance, and recovery. During initiation, renal blood flow decreases, leading to cellular ATP depletion and injury. Extension phase involves hypoxia and inflammation, with increased vascular resistance and leukocyte infiltration. Maintenance phase involves cellular repair and proliferation, while recovery phase restores normal function. Hemodynamic changes in AKI include increased renal vascular resistance, influenced by factors such as tubuloglomerular feedback, adenosine, sympathetic nervous system, angiotensin II, endothelin, prostaglandins, and platelet-activated factor. These factors contribute to reduced GFR and renal perfusion. Inflammation is a key component of AKI, with leukocyte infiltration and adhesion playing a significant role. T cells and macrophages are involved in the inflammatory response, with T cells contributing to injury through IFN-γ production. Macrophages can exacerbate injury by producing pro-inflammatory cytokines, but M2 macrophages may aid in tissue repair. Dendritic cells and inflammatory signals also play roles in AKI, with inflammatory mediators promoting a positive feedback loop that worsens kidney injury. Understanding these mechanisms is crucial for developing effective therapies for AKI.