Acute kidney injury is a sudden decline in kidney function that leads to accumulation of waste products, fluid imbalance and disturbances in electrolytes such as potassium. It often occurs in hospitalized and critically ill patients, especially after major surgery, sepsis, shock, or exposure to nephrotoxic drugs like some antibiotics, contrast agents and chemotherapy.

Diagnosis relies on changes in serum creatinine and urine output, but these are delayed markers and may miss early, reversible injury. Recent research has focused on more sensitive biomarkers that reflect structural kidney damage, such as neutrophil gelatinase associated lipocalin, kidney injury molecule 1, interleukin 18 and cell cycle arrest markers like TIMP 2 and IGFBP7. These biomarkers aim to enable earlier detection, better risk stratification and targeted preventive strategies in high risk patients.

Pathophysiologically, acute kidney injury involves complex interactions among reduced renal blood flow, tubular cell injury, inflammation, oxidative stress, microvascular dysfunction and impaired repair. Persistent or severe injury can lead to incomplete recovery, fibrosis and transition to chronic kidney disease, which increases long term cardiovascular risk and mortality.

Management currently focuses on identifying and correcting the underlying cause, optimizing hemodynamics, avoiding further nephrotoxins, carefully managing fluids and electrolytes and providing renal replacement therapy when needed. There is active investigation into pharmacologic interventions that might protect renal tubules, modulate inflammation or enhance repair, but no specific drug therapy is yet established in routine practice. Ongoing research emphasizes early risk prediction, standardized definitions and staging, and long term follow up to understand and mitigate the lasting consequences of acute kidney injury.