Acute kidney injury (AKI) is a sudden decline in kidney function that impairs the body’s ability to filter waste, balance fluids and regulate electrolytes. It often develops over hours to days in hospitalized or critically ill patients and is associated with high rates of illness and death.

Research distinguishes three main causes. Prerenal AKI arises from reduced blood flow to the kidneys, often due to dehydration, blood loss, heart failure or sepsis. Intrinsic AKI reflects direct injury to kidney tissue, such as acute tubular necrosis from prolonged ischemia, nephrotoxic drugs like certain antibiotics or contrast agents, and inflammatory diseases like glomerulonephritis. Postrenal AKI results from obstruction of urine flow by conditions such as kidney stones, tumors or prostate enlargement.

Diagnosis relies on rising serum creatinine, declining urine output and clinical context. However, creatinine is a delayed marker, so there is intense research into earlier biomarkers, including neutrophil gelatinase associated lipocalin, kidney injury molecule 1 and cystatin C, which may detect injury before functional decline is evident.

Management focuses on identifying and reversing the cause, optimizing hemodynamics, avoiding further nephrotoxins and carefully managing fluids and electrolytes. In severe cases, renal replacement therapy with dialysis is required. Studies highlight that even mild AKI episodes increase long term risks of chronic kidney disease, cardiovascular events and mortality.

Current research priorities include refining risk prediction tools, validating early biomarkers, better understanding the transition from AKI to chronic kidney disease and testing interventions that could protect or regenerate kidney tissue, such as cell based therapies and pharmacologic agents targeting inflammation and oxidative stress.