NSAIDS acute kidney injury is one of the common clinical adverse drug reactions, most of which can recover on their own after drug discontinuation, while a few can cause severe kidney damage or even death. Pathogenesis: NSAIDS can lead to two different types of acute kidney injury: 1. Hemodynamically mediated acute kidney injury, such as renal anterior injury and/or acute tubular necrosis. Prostaglandins can dilate the small renal inflow arteries, increasing renal blood perfusion and glomerular filtration rate, and thus are essential for maintaining both renal blood supply and renal filtration function. NSAIDS reduces PG production through inhibition of COX, resulting in a decrease in renal blood perfusion and glomerular filtration rate, causing acute renal functional and structural damage, and in severe cases, even tubular necrosis. This inhibition is reversible, and both the efficacy and toxicity are closely related to the blood concentration. Therefore, toxic side effects usually occur at steady-state plasma concentrations where COX activity is maximally inhibited, usually in 3-7 days. 2. Immune-mediated acute kidney injury, such as acute interstitial nephritis. The exact mechanism by which NSAIDS causes acute interstitial nephritis is not yet clear. It has been proposed that the preferential conversion of arachidonic acid to leukotrienes caused by the inhibition of COX triggers the onset of autoimmune reactions.