Nonsteroidal anti-inflammatory drugs (NSAIDs) are a class of medications used for analgesic and anti-inflammatory benefits. NSAIDs can induce several different forms of kidney injury including hemodynamically mediated acute kidney injury (AKI); electrolyte and acid-base disorders; acute interstitial nephritis (AIN), which may be accompanied by the nephrotic syndrome; and papillary necrosis (table 1).
This topic reviews hemodynamically mediated AKI. The roles of NSAIDs in AIN, chronic kidney disease, and electrolytes disorders are discussed elsewhere. (See "Clinical manifestations and diagnosis of acute interstitial nephritis" and "Analgesic-related chronic kidney disease" and "NSAIDs: Electrolyte complications".)
The mechanism of action, therapeutic action, and non-renal-related adverse effects of NSAIDs are also discussed elsewhere. (See "NSAIDs: Mechanism of action" and "NSAIDs: Therapeutic use and variability of response in adults" and "Nonselective NSAIDs: Overview of adverse effects" and "Nonselective NSAIDs: Adverse cardiovascular effects".)
Adverse renal events occur in approximately 1 to 5 percent of all patients using NSAIDs . Because of the large number of patients that take NSAIDs (estimates of more than 70 million prescriptions and 30 billion over-the-counter doses annually), this translates to upwards of 2.5 million patients experiencing a nephrotoxic event annually .
AKI can occur with any class of traditional, nonselective NSAID or cyclooxygenase-2 (COX-2) specific NSAIDs [3-8]. As an example, in a nested case-control study that included 121,722 older patients, an increased risk of hospitalization within 30 days was associated with initiation of nonselective NSAIDs (other than naproxen), naproxen, rofecoxib, and celecoxib with relative risks (RR) of 2.3, 2.4, 2.3, and 1.5, respectively, compared with unexposed individuals .