Kidney Function Impairment: Do Relevant Differences between Non-Steroidal Anti-Inflammatory Drugs Exist?

Non-steroidal anti-inflammatory drugs (NSAIDs) include such diverse substances as salicylates (aspirin, sodium salicylate, diflunisal, trisalicylate), pyra-zoles (phenylbutazone, oxyphenbutazone, azapropazone, feprazone), indene derivatives (indomethacin, sulindac, tolmetin, zomepirac), propionic acid derivatives (fenoprofen, flurbiprofen, ibuprofen, naproxen), fenamates (mefenamic acid, flufenamic acid), oxicams (piroxicam), and acetic acid derivatives (diclofenac, fenclofenac). The therapeutic effectiveness and a substantial part of the adverse effects (AEs) of NSAIDs have been attributed principally to their ability to decrease prostanoid formation by inhibition of the cyclooxygenase activity of prostaglandin endoperoxide synthase (EC 1.14.99.1), the initial enzyme in the synthetic pathway for prostaglandins (PGs) and thromboxanes (TXs) [1–3]. A good correlation exists between the rank order of potencies for inhibiting prostaglandin formation and the reduction of experimental edema in vivo [4]. Prostanoids sensitize peripheral nociceptors in the presence of a definite degree of tissue damage, which may explain why NSAIDs are not analgesic in the absence of inflammation. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.