Gambaro G, Perazella M A
Department of Medical and Surgical Sciences, Division of Nephrology, University Hospital, Padua, Italy.
J Intern Med. 2003 Jun;253(6):643-52. doi: 10.1046/j.1365-2796.2003.01146.x.
Conventional nonsteroidal anti-inflammatory drugs (NSAIDs), i.e. nonselective cyclooxygenase COX inhibitors have well-documented nephrotoxicity. Adverse renal effects occur because of inhibition of the synthesis of cyclooxygenase-derived prostaglandins which act to modulate pathologic processes that would normally impair various renal functions. The introduction of the selective COX-2 inhibitors raised hope that this class of drugs would reduce injury in both the gastrointestinal tract and the kidneys. Animal and human data, however, suggest that COX-2 synthesized prostaglandins are important in the modulation of renal physiology during adverse conditions. Hence, it appears that these drugs are equal in causing nephrotoxicity as the nonselective COX inhibitors.
传统的非甾体抗炎药（NSAIDs），即非选择性环氧化酶COX抑制剂，具有充分记录的肾毒性。由于抑制了环氧化酶衍生的前列腺素的合成，从而产生不良肾脏效应，而这些前列腺素的作用是调节通常会损害各种肾功能的病理过程。选择性COX-2抑制剂的引入带来了希望，即这类药物将减少胃肠道和肾脏的损伤。然而，动物和人类数据表明，COX-2合成的前列腺素在不利条件下对肾脏生理调节中很重要。因此，看来这些药物在引起肾毒性方面与非选择性COX抑制剂相当。
