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Adverse renal effects of anti-inflammatory agents: evaluation of selective and nonselective cyclooxygenase inhibitors Gambaro G; Perazella MAJ Intern Med 2003[Jun]; 253 (6): 643-52Conventional 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.|Acute Kidney Injury/*chemically induced/metabolism/physiopathology[MESH]|Animals[MESH]|Anti-Inflammatory Agents, Non-Steroidal/*adverse effects/metabolism[MESH]|Contraindications[MESH]|Cyclooxygenase 2[MESH]|Cyclooxygenase 2 Inhibitors[MESH]|Cyclooxygenase Inhibitors/*adverse effects/metabolism[MESH]|Edema/metabolism[MESH]|Glomerular Filtration Rate/drug effects[MESH]|Humans[MESH]|Hypertension, Renal/chemically induced/metabolism[MESH]|Isoenzymes/metabolism[MESH]|Kidney/*drug effects/metabolism/physiopathology[MESH]|Leukotrienes/metabolism[MESH]|Membrane Proteins[MESH]|Prostaglandin-Endoperoxide Synthases/metabolism[MESH]|Prostaglandins/metabolism[MESH] |
