Selective
cyclooxygenase-2 (COX-2) inhibitors have provided relief for patients suffering from
chronic pain and other inflammatory conditions and have reduced adverse gastrointestinal effects. The documented reduction in gastric erosions, ulcerations, and perforations during the use of COX-2-selective inhibitors raises the question: would the kidney be similarly spared? Our understanding of these
enzyme isoforms in the kidney is incomplete. However, kidney tissue seems to possess "constitutive" or homeostatic COX-2
enzyme, suggesting a role for
prostaglandins produced by this
isoform. In addition, studies evaluating the renal effects of the selective nonsteroidal anti-inflammatory drugs (
NSAIDs) are inconclusive, and available data on the renal effects of COX-2-selective inhibitors are conflicting. Inadequate numbers, varied baseline patient characteristics, and different doses and lengths of
drug treatment hampers comparison of the small number of clinical investigations available for review. Therefore, this article reviews the role of
cyclooxygenase enzyme activity and associated
prostaglandins in the kidney and the adverse renal effects of nonselective
NSAIDs. We also touch on the COX-1/COX-2 selectivity of
NSAIDs, the localization of COX
enzymes in kidneys, and clinical studies examining the renal effects of selective
COX-2 inhibitors.