Journal
JOURNAL OF INTERNAL MEDICINE
Volume 253, Issue 6, Pages 643-652Publisher
WILEY
DOI: 10.1046/j.1365-2796.2003.01146.x
Keywords
cyclooxygenase; hypertension; nonsteroidal anti-inflammatory drugs; oedema; renal failure
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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.
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