NSAID nephrotoxicity

Wai Y. Tse and Dwomoa Adu

in Rheumatology and the Kidney

Second edition

Published on behalf of Oxford University Press

Published in print April 2012 | ISBN: 9780199579655
Published online February 2013 | e-ISBN: 9780191763472 | DOI:

Series: Oxford Clinical Nephrology Series

NSAID nephrotoxicity

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1. Although uncommon, the widespread use of NSAIDs means that renal complications are likely to be seen frequently. 2. Two isoforms of COX (COX-1 and COX-2) have been identified in mammalian cells. COX-1, which is constitutively expressed, mediates gastric cytoprotection and vascular homeostasis. COX-2 expression is regulated by salt and water intake, medullary tonicity, growth factors, cytokines and adrenal steroids and produces prostaglandins in inflamed tissues. 3. Constitutive COX-2 mRNA, as well as inducible COX-2 mRNA, is present in the kidney. 4. In circumstances where there is poor renal perfusion with high renin levels, non-selective and COX-2 selective NSAIDs can reduce glomerular filtration rate resulting in acute renal failure. 5. Acute renal failure and hyperkalaemia have been observed after the administration of COX-2 selective inhibitors to patients with risk factors for NSAID-induced acute renal insufficiency. 6. NSAIDs of different chemical classes have been associated with acute tubulo-interstitial nephritis and renal failure. 7. On balance, it seems likely that chronic usage of NSAIDs may be associated with a slightly increased risk for the development of chronic renal failure. 8. Both non-selective NSAIDs and COX-2 inhibitors can raise blood pressure especially in hypertensive, elderly patients and there is no substantial evidence to suggest that COX-2 inhibitors are safer in this respect.

Chapter.  7890 words.  Illustrated.

Subjects: Nephrology

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