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NSAID nephrotoxicity 

NSAID nephrotoxicity
Chapter:
NSAID nephrotoxicity
Author(s):

Wai Y. Tse

and Dwomoa Adu

DOI:
10.1093/med/9780199579655.003.0136
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date: 23 September 2020

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.

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