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G Ital Nefrol. 2002 Mar-Apr;19(2):199-203.

[Case report: reversible acute renal failure following therapy with both ketorolac (non-selective non-steroidal anti-inflammatory drug NSAID) and celecoxib (COX-2 selective) in the same patient].

[Article in Italian]

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U.O. Nefrologia e Dialisi, Ospedale Maggiore, Trieste, Italy.



We present the case of acute renal failure complicating the course of therapy with both ketorolac (non-selective Non-Steroidal Anti-inflammatory Drug, NSAID), and celecoxib (COX-2 Selective Inhibitor) in an elderly woman with chronic liver disease, heart failure and chronic renal failure. The main effect of NSAIDs is the inhibition of cyclooxygenase (COX), the enzyme involved in prostaglandins synthesis. The nephrotoxicity of NSAIDs is linked to this effect since prostaglandins not only act in response to inflammatory stimuli, but also play a role as modulators of some physiological renal functions. Under conditions of reduced renal perfusion, acute renal failure secondary to NSAIDs use may occur if the vasoconstrictive forces stimulated to maintain the filtrating function are not balanced by prostaglandin-induced vasodilatation. About ten years ago, two COX isoforms were demonstrated: COX-1 whose products are involved in regulating physiological functions and COX-2 which is expressed by a number of inflammatory stimuli. The discovery of molecular differences between COX-1 and COX-2 allowed the development of pharmacological agents selectively inhibiting COX-1 or COX-2. Selective inhibitors of COX-2 are now available. However, COX-1 products are involved in inflammatory reactions, whereas COX-2 products play a physiological role in many tissues and organs, including the kidney. These observations raised many doubts regarding the renal safety of COX-2 Inhibitors before they became commercially available. These doubts have been recently confirmed in the Literature.


The case we report seems to confirm that, in patients at risk, the renal adverse effects of non-selective NSAIDs and of COX-2 Inhibitors could be the same due to the similar physiological role of COX-1 and COX-2-dependent prostaglandins.

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