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Nephrol Dial Transplant (2002) 17: 1159-1162
© 2002 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Strategies to safely interfere with prostanoid activity while avoiding adverse renal effects: could COX-2 and COX-LOX dual inhibition be the answer?

Giovanni Gambaro

Department of Medical and Surgical Sciences, Division of Nephrology, University Hospital, Padua, Italy

Keywords: COX-2; Coxib; COX-LOX; non-steroidal anti-inflammatory drugs

The first 150 words of the full text of this article appear below.

Introduction

A major expectation of cyclo-oxygenase-2 (COX-2) inhibitor therapy has been the (Coxib) reduction of untoward renal effects of non-steroidal anti-inflammatory drugs (NSAIDs). The idea that COX-isoform functions are mutually exclusive, with COX-1 involved in maintenance of normal renal physiology and COX-2 not normally expressed but rapidly induced in response to inflammation, inspired hopes of exciting new therapeutic possibilities. However, recent reports of acute renal failure [1] and interstitial nephritis [2] in patients taking celecoxib or rofecoxib has dampened enthusiasm for these inhibitors. Evolving knowledge of the activities of COX-1 and COX-2 has indicated that the original paradigm was an over-simplification. While it is true that COX-2 is induced at inflammation sites and plays a major role in prostanoid synthesis, COX-1 may also contribute to these mechanisms [3]. However, and more important, a critical role for COX-2 in renal function has recently come to light . . . [Full Text of this Article]

COX-2 in renal pathology

Leukotrienes in renal disease

Putative risks of selective inhibition of prostanoid synthetic pathways

COX activity and thrombosis (COX-1 and -2 inhibition vs COX-2 inhibition)
Aspirin-intolerant asthma and inflammatory renal disease induced by NSAIDs (COX inhibition and LT-related disorders)
COX-LOX dual inhibition

Conclusion


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