COX-2 inhibitors and the kidney

Cyclooxygenase-2 (COX-2) selective inhibitors are now extensively used for their anti-inflammatory and analgesic efficacy. Several large controlled trials provide evidence to support the proposition that they cause fewer major gastro-intestinal side effects and less toxicity than routine nonsteroidal antiinflammatory drugs (NSAIDs). In view of the documented different localizations of the cyclooxygenase-1 and COX-2 enzymes in the kidney, it was initially hoped that COX-2 inhibitors would be associated with fewer renal side effects than other NSAIDs. This has not been borne out by subsequent studies. Like other NSAIDs, COX-2 inhibitors can cause salt and water retention, leading to edema and worsening hypertension. They can also cause acute declines in renal function and glomerular filtration rate. These events are, however, uncommon in large rheumatology populations and infrequently lead to discontinuation of the medications. Judicious use of COX-2 inhibitors in high-risk patients (such as those with chronic renal insufficiency, diabetes or congestive heart failure) will lead to a decreased incidence of adverse renal events.