Abstract
In the clinical setting of reduced renal perfusion, as seen in patients with renal, cardiac, or liver disease, dehydration, or aging kidneys, renal prostaglandin production (mediated primarily by cyclooxygenase [COX]-1 and possibly by COX-2) plays a major role in compensatory renal hemodynamics. Inhibition of the synthesis of renal prostaglandins by conventional nonsteroidal anti-inflammatory drugs (NSAIDs) may result in several nephrotoxic syndromes, including fluid and electrolyte abnormalities, acute renal failure, nephrotic syndrome, and renal papillary necrosis. Moreover, NSAIDs may adversely influence blood pressure control in treated hypertensive individuals and also may decompensate the clinical stability of diuretic-treated patients with chronic heart failure. The recently approved COX-2–specific inhibitors celecoxib and rofecoxib offer the potential for sparing homeostatic COX-1 activity in the kidney while inhibiting COX-2–mediated pain and inflammation. Emerging clinical data are helping to quantify the renal and related cardiovascular risks associated with the use of COX-2–specific versus conventional NSAIDs.
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