Commentary: Renal Effects of Cyclooxygenase-2-Selective Inhibitors

Abstract

Since the discovery of the first nonselective nonsteroidal anti-inflammatory drug (NSAID), aspirin, in 1897, physicians have been managing NSAID-induced adverse events, including gastrointestinal ulceration and bleeding and renal effects (e.g., renal dysfunction, changes in blood pressure, peripheral edema, and hyperkalemia). The cyclooxygenase (COX)-2-specific inhibitors (coxibs) were developed as a safer alternative to NSAIDs in patients at risk for developing gastrointestinal toxicity. However, through inhibition of constitutive COX-2 in the kidneys, the production of prostaglandins, which are responsible for regulating electrolyte and water balance and vascular tone, may be decreased, leading to such renal effects as sodium and potassium retention, peripheral edema, and acute reversible renal dysfunction.