THE NONSTEROIDAL anti-inflammatory drugs (NSAIDs), whose volume of use is among the highest of all therapeutic agents, function as anti-inflammatory modalities by inhibiting the production of prostaglandins involved in inflammation. As a corollary, prostaglandin inhibition also causes the most common form of NSAID-induced kidney impairment.1
Within the kidney, prostaglandins, primarily prostaglandin E2 and prostaglandin I2, are synthesized in discrete regions along the course of the nephron. Their effects are localized to the immediate areas of origin.2 Stimulation of intrarenal prostaglandin production causes dilatation of the renal vasculature, reduces salt and water reabsorption, and increases renin release. During a normal state of volemia, production of these prostaglandins is minimal, and they have little part to play in minute to minute regulation of renal function. However, in clinical situations with decreased effective blood volume, their role may become critical. Such situations include congestive heart failure, cirrhosis, nephrotic syndrome,