Clinical acute renal failure with nonsteroidal anti-inflammatory drugs

Abstract

Under baseline euvolemic conditions, prostaglandins play little to no role in the minute-to-minute regulation of renal function. Where these compounds come to serve a major role is in the setting of a systemic or intrarenal circulatory disturbance. In the setting of a decreased absolute or effective circulatory volume, a number of vasoconstrictor effectors are stimulated whose function is to preserve the systemic circulation. At the same time, these compounds stimulate the synthesis of renal vasodilatory prostaglandins. In turn, prostaglandins oppose the vasoconstrictive effect of these effectors such that the renal circulation remains well-preserved while the rest of the circulation is clamped down. Predictably, inhibition of prostaglandin synthesis would lead to unopposed renal vasoconstriction, resulting in a precipitous decline in renal function. Clinical conditions in which the renal circulation is critically dependent on the effect of vasodilatory prostaglandins include volume depletion, congestive heart failure, and cirrhosis. There are other conditions in which the circulatory volume is normal, but due to the intrarenal generation of vasoconstrictors, the kidney is similarly dependent on vasodilatory prostaglandins. Such conditions include glomerulonephritis and urinary tract obstruction.