Renal consequences of prostaglandin inhibition in heart failure

Prostaglandins are products of intracellular arachidonate metabolism via the cyclooxygenase pathways. In the kidney, prostaglandins are modulators of afferent arteriole autoregulation. In diminished effective intravascular volume, vasodilatory prostaglandins reduce afferent arteriolar resistance, helping to maintain overall glomerular filtration. In subjects who have a low perfusion state, as in congestive heart failure, arthrosclerosis, hepatorenal syndrome, and cirrhosis, impaired renal autoregulation occurs, predisposing to kidney injury. Adverse effects of prostaglandin inhibition include acute kidney injury, hyperkalemia, hypertension, and edema. Hypertension and edema can occur because prostaglandins play an important role in renal regulation of salt and water balance. This review summarizes the renal consequences of using prostaglandin inhibitors in subjects who have congestive heart failure.