The pathophysiologic role of prostaglandins in clinical renal disease is not fully understood. Animal models such as the ureteral-obstructed rabbit provide strong evidence that increased renal PGE2 synthesis may reduce renal vascular resistance and increase renal perfusion; whereas thromboxane A2 biosynthesis may increase renal vascular resistance in states of increased interstitial pressure. The effects of cyclooxygenase inhibitors to reduce renal blood flow may be beneficial in some patients with nephrotic syndrome. However, by inhibiting compensatory vasodilator prostaglandin synthesis in conditions of impaired renal perfusion such as cirrhosis with ascites, these drugs may also markedly impair renal function.
|Number of pages
|Mineral and Electrolyte Metabolism
|Published - 1981