Renal prostaglandins are gaining increasing recognition as important modulators of hemodynamics and excretory function in the mammalian kidney. Synthesis of these unsaturated fatty acids from arachidonate precursors is closely regulated by intrarenal factors, and circulating angiotensin II, catecholamines, arginine vasopressin and bradykinin. Endogenous prostaglandins exert little influence on renal blood flow and glomerular filtration rate in the basal state, but inhibition of arachidonate metabolism when renal perfusion is impaired causes marked alterations in these parameters. Renal salt and water excretion is modified by the effects of prostaglandins on glomerular filtration rate, proximal tubule fluid reabsorption, medullary solute gradients, and the intrinsic water and ion reabsorptive properties of distal nephron segments. Prostaglandins also mediate renin release under basal conditions and in response to intravascular volume depletion. Abnormalities of renal prostaglandins are evident in various clinical disorders of renal function including hypertension, ureteral obstruction, Bartter syndrome, hypokalemic nephropathy and drug-induced disorders of water metabolism. Appropriate clinical use of nonsteroidal anti-inflammatory agents requires consideration of the potential renal consequences of inhibiting prostaglandin biosynthesis.