Renal eicosanoids as determinants of renal function in liver disease.

The available data suggest that alterations in renal prostaglandin metabolism participate in the pathogenesis of at least two prominent renal complications of liver disease: (a) sodium retention and (b) HRS. Although the data are highly suggestive, additional studies, including experimental manipulations that augment vasodilatory prostaglandins while diminishing vasoconstrictor metabolites of arachidonic acid, will be required to establish the role of prostaglandins or other arachidonic acid metabolites in mediating these renal abnormalities. The clinical caveat emerging from these observations is that every attempt should be made to avoid prescribing drugs which possess cyclooxygenase inhibitory activity to patients with decompensated liver disease who are sodium-avid.