Urinary thromboxane B2 and prostaglandin E2 in the hepatorenal syndrome: Evidence for increased vasoconstrictor and decreased vasodilator factors

Abstract Vasodilatory prostaglandins function to maintain renal perfusion in patients with cirrhosis and ascites. To evaluate the potential contribution of the vasodilator prostaglandin E 2 and the vasoconstrictor metabolite thromboxane B 2 to the development of the hepatorenal syndrome, we measured urinary excretion of these products in 14 patients with hepatorenal syndrome and in control populations with acute or chronic liver or kidney failure. Radioimmunoassay measurements were confirmed by bioassay and by mass spectrometry. Prostaglandin E 2 was decreased compared with healthy controls (2.2 ± 0.3 vs. 6.3 ± 0.8 ng/h, p 2 concentration was normal in patients with alcoholic hepatitis (0.12 ± 0.02 vs. 0.15 ± 0.03 ng/ml) and minimally increased in acute renal failure (0.18 ± 0.15 ng/ml), but markedly elevated in hepatorenal syndrome (0.69 ± 0.15 ng/ml, p 2 concentration fell with improved renal function in 3 patients who survived. These data suggest an imbalance of vasodilator and vasoconstrictor metabolites of arachidonic acid in patients with the hepatorenal syndrome.