[Urinary prostaglandins in the hepatorenal syndrome of cirrhotic patients: role of thromboxane A2 and an imbalance of precursor polyunsaturated fatty acids].

The hepatorenal syndrome is considered to be a functional renal failure due to active renal vasoconstriction. The purpose of this work was to study the urinary elimination of prostaglandins and the plasmatic polyunsaturated fatty acid precursors of prostaglandins. The urinary elimination of PGE2 was not significantly different in the groups of patients studied: controls, group I (193 +/- 42 ng/24 h), cirrhotic patients without ascites, group II (274 +/- 43 ng/24 h), cirrhotic patients with ascites, group III (269 +/- 41 ng/24 h). The urinary elimination of PGE1 and PGF2 alpha varied in the same way as PGE2. In cirrhotics with hepatorenal syndrome (group IV) the urinary elimination of vasodilating prostaglandins was greatly decreased (p less than 0.001); PGE2 (53 +/- 16 ng/24 h), PGE1 (65 +/- 11 ng/24 h). The urinary elimination of PGF2 alpha was also decreased (293 +/- 75 ng/24 h). On the other hand, the urinary elimination of thromboxane, a vasoconstrictor, increased progressively from group I (287 +/- 75 ng/24 h) to group IV (980 +/- 266 ng/24 h) (p less than 0.05). Plasmatic arachidonic acid was significantly decreased in group IV (5.0 +/- 0.6 p. 100) compared to group I (10.0 +/- 0.6 p. 100) (p less than 0.001), to group II (10.3 +/- 0.5 p. 100) (p less than 0.001), and to group III (8.5 +/- 0.7 p. 100) (p less than 0.05). In conclusion, in hepatorenal patients, urinary excretion of a vasoconstricting prostaglandin (thromboxane) is increased while urinary excretion of vasodilating prostaglandins is decreased. This decrease could be secondary to a lack of plasmatic arachidonic acid, precursor of prostaglandins.