The pathogenic mechanism of hepatorenal syndrome is not well established.
Dr Luis Ruiz-del-Arbol and colleagues investigated the circulatory function in cirrhosis before and after the development of hepatorenal syndrome.
The investigators measured systemic and hepatic hemodynamics and the activity of endogenous vasoactive systems.
The investigative team included 66 patients who had cirrhosis with tense ascites and normal serum creatinine levels.
The team repeated measurements at follow-up in 27 cases in whom hepatorenal syndrome had developed.
|Hepatorenal syndrome occurred with a reduction in mean arterial pressure from 83 mmHg to 75 mmHg|
At baseline, the team found that mean arterial pressure and cardiac output were significantly higher in patients who did not develop hepatorenal syndrome.
Hepatic venous pressure gradient, plasma renin activity, and norepinephrine concentration were lower compared with those presenting with this complication.
The investigators noted that peripheral vascular resistance was decreased to the same extent in the 2 groups.
The team showed that plasma renin activity and cardiac output were the only independent predictors of hepatorenal syndrome.
The investigators observed that hepatorenal syndrome occurred in the setting of a significant reduction in mean arterial pressure from 83 mmHg to 75 mmHg.
Hepatorenal syndrome occurred with a reduction of cardiac output from 6 L/min to 5 L/min, and wegded pulmonary pressure from 9 mmHg 8 mmHg.
The team also found that hepatorenal syndrome occurred with an increase in plasma renin activity from 10 to 18 ng/mL.
An increase in norepinephrine concentration from 571 to 965 pg/mL, and increases in hepatic venous pressure gradient were observed with hepatorenal syndrome.
The team observed no changes in peripheral vascular resistance.
Dr Ruiz-del-Arbol's team concludes, “These data indicate that hepatorenal syndrome is the result of a decrease in cardiac output in the setting of a severe arterial vasodilation.”