Circulatory function and hepatorenal syndrome in cirrhosis

Authors

  • Luis Ruiz-del-Arbol,

    Corresponding author
    1. Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, Spain
    • Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, Ctra. de Colmenar Viejo Km 9.1, 28034 Madrid, Spain
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    • fax: (34) 91-336-80-85

  • Alberto Monescillo,

    1. Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, Spain
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  • Carlos Arocena,

    1. Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, Spain
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  • Paz Valer,

    1. Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, Spain
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  • Pere Ginès,

    1. Liver Unit, Institute of Digestive and Metabolic Diseases, Hospital Clínic, Institut d'Investigacions Biomèdiques, August Pi-Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain
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  • Víctor Moreira,

    1. Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, Spain
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  • José María Milicua,

    1. Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, Spain
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  • Wladimiro Jiménez,

    1. Hormonal Laboratory, IDIBAPS, Hospital Clinic, University of Barcelona, Barcelona, Spain
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  • Vicente Arroyo

    1. Liver Unit, Institute of Digestive and Metabolic Diseases, Hospital Clínic, Institut d'Investigacions Biomèdiques, August Pi-Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain
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  • Potential conflict of interest: Nothing to report.

Abstract

The pathogenic mechanism of hepatorenal syndrome is not well established. We investigated the circulatory function in cirrhosis before and after the development of hepatorenal syndrome. Systemic and hepatic hemodynamics and the activity of endogenous vasoactive systems were measured in 66 patients who had cirrhosis with tense ascites and normal serum creatinine levels; measurements were repeated at follow-up in 27 cases in whom hepatorenal syndrome had developed. At baseline, mean arterial pressure and cardiac output were significantly higher, and hepatic venous pressure gradient, plasma renin activity, and norepinephrine concentration were significantly lower in patients who did not develop hepatorenal syndrome compared with those presenting with this complication. Peripheral vascular resistance was decreased to the same extent in the two groups. Plasma renin activity and cardiac output were the only independent predictors of hepatorenal syndrome. Hepatorenal syndrome occurred in the setting of a significant reduction in mean arterial pressure (83 ± 9 to 75 ± 7 mmHg; P < .001), cardiac output (6.0 ± 1.2 to 5.4 ± 1.5 L/min; P < .01), and wegded pulmonary pressure (9.2 ± 2.6 to 7.5 ± 2.6 mmHg; P < .001) and an increase in plasma renin activity (9.9 ± 5.2 to 17.5 ± 11.4 ng/mL · hr; P < .001), norepinephrine concentration (571 ± 241 to 965 ± 502 pg/mL; P < .001), and hepatic venous pressure gradient. No changes were observed in peripheral vascular resistance. In conclusion, these data indicate that hepatorenal syndrome is the result of a decrease in cardiac output in the setting of a severe arterial vasodilation. (HEPATOLOGY 2005.)

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