Renal sodium retention complicating alcoholic liver disease: Relation to portosystemic shunting and liver function

Authors

  • William G. Rector Jr. M.D.,

    Corresponding author
    1. Department of Medicine, Division of Gastroenterology, University of Colorado Health Sciences Center, Denver General Hospital, Denver, Colorado 80204
    • Box 4001, Denver General Hospital, 777 Bannock St., Denver, CO 80204
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  • Frederick Lewis,

    1. Department of Medicine, Division of Gastroenterology, University of Colorado Health Sciences Center, Denver General Hospital, Denver, Colorado 80204
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  • Alastair D. Robertson,

    1. Department of Medicine, Division of Gastroenterology, University of Colorado Health Sciences Center, Denver General Hospital, Denver, Colorado 80204
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  • Gregory T. Everson

    1. Department of Medicine, Division of Gastroenterology, University of Colorado Health Sciences Center, Denver General Hospital, Denver, Colorado 80204
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    • With the technical assistance of Georgia DeRoche.


Abstract

The aim of this study was to determine whether liver function and portosystemic shunting are related to renal sodium retention in alcoholic liver disease. Twenty-three studies were performed; 10 patients had ascites. Liver function was assessed from the plasma elimination rates of antipyrine, caffeine and stable isotopes of cholic acid, the latter administered both orally [2,2,4,4-2H] and intravenously [24-13C]. Portosystemic shunt fraction was calculated as the ratio of the intravenous and oral clearances of the isotopes of cholic acid.

Portosystemic shunt fraction was similar in patients with and without ascites (61% ± 16% vs. 64% ± 11%) and unrelated to urinary sodium excretion in patients with ascites (r = −0.145). Patients with ascites had significantly lower elimination rates of all administered compounds as compared with patients without ascites (antipyrine = 0.012 ± 0.007 vs. 0.031 ± 0.016/hr, p < 0.001; caffeine = 0.014 ± 0.013 vs. 0.061 ± 0.041/hr, p < 0.002; intravenous cholic acid = 1.355 ± 0.442 vs. 2.284 ± 0.885/hr, p = 0.005; orally administered cholic acid = 2.178 ± 0.841 vs. 4.056 ± 1.837/hr, p = 0.007). However, urinary sodium excretion in patients with ascites was not related to the elimination constants of these compounds (r = 0.360, 0.319, 0.067, –0.073, respectively).

Ascites complicating alcoholic liver disease is associated with impaired liver function but not the extent of portosystemic shunting. (HEPATOLOGY 1990;12:455–459).

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