Effects of bile duct ligation on calcium excretion in the rat

Authors

  • Nimish Vakil M.D., F.A.C.P.,

    Corresponding author
    1. Divisions of Gastroenterology and Nephrology, Department of Medicine, University of Rochester, Rochester, New York 14642
    • University of Wisconsin Medical School–Milwaukee Campus, 945 North 12th Street, A 324 A, Milwaukee, WI 53233
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  • Anil Sharma,

    1. Divisions of Gastroenterology and Nephrology, Department of Medicine, University of Rochester, Rochester, New York 14642
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  • Yoram Yagil

    1. Divisions of Gastroenterology and Nephrology, Department of Medicine, University of Rochester, Rochester, New York 14642
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  • Presented in part at the American Gastroenterological Association Annual Meeting, San Francisco, 1992.

Abstract

In an earlier study we showed that bile duct–ligated rats were highly susceptible to gentamicin nephrotoxicity and that oral calcium administration had a pronounced protective effect. The mechanism by which this occurs is unclear. Because cations compete with gentamicin for tubule binding sites, it has been suggested that the increased susceptibility of the kidney to gentamicin after bile duct ligation might result from decreased cation excretion. The aim of this study was to determine the effect of bile duct ligation on calcium excretion in relation to overall renal function. Male Sprague-Dawley rats underwent bile duct ligation and division. Pair-fed sham-operated rats served as controls. Metabolic and clearance studies were carried out at 3, 5, 7, 14 and 21 days after surgery. Urine output was higher in bile duct–ligated rats, and they excreted more calcium at 3, 5, 7 and 14 days, while excreting less sodium than controls. We conclude that after bile duct ligation, there is increased calcium excretion, which is independent of the abnormality in sodium excretion. Enhanced nephrotoxicity with aminoglycosides in the bile duct–ligated rat model cannot be explained by decreased calcium excretion. (Hepatology 1994;19:457–463).

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