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      Acute Bile Duct Ligation Ameliorates Ischemic Renal Failure

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          Background: Biliary obstruction affects the renal response to ischemia and also elicits a hepatic cytokine response. Using a murine model, we now test the hypothesis that these hepatic cytokines help determine the outcome of ischemic acute renal failure. Methods: C3H/HEN mice were subjected to bile duct ligation 24 h (ABDL) or 7 days (CBDL) prior to induction of acute ischemic renal failure (ARF). Serum creatinine (Scr), cytokine mRNA abundance, and renal histology were studied 24 h after renal ischemia. Results: ABDL prior to ARF resulted in amelioration of renal injury (Scr 0.7 ± 0.1 mg/dl compared to 2.5 ± 0.1 mg/dl in sham/ARF group, (mean ± SE, n = 11/group). CBDL exacerbated renal injury. Increased hepatic mRNA for interleukin-10 (IL10) and interleukin-1 receptor antagonist (IL1RA) was detected in the ABDL/ARF group but not in the CBDL/ARF group. These data suggest that hepatic production of IL10 and IL1RA in response to ABDL ameliorates ischemic ARF, an effect that is lost after several days of BDL. Conclusion: Our data support the concept that hepatic cytokines modulate renal injury. This adds a new dimension in our understanding of renal injury in the setting of hepatic disease.

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          Most cited references 11

          • Record: found
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          The role of the interleukin-1-receptor antagonist in blocking inflammation mediated by interleukin-1.

           C Dinarello (2000)
            • Record: found
            • Abstract: not found
            • Article: not found

            Identification of the CD4+ T cell as a major pathogenic factor in ischemic acute renal failure

              • Record: found
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              • Article: not found

              IL-1 receptor antagonist prevents apoptosis and caspase-3 activation after spinal cord injury.

               Y. Xu,  O Nesic,  K High (2001)
              One of the consequences of cytokine-orchestrated inflammation after CNS trauma is apoptosis. Our hypothesis is that cell death in the spinal cord after injury results in part from increased synthesis and release of IL-1beta. Using a ribonuclease protection assay, we demonstrated that there is increased transient expression of IL-1beta mRNA and, by using IL-1beta protein ELISA assay, that there are increased IL-1beta protein levels in the contused rat spinal cord, initially localized to the impact region of the spinal cord (segment T8). Using an ELISA cell death assay, we showed that there is apoptosis in the spinal cord 72 h after injury, a finding that was confirmed by measuring caspase-3 activity, which also significantly increased at the site of injury 72 h after trauma. Treatment of the contused spinal cord at the site of injury with the IL-1 receptor antagonist (rmIL-lra, 750 ng/mL) for 72 h using an osmotic minipump completely abolished the increases in contusion-induced apoptosis and caspase-3 activity.

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                October 2003
                12 November 2003
                : 95
                : 2
                : p28-p35
                Departments of aSurgery, bInternal Medicine (Division of Nephrology), cPathology, and dDivision of Cell and Molecular Biology (Graduate Program in Immunology), Southwestern Medical School, Dallas, Tex., USA
                73677 Nephron Physiol 2003;95:p28–p35
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 6, References: 42, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/73677
                Original Paper


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