Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/44185
Title: Renal dysfunction as a consequence of acute liver damage by bile duct ligation in cirrhotic rats
Author: Rivera-Huizar, S.
Rincon-Sanchez, A.R.
Covarrubias-Pinedo, A.
Islas-Carbajal, M.
Gabriel-Ortiz, G.
Pedraza-Chaverri, J.
Alvarez-Rodriguez, A.
Meza-Garcia, E.
Armendariz-Borunda, J.
Issue Date: 2006
Abstract: Renal failure is a common complication in patients with alcohol-induced cirrhosis who undergo a superimposed severe alcoholic hepatitis. Aim: Our aim was to evaluate renal dysfunction established as a consequence of acute liver damage (ALD) induced by bile duct ligation (BDL) in cirrhotic rats. Hepatic and renal functional assays were performed. Results: Hiperbilirubinemia and increased alanine aminotransferase and aspartate aminotransferase (p < 0.05) in rats with BDL were observed since the first day of bile obstruction in cirrhotic rats. Urinary volume and urinary sodium concentration showed a significant reduction (p < 0.05) on days 3 and 5 after BDL. Plasma renin activity, plasma renin concentration, serum creatinine, and BUN values increased (p < 0.05) from day 1 to day 7 after BDL. Glomerular filtration rate was substantially decreased from day 1 to day 7. Histological changes became apparent since day 3 after BDL in which glomeruli with mesangial hipercellularity took place in the absence of tubular necrosis; with portal inflammation and proliferation of biliar conduits. Results of the present work demonstrate that ALD induced by BDL in cirrhotic rats produces changes in renal function. In conclusion, this experimental model demonstrates that an ALD of variable etiology, either surgical or induced by CCl4, can cause important damage that eventually results in renal function deterioration. This experimental model may be suitable, to study the physiopathology of this syndrome, as well as for the evaluation of different pharmacological therapies. � 2006 Elsevier GmbH. All rights reserved.
URI: http://www.scopus.com/inward/record.url?eid=2-s2.0-33750314611&partnerID=40&md5=6203a290d143c7df857f424ab56d3591
http://hdl.handle.net/20.500.12104/44185
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