Letters To The Editor
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Jan 7, 2009; 15(1): 121-123
Published online Jan 7, 2009. doi: 10.3748/wjg.15.121
Bile duct ligation in rats: A reliable model of hepatorenal syndrome?
Stelios F Assimakopoulos, Constantine E Vagianos
Stelios F Assimakopoulos, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece
Constantine E Vagianos, First Surgical Department, “Saint Panteleimon” General Hospital of Nikaia, Piraeus 18454, Greece
Author contributions: Assimakopoulos SF wrote this commentary and Vagianos CE revised it.
Correspondence to: Stelios F Assimakopoulos, MD, PhD, Department of Internal Medicine, School of Medicine, University of Patras, Vironos 18, 26224, Patras, Greece. sassim@upatras.gr
Telephone: +30-2610-346946
Fax: +30-2610-990775
Received: October 18, 2008
Revised: December 6, 2008
Accepted: December 13, 2008
Published online: January 7, 2009
Abstract

The two most widely used experimental models of advanced liver disease are the administration of carbon tetrachloride, and common bile duct ligation (BDL), however, neither has been systematically evaluated as a model of hepatorenal syndrome (HRS). The BDL model in rats, studied at diverse time points, induced a progressive renal dysfunction without structural changes in the kidney. The authors concluded that BDL is a good model for further studies of HRS and its treatment. However, the renal impairment observed at the acute phase of the BDL model is based on a different pathophysiology than that of HRS. Specifically, in acute obstructive jaundice, cholemia predominates over parenchymal liver disease (reversible at this stage without portal hypertension or cirrhosis) and independently induces negative inotropic and chronotropic effects on the heart, impaired sympathetic vasoconstriction response and profound natriuresis and diuresis that might lead to volume depletion. In addition, systemic endotoxemia contributes to the prerenal etiology of renal impairment and promotes direct nephrotoxicity and acute tubular necrosis. On the other hand, the renal failure observed in the chronic BDL model (with development of biliary cirrhosis, portal hypertension and ascites) shares pathophysiological similarities with HRS, but the accordance of the chronic BDL model to the diagnostic criteria of HRS (e.g. absence of spontaneous bacterial peritonitis, no renal function improvement after plasma volume expansion) should have been confirmed. In conclusion, we think that the BDL model is not suitable for the study of the natural history of HRS, but the chronic BDL model might be valid for the study of established HRS and its potential therapies.

Keywords: Obstructive jaundice; Rats; Bile duct ligation; Hepatorenal syndrome; Renal failure