Copyright ©2010 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Nov 7, 2010; 16(41): 5139-5147
Published online Nov 7, 2010. doi: 10.3748/wjg.v16.i41.5139
Terlipressin and hepatorenal syndrome: What is important for nephrologists and hepatologists
Ahmed A Magan, Atif A Khalil, Mohamed H Ahmed
Ahmed A Magan, Department of Surgery, Cambridge University Hospital NHS foundation Trust, Hills Road, Cambridge CB2 0QQ, United Kingdom
Atif A Khalil, Department of Nephrology, Royal Liverpool and Broadgreen University Hospitals, Liverpool L7 8XP, United Kingdom
Mohamed H Ahmed, Division of Acute Medicine, James Cook University Hospital, Marton Road, Middlesbrough TS4 3BW, United Kingdom
Author contributions: All authors contributed equally to the manuscript.
Correspondence to: Mohamed H Ahmed, MD, PhD, Division of Acute Medicine, James Cook University Hospital, Marton Road, Middlesbrough TS4 3BW, United Kingdom. elziber@yahoo.com
Telephone: +44-1642-854501 Fax: +44-1642-835507
Received: May 1, 2010
Revised: June 7, 2010
Accepted: June 14, 2010
Published online: November 7, 2010

Hepatorenal syndrome (HRS) is a reversible form of functional renal failure that occurs with advanced hepatic cirrhosis and liver failure. Despite mounting research in HRS, its etiology and medical therapy has not been resolved. HRS encompasses 2 distinct types. Type 1 is characterized by the rapid development of renal failure that occurs within 2 wk and involves a doubling of initial serum creatinine. Type 2 has a more insidious onset and is often associated with ascites. Animal studies have shown that both forms, in particular type 1 HRS, are often precipitated by bacterial infections and circulatory changes. The prognosis for HRS remains very poor. Type 1 and 2 both have an expected survival time of 2 wk and 6 mo, respectively. Progression of liver cirrhosis and the resultant portal hypertension leads to the pooling of blood in the splanchnic vascular bed. The ensuing hyperdynamic circulation causes an ineffective circulatory volume which subsequently activates neurohormonal systems. Primarily the sympathetic nervous system and the renin angiotensin system are activated, which, in the early stages of HRS, maintain adequate circulation. Both advanced cirrhosis and prolonged activation of neurohormonal mechanisms result in fatal complications. Locally produced nitric oxide may have the potential to induce a deleterious vasodilatory effect on the splanchnic circulation. Currently medical therapy is aimed at reducing splanchnic vasodilation to resolve the ineffective circulation and maintain good renal perfusion pressure. Terlipressin, a vasopressin analogue, has shown potential benefit in the treatment of HRS. It prolongs both survival time and has the ability to reverse HRS in the majority of patients. In this review we aim to focus on the pathogenesis of HRS and its treatment with terlipressin vs other drugs.

Keywords: Heptorenal syndrome, Terlipressin, Kidney, Liver