Objective: Hepatorenal syndrome (HRS) is a life-threatening complication of end-stage liverdisease. Better knowledge of the disease may contribute to targeted and quick diagnosis andeffective treatment of those affected. In the present paper, an overview of hepatorenal syndrome ispresented, including the most recent advances in pathophysiology; as well as diagnostic, clinicaland therapeutic aspects.
Methods: Review of literature presented over the last 10 years by searching through the PubMedand Cochrane databases using the terms “hepatorenal syndrome”, “cirrhosis AND acute renalfailure” ,” cirrhosis AND hepatorenal syndrome". I have also looked over some review-articles thatwere most frequently cited by other authors.
Results and conclusion: HRS is best described as an acute functional kidney failure (AKI),resulting from severe impairment in systemic circulatory function seen in the advanced stages ofcirrhosis. The pathophysiological hallmark is intense renal vasoconstriction, which traditionally hasbeen considered to be the consequence of the extreme splanchnic arterial vasodilatation occurring inthese patients. However, recent data indicate that a reduction in cardiac output also plays asignificant role, and that HRS in cirrhosis is a complex syndrome that affects organs other than thekidney. HRS is a diagnosis of exclusion and all other causes of acute renal failure have to beconsidered and ruled out. Despite its functional nature, the prognosis is very poor.The most recent advances in the understanding of the pathophysiology of HRS are the basis of thenew therapeutic interventions. Until recently, liver transplantation was the only viable option fortreatment. More recently, several studies have been performed to unravel newer promisingtreatment modalities. Combined use of vasoconstrictors and albumin can act as bridges to earlyliver transplantation (or combined liver-kidney transplantation in selected patients). However,further research is necessary to determine its clinical usefulness.