A Review of Hepatorenal Syndrome

Abstract

Renal dysfunctions are not uncommon occurrences in liver cirrhosis and hepatorenal syndrome (HRS) is a major one with a very high morbidity and mortality. The major pathophysiological mechanisms have been mostly unravelled, consisting of splanchnic vasodilation and renal cortical vasoconstriction. These vascular anomalies stem from the endogenous release of vasodilatory biomolecules such as nitric oxide in the face of high hepatic sinusoidal pressure and portal hypertension. The vasodilatation leads to ineffective tissue perfusion and subsequently triggering the release of vasoconstricting substances via the renin-angiotensin-aldosterone system, thus leading to a vicious cycle. Therapeutic intervention is anchored on the reversal of the splanchnic vasodilation and renal ischaemia. Measures that have shown promise include the use of vasopressin analogues like terlipressin or ornipressin and alpha adrenergic agonists like midodrine and norepinephrine. The use of these vasoactive substances has been combined effectively with plasma expanders especially albumin infusion, using extracorporeal albumin dialysis (ECAD). The most effective therapy, however, is liver transplantation, though the mortality of this procedure is higher than in non-HRS patients. Transjugular intrahepatic portocaval shunt (TIPS) has also been found useful, with a good patient selection. Prevention of HRS is principally by prevention of precipitating factors like spontaneous bacterial peritonitis, gastrointestinal haemorrhage and depletion of the intravascular volume.