Hepatorenal syndrome: management
The management of hepatorenal syndrome (HRS) is notoriously difficult. The ideal treatment is liver transplantation but patients are often too unwell to have surgery and there is a shortage of donors
The most accepted theory regarding the pathophysiology of HRS is that vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in 'underfilling' of the kidneys. This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation.
Hepatorenal syndrome has been categorized into two types:
Management options
The most accepted theory regarding the pathophysiology of HRS is that vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in 'underfilling' of the kidneys. This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation.
Hepatorenal syndrome has been categorized into two types:
| Type 1 HRS | Type 2 HRS |
|---|---|
| Rapidly progressive Doubling of serum creatinine to > 221 µmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks Very poor prognosis | Slowly progressive Prognosis poor, but patients may live for longer |
Management options
- vasopressin analogues, for example terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation
- volume expansion with 20% albumin
- transjugular intrahepatic portosystemic shunt