From the Guidelines
Management of hepatorenal syndrome (HRS) should focus on improving renal function by addressing the underlying circulatory dysfunction, with the first-line treatment involving vasoconstrictors combined with albumin, as recommended by the most recent guidelines 1. The treatment of choice for HRS-AKI is vasoconstrictor drugs in combination with albumin, with terlipressin being the preferred drug, administered either as IV bolus or continuous IV infusion 1.
Key Components of HRS Management
- Vasoconstrictor therapy: Terlipressin (1 g/kg on day 1 followed by 20-40 g daily) is the preferred regimen, continued for up to 14 days or until serum creatinine improves, as supported by recent studies 1.
- Albumin infusion: Helps expand plasma volume and improve effective arterial blood volume, with a dose of 1 g/kg on day 1 followed by 20-40 g daily 1.
- Supportive care: Includes careful fluid management, avoiding nephrotoxic medications, treating precipitating factors like infections or gastrointestinal bleeding, and discontinuing diuretics 1.
- Renal replacement therapy: May be needed as a bridge to liver transplantation in severe cases 1.
- Liver transplantation: Remains the definitive treatment for eligible patients with HRS, as it addresses the underlying liver dysfunction that causes the splanchnic vasodilation and renal hypoperfusion characteristic of this condition 1.
Alternative Treatment Options
- Norepinephrine: Can be used if terlipressin is unavailable, with a dose of 0.5-3 mg/hour, as supported by recent studies 1.
- Midodrine plus octreotide: Can be used as an alternative, although its efficacy is lower, with a dose of 7.5-12.5mg orally three times daily plus octreotide 100-200mcg subcutaneously three times daily 1.
From the FDA Drug Label
Terlipressin is thought to increase renal blood flow in patients with hepatorenal syndrome by reducing portal hypertension and blood circulation in portal vessels and increasing effective arterial volume and mean arterial pressure (MAP).
The management of Hepatorenal Syndrome (HRS) with terlipressin involves increasing renal blood flow by reducing portal hypertension and increasing effective arterial volume and mean arterial pressure (MAP) 2.
- Key mechanism: Terlipressin acts as a vasopressin receptor agonist to reduce portal hypertension and increase renal blood flow.
- Clinical effect: Increase in diastolic, systolic, and mean arterial pressure (MAP), and decrease in heart rate are evident within 5 minutes after dosing and are maintained for at least 6 hours after dosing 2.
- Pharmacodynamics: The maximum change in blood pressure and heart rate occurred at 1.2 to 2 hours post dose, with an estimated maximum effect of an increase of 16.2 mmHg in MAP and a decrease of 10.6 beats/minute in heart rate 2.
From the Research
Management of Hepatorenal Syndrome (HRS)
The management of HRS involves various treatment options, including:
- Liver transplantation, which is the preferred definitive treatment option 3
- Pharmacologic therapies, such as terlipressin with albumin, which is the preferred treatment for patients with HRS 3, 4
- Alternative pharmacologic therapies, such as norepinephrine and vasopressin, which can be used in countries where terlipressin is not available 3
- Midodrine plus octreotide, which appears to be an effective pharmacologic regimen for patients with Type II HRS 3, 5
- Non-pharmacologic options, such as artificial hepatic support devices, renal replacement therapy, and transjugular intrahepatic portosystemic shunt (TIPS) 3, 6
Treatment Response Rates
Standardizing the treatment regimen with albumin, midodrine, and octreotide may improve treatment response rates in patients with HRS 7
- A study found that 25% of patients achieved full response in the poststandardization group compared to 10% in the prestandardization group 7
- Standardized therapy led to significantly lower rates of renal replacement therapy and liver transplantation 7
Treatment Goals
The main goal of treatment is to reverse the mechanisms underlying HRS, including portal hypertension, splanchnic vasodilation, and/or renal vasoconstriction 3