Our Focus: HRS-AKI
HRS-AKI: A Complex Disease with Severely Limited Treatment Options
Hepatorenal syndrome with acute kidney injury (HRS-AKI) is a serious and rapidly progressive complication of end-stage liver disease that may occur in patients with advanced liver disease and is believed to result from inadequate renal perfusion and intense renal vasoconstriction. While initially reversible, it can lead to irreversible renal failure if inadequately treated.
Determination of the exact prevalence of HRS-AKI has been difficult, in part because the previously utilized diagnostic criteria for hepatorenal syndrome proved to be inadequate for diagnosing HRS-AKI. As a result, the diagnostic criteria for HRS-AKI have been updated to allow for better identification and treatment. Consequently, it is estimated that HRS-AKI impacts approximately 50,000 individuals in the United States per year and is associated with a mortality rate of more than 50 percent at 90 days following diagnosis.
HRS-AKI is a complication of ESLD-induced portal hypertension that leads to splanchnic vasodilation, plasma leakage throughout the abdomen and a significant drop in arterial pressure. This acute drop in arterial pressure triggers a large renal vasoconstriction response resulting in a substantial drop in renal perfusion. Treating HRS-AKI requires improving renal perfusion to avoid acute kidney injury.
Treatment options for HRS-AKI are quite limited, but recent clinical advances in vasopressin 1a (V1a) receptor agonists are now providing promising new options. As a result of their ability to reduce portal hypertension through increasing splanchnic arteriolar vasoconstriction, finely tuned V1a receptor agonists have the potential to redistribute blood volume back to the systemic circulation, reversing the renal vasoconstriction and improving renal perfusion with the additional benefit of enhanced safety profiles compared to other drugs currently utilized for this indication.
Liver Portal Hypertension