Current position of vasoconstrictor and albumin infusion for type 1 hepatorenal syndrome

Abstract

Spontaneous bacterial peritonitis (SBP), refractory ascites, hepatorenal syndrome (HRS), hyponatremia and hepatic encephalopathy are complications which frequently happen during a clinical course of decompensated cirrhosis. Splanchnic and peripheral vasodilatation, increased intrarenal vasoconstriction and impaired cardiac responsive function are pathological changes causing systemic and hemodynamic derangement. Extreme renal vasoconstriction leads to severe reduction of renal blood flow and glomerular filtration rate, which finally evolves into the clinical feature of HRS. Clinical manifestations of type 1 and type 2 HRS come to medical attention differently. Patients with type 1 HRS present as acute kidney injury whereas those with type 2 HRS will have refractory ascites as the leading problem. Prompt diagnosis of type 1 HRS can halt the progression of HRS to acute tubular necrosis if the combined treatment of albumin infusion and vasoconstrictors is started timely. HRS reversal was seen in 34%-60% of patients, followed with decreasing mortality. Baseline serum levels of creatinine less than 5 mg/dL, bilirubin less than 10 mg/dL, and increased mean arterial pressure of over 5 mmHg by day 3 of the combined treatment of vasoconstrictor and albumin are the predictors of good response. Type 1 HRS can be prevented in some conditions such as albumin infusion in SBP, prophylactic antibiotics for upper gastrointestinal hemorrhage, albumin replacement after large volume paracentesis in cirrhotic patients with massive ascites. The benefit of albumin infusion in infection with primary source other than SBP requires more studies.

Liver cirrhosis: current status and treatment options using western or traditional Chinese medicine

“…At present, global scholars have not fully understood the pathogenesis of HRS. Existing studies have found that due to the influence of end-stage liver diseases such as cirrhosis, the inactivation of vasodilator factors in vivo is reduced, which leads to the dilation of visceral and peripheral arteries, the contraction of renal vessels, the reduction of glomerular filtration rate and the decrease of renal blood flow, and finally the occurrence of HRS ( Sobhonslidsuk, 2015 ; Simonetto et al, 2020 ; Wu et al, 2024 ). At the same time, liver inflammation, intestinal flora displacement and concurrent infection caused by cirrhosis lead to the release of a large number of inflammatory factors and endotoxemia, causing renal microcirculation dysfunction, which can induce renal function injury ( Rad et al, 2024 ).…”