Management of hepatorenal syndrome

Abstract

Hepatorenal syndrome (HRS) is defined as development of renal dysfunction in patients with chronic liver diseases due to decreased effective arterial blood volume. It is the most severe complication of cirrhosis because of its very poor prognosis. In spite of several hypotheses and research, the pathogenesis of HRS is still poorly understood. The onset of HRS is a progressive process rather than a suddenly arising phenomenon. Since there are no specific tests for HRS diagnosis, it is diagnosed by the exclusion of other causes of acute kidney injury in cirrhotic patients. There are two types of HRS with different characteristics and prognostics. Type 1 HRS is characterized by a sudden onset acute renal failure and a rapid deterioration of other organ functions. It may develop spontaneously or be due to some precipitating factors. Type 2 HRS is characterized by slow and progressive worsening of renal functions due to cirrhosis and portal hypertension and it is accompanied by refractory ascites. The only definitive treatment for both Type 1 and Type 2 HRS is liver transplantation. The most suitable bridge treatment or treatment for patients who are not eligible for transplantation is a combination of terlipressin and albumin. For the same purpose, it is possible to try hemodialysis or renal replacement therapies in the form of continuous veno-venous hemofiltration. Artificial hepatic support systems are important for patients who do not respond to medical treatment. Transjugular intrahepatic portosystemic shunt may be considered as a treatment modality for unresponsive patients to medical treatment. The main goal of clinical surveillance in a cirrhotic patient is prevention of HRS before it develops. The aim of this article is to provide an updated review about the physiopathology of HRS and its treatment.

Hepatorenal Syndrome: Diagnosis and Treatment – newsreel –

“…Other vasoconstrictor agents used in practice in HRS treatment are somatostatin analogues (octreotide), alpha adrenergic agonists, midodrine and norepinephrine. Several studies have proved their effectiveness, some of which found that they are less effective than terlipressin and some others found that their effectiveness is similar to terlipressin [26]. Therapy with terlipressin and albumin, on the one hand, and albumin alone, on the other hand, were compared in a multicentre randomized controlled trial in 46 patients with HRS, showed improved renal function in the former group (43.5% versus 8.7%, p = 0.017), but no survival advantage in either group at three months (27% versus 19%, p = 0.7) [27].…”

Perioperative Risk Assessment and Management of Cirrhotic Patients

“…Although not available in the U.S., terlipressin plus albumin maintains better MAP [72] with a higher rate of renal recovery at 70% compared to midodrine and octreotide plus albumin in the treatment of HRS at 28.6% [74], despite higher rates of cardiovascular side effects [75]. However, there tends to be a 50% recurrence rate after cessation of therapy [75].…”

“…HRS-1/2 should be referred for LT, and managed with albumin 1 g/kg/d increasing to 100 g loading dose followed by 20-40 g/d [72] combined with vasconstrictor treatment [65,73]. Although not available in the U.S., terlipressin plus albumin maintains better MAP [72] with a higher rate of renal recovery at 70% compared to midodrine and octreotide plus albumin in the treatment of HRS at 28.6% [74], despite higher rates of cardiovascular side effects [75]. However, there tends to be a 50% recurrence rate after cessation of therapy [75].…”

Renal dysfunctions in cirrhosis

“…The major hemodynamic changes in HRS are splanchnic vasodilation associated with portal hypertension, decrease in the effective blood volume and the resultant decrease in renal perfusion. As renal perfusion decreases glomerular filtration rate and sodium (Na) excretion also decrease resulting in renal dysfunction (12). The diagnostic criteria for hepatorenal syndrome proposed by International Ascites Club in 2007 are shown in table 1.…”