What is hepatorenal syndrome?

What is hepatorenal syndrome?

Hepatorenal syndrome (HRS) is a type of progressive kidney failure. As the kidneys stop functioning, toxins begin to build up in the body. Eventually, this leads to liver failure. It is only seen in people with severe liver damage and is almost always caused by cirrhosis. There are two forms of HRS. Type 1 HRS is associated with rapid kidney failure. There is also an overproduction of creatinine. Type 2 HRS is associated with more gradual kidney damage. It generally progresses more slowly. Symptoms are generally subtler. HRS is an extremely serious condition. It is almost always fatal. According to an article inClinical Biochemist Reviews, people with type 1 HRS have a median survival time of two weeks. Almost everyone with this type of the disease will die within eight to 10 weeks. The median survival time for type 2 is six months.

What causes hepatorenal syndrome?

Hepatorenal syndrome usually affects individuals with cirrhosis and elevated pressures in the portal vein system (termed portal hypertension). While HRS may develop in any type of cirrhosis, it is most common in individuals with alcoholic cirrhosis, particularly if there is concomitant alcoholic hepatitis identifiable on liver biopsies.[8] HRS can also occur in individuals without cirrhosis, but with acute onset of liver failure, termed fulminant hepatic failure.[3][8]

Certain precipitants of HRS have been identified in vulnerable individuals with cirrhosis or fulminant hepatic failure. These include bacterial infection, acute alcoholic hepatitis, or bleeding in the upper gastrointestinal tract. Spontaneous bacterial peritonitis, which is the infection of ascites fluid, is the most common precipitant of HRS in cirrhotic individuals. HRS can sometimes be triggered by treatments for complications of liver disease: iatrogenic precipitants of HRS include the aggressive use of diuretic medications or the removal of large volumes of ascitic fluid by paracentesis from the abdominal cavity without compensating for fluid losses by intravenous replacement.[8]

Hepatorenal syndrome may complicate any form of severe liver disease. Many liver transplantations are performed in children with chronic liver disease secondary to biliary atresia. In children, 50% of all cases of acute hepatic failure are secondary to acute viral hepatitis. Other etiologies include acetaminophen toxicity, Wilson disease, liver malignancy, and autoimmune hepatitis.

Among adults with cirrhosis and portal hypertension, several precipitating factors have been implicated in the progression to hepatorenal syndrome. These factors include spontaneous bacterial peritonitis, large volume paracentesis without simultaneous or subsequent plasma expansion, and GI or variceal bleeding.

Patients with hepatic failure and ascites are prone to develop spontaneous bacterial peritonitis. In approximately 20% of adults with advanced liver disease and spontaneous bacterial peritonitis, their condition progresses to hepatorenal syndrome.

Large-volume paracentesis without plasma volume replacement is associated with the development of hepatorenal syndrome in as many as 15% of patients with ascites. Renal failure is attributed to a circulatory dysfunction after paracentesis and is preventable by administering an isotonic solution, or preferably intravenous (IV) albumin, during or soon after the procedure.

Hepatorenal syndrome develops in as many as 10% of adults after a clinically significant upper or lower GI bleed. Care must be taken to rule out acute tubular necrosis from volume depletion as the etiology of the renal failure after a GI bleed because hepatorenal syndrome is a diagnosis of exclusion.