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Hepatorenal syndrome (HRS) refers to acute renal failure that occurs in the setting of cirrhosis or fulminant liver failure, sometimes also associated with portal hypertension, usually in the absence of other disease of the kidney.[1][2] The pathology involved in the development of hepatorenal syndrome is thought to be an alteration in blood flow and blood vessel tone in the circulation that supplies the intestines (the splanchnic circulation) and the circulation that supplies the kidney.[3] It is usually indicative of an end-stage of perfusion, or blood flow to the kidney, due to deteriorating liver function. Patients with hepatorenal syndrome are very ill, and, if untreated, the condition is usually fatal. Treatment usually involves medical therapy or TIPS as a bridge to liver transplantation.[2] Interestingly, kidneys from patients with the hepatorenal syndrome have been used successfully for renal transplant.
The hepatorenal syndrome is defined as renal failure that occurs in the setting of liver disease as follows:[1]
Type I HRS is characterized by rapidly progressive renal failure with a doubling of serum creatinine to a level greater than 221 µmol/L (2.5 mg/dL) or a halving of the creatinine clearance to less than 20 mL/min over a period of less than 2 weeks. Type I HRS carries a very poor prognosis, usually with less than 50% survival at one month.[3] Patients with type I hepatorenal syndrome are usually ill, may have low blood pressures, and may require therapy with inotropes, or intravenous drugs to maintain blood pressure.[4]
Type II HRS is characterized by a slowly progressive:
It is typically associated with ascites that is unresponsive to diuretic medications, and also carries a poor, if somewhat longer (median survival ~6 months) outlook,[6] unless the patient undergoes liver transplantation.
It can be challenging to distinguish hepatorenal syndrome from other entities that cause renal failure in the setting of advanced liver disease. As a result, additional major and minor criteria have been proposed to assist in the diagnosis of the hepatorenal syndrome.[1]
The major criteria include liver disease in the setting of portal hypertension; renal failure; the absence of shock, infection, recent treatment with medications that affect the kidney’s function (nephrotoxins), and fluid losses; the absence of sustained improvement in renal function despite treatment with 1.5 litres of intravenous normal saline; the absence of proteinuria, or protein in the urine; and, the absence of renal disease or obstruction of renal outflow as seen on ultrasound.
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