Hepatorenal syndrome HRS is a severe complication in patients with cirrhosis and ascites. Renal insufficiency is functional and is caused by renal vasoconstriction. Diagnosis of HRS is based on ruling out other causes of renal insufficiency. There are two types of HRS: type 1 has rapid onset and progressive course and a mean survival of 15 days without treatment, while type 2 is less severe and progressive, with a mean survival of 6 months. Definitive treatment of HRS is liver transplantation. However, in the last few years administration of vasoconstrictive drugs or placement of portosystemic shunts have been shown to be effective in reversing HRS.
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Classification[ edit ] The development of ascites as shown on this abdominal ultrasound in cirrhotics that is refractory to the use of diuretic medications is associated with type 2 HRS. Hepatorenal syndrome is a particular and common type of kidney failure that affects individuals with liver cirrhosis or, less commonly, with fulminant liver failure. In both categories, the deterioration in kidney function is quantified either by an elevation in creatinine level in the blood, or by decreased clearance of creatinine in the urine.
Vasoconstrictors and volume expanders are the mainstay of treatment. Type 2 HRS is thought to be part of a spectrum of illness associated with increased pressures in the portal vein circulation , which begins with the development of fluid in the abdomen ascites. The spectrum continues with diuretic-resistant ascites, where the kidneys are unable to excrete sufficient sodium to clear the fluid even with the use of diuretic medications. Most individuals with type 2 HRS have diuretic-resistant ascites before they develop deterioration in kidney function.
As these phenomena may not necessarily produce symptoms until late in their course, individuals with hepatorenal syndrome are typically diagnosed with the condition on the basis of altered laboratory tests.
Most people who develop HRS have cirrhosis, and may have signs and symptoms of the same, which can include jaundice , altered mental status , evidence of decreased nutrition, and the presence of ascites. Oliguria , which is a decrease in urine volume, may occur as a consequence of kidney failure; however, some individuals with HRS continue to produce a normal amount of urine.
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. 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.
Consequently, it is a challenge to distinguish hepatorenal syndrome from other entities that cause kidney failure in the setting of advanced liver disease.
As a result, additional major and minor criteria have been developed to assist in the diagnosis of hepatorenal syndrome. Individuals with pre-renal kidney failure do not have damage to the kidneys, but as in individuals with HRS, have kidney dysfunction due to decreased blood flow to the kidneys. Also, similarly to HRS, pre-renal kidney failure causes the formation of urine that has a very low sodium concentration.
In contrast to HRS, however, pre-renal kidney failure usually responds to treatment with intravenous fluids, resulting in reduction in serum creatinine and increased excretion of sodium. Because of the damage to the tubules, ATN affected kidneys usually are unable to maximally resorb sodium from the urine. As a result, ATN can be distinguished from HRS on the basis of laboratory testing, as individuals with ATN will have urine sodium measurements that are much higher than in HRS; however, this may not always be the case in cirrhotics.
Diagram showing hypothesized correlation between clinical features and pathophysiology of ascites and hepatorenal syndrome. The kidney failure in hepatorenal syndrome is believed to arise from abnormalities in blood vessel tone in the kidneys. The underfill theory involves activation of the renin—angiotensin—aldosterone system, which leads to an increase in absorption of sodium from the kidney tubule termed renal sodium avidity mediated by aldosterone , which acts on mineralocorticoid receptors in the distal convoluted tubule.
It has been hypothesized that the progression from ascites to hepatorenal syndrome is a spectrum where splanchnic vasodilation defines both resistance to diuretic medications in ascites which is commonly seen in type 2 HRS and the onset of kidney vasoconstriction as described above leading to hepatorenal syndrome.
Bleeding from esophageal varices can be a precipitant for hepatorenal syndrome in individuals with cirrhosis , and can be prevented by early diagnosis and treatment. The risk of death in hepatorenal syndrome is very high; consequently, there is a significant emphasis on the identification of patients who are at risk for HRS, and prevention of triggers for onset of HRS.
As infection specifically spontaneous bacterial peritonitis and gastrointestinal hemorrhage are both complications in individuals with cirrhosis, and are common triggers for HRS, specific care is made in early identification and treatment of cirrhotics with these complications to prevent HRS.
The aggressive use of diuretic medications should be avoided. In addition, many medications that are either used to treat cirrhotic complications such as some antibiotics or other conditions may cause sufficient impairment in kidney function in the cirrhotic to lead to HRS. The concomitant infusion of albumin can avert the circulatory dysfunction that occurs after large-volume paracentesis and may prevent HRS.
These include the use of intravenous albumin infusion, medications for which the best evidence is for analogues of vasopressin , which causes splanchnic vasoconstriction , radiological shunts to decrease pressure in the portal vein , dialysis , and a specialized albumin-bound membrane dialysis system termed molecular adsorbents recirculation system MARS or liver dialysis. The medications are respectively systemic vasoconstrictors and inhibitors of splanchnic vasodilation, and were not found to be useful when used individually in treatment of hepatorenal syndrome.
A transjugular intrahepatic portosystemic shunt TIPS involves the decompression of the high pressures in the portal circulation by placing a small stent between a portal and hepatic vein.
This is done through radiologically guided catheters which are passed into the hepatic vein either through the internal jugular vein or the femoral vein. Theoretically, a decrease in portal pressures is thought to reverse the hemodynamic phenomena that ultimately lead to the development of hepatorenal syndrome. TIPS has been shown to improve kidney function in patients with hepatorenal syndrome. The molecular adsorbents recirculation system MARS has shown some utility as a bridge to transplantation in patients with hepatorenal syndrome, yet the technique is still nascent.
In patients who undergo hemodialysis , there may even be an increased risk of mortality due to low blood pressure in patients with HRS, although appropriate studies have yet to be performed. As a result, the role of renal replacement therapy in patients with HRS remains unclear. The first systematic attempt to define hepatorenal syndrome was made in by the International Ascites Club, a group of liver specialists. The more recent history of HRS has involved elucidation of the various vasoactive mediators that cause the splanchnic and kidney blood flow abnormalities of the condition.