Hepatorenal syndrome

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Hepatorenal syndrome

مشاركةبواسطة دكتور كمال سيد » الأحد يناير 11, 2015 6:18 pm

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Hepatorenal syndrome


The hepatorenal syndrome is one of many potential causes of acute kidney injury in patients with acute or chronic liver disease. Affected patients usually have portal hypertension due to cirrhosis, severe alcoholic hepatitis, or (less often) metastatic tumors, but can also have fulminant hepatic failure from any cause. (See 'Introduction' above.)
●Arterial vasodilatation in the splanchnic circulation, which is triggered by portal hypertension, appears to play a central role in the hemodynamic changes and the decline in renal function in the hepatorenal syndrome. The presumed mechanism is increased production or activity of vasodilators, mainly in the splanchnic circulation, with nitric oxide thought to be most important. As the hepatic disease becomes more severe, there is a progressive rise in cardiac output and fall in systemic vascular resistance; the latter change occurs despite local increases in renal and femoral vascular resistance that result in part from hypotension-induced activation of the renin-angiotensin and sympathetic nervous systems (figure 1). (See 'Pathogenesis' above.)
●Patients who develop the hepatorenal syndrome usually have portal hypertension due to cirrhosis, severe alcoholic hepatitis, and, less often, metastatic tumors. However, patients with fulminant hepatic failure from any cause may develop hepatorenal syndrome. In patients with cirrhosis and ascites, the hepatorenal syndrome occurs in approximately 20 and 40 percent at one and five years, respectively. In patients with acute liver disease, the hepatorenal syndrome occurs in approximately 25 to 30 percent. (See 'Epidemiology' above.)
●The hepatorenal syndrome is usually characterized by the following features in a patient who has established or clinically evident acute or chronic liver disease (see 'Clinical presentation' above):
•A progressive rise in serum creatinine
•A benign urine sediment
•No or minimal proteinuria (less than 500 mg per day)
•A very low rate of sodium excretion (ie, urine sodium concentration less than 10 meq/L)
•Oliguria
●Based upon the rapidity of the decline in kidney function, two forms of hepatorenal syndrome have been described (see 'Clinical presentation' above):
•Type 1 hepatorenal syndrome – Type 1 hepatorenal syndrome is the more serious type; it is defined as at least a twofold increase in serum creatinine (reflecting a 50 percent reduction in creatinine clearance) to a level greater than 2.5 mg/dL (221 micromol/L) during a period of less than two weeks. At the time of diagnosis, some patients with type 1 hepatorenal syndrome have a urine output less than 400 to 500 mL per day.
•Type 2 hepatorenal syndrome – Type 2 hepatorenal syndrome is defined as renal impairment that is less severe than that observed with type 1 disease. The major clinical feature in patients with type 2 hepatorenal syndrome is ascites that is resistant to diuretics.
●The onset of renal failure is typically insidious but can be precipitated by an acute insult, such as bacterial infection (often spontaneous bacterial peritonitis) or gastrointestinal bleeding. Diuretics do not cause hepatorenal syndrome. (See 'Precipitants' above.)
●Patients with hepatorenal syndrome may have renal dysfunction that is substantially more severe than is suggested by the serum creatinine. (See 'Problems with estimating kidney function' above.)
●Hepatorenal syndrome is diagnosed based upon clinical criteria. There is no one specific test that can establish the diagnosis. The following definition and diagnostic criteria have been proposed for the hepatorenal syndrome (see 'Diagnosis' above):
•Chronic or acute hepatic disease with advanced hepatic failure and portal hypertension.
•A serum creatinine above 1.5 mg/dL (133 micromol/L) that progresses over days to weeks (ie, acute or subacute kidney injury). As noted above, the rise in serum creatinine with reductions in glomerular filtration rate (GFR) may be minimal due to the marked reduction in creatinine production among such patients.
•The absence of any other apparent cause for the acute kidney injury, including shock, current, or recent treatment with nephrotoxic drugs, and the absence of ultrasonographic evidence of obstruction or parenchymal renal disease. Spontaneous bacterial peritonitis is complicated by acute kidney injury that may be reversible in 30 to 40 percent of patients. It can be associated with acute tubular necrosis (ATN), but it is also a major precipitant of the hepatorenal syndrome. Thus, ongoing infection with spontaneous bacterial peritonitis should not exclude the possibility of hepatorenal syndrome. This means that therapy for hepatorenal syndrome can commence while the bacterial infection is still being treated. In addition, hepatorenal syndrome can occur in patients with preexisting chronic KIDNEY DISEASE. Thus, the presence of another renal diagnosis (eg, diabetic nephropathy) does not necessarily exclude hepatorenal syndrome.
•In conjunction with excluding other apparent causes of renal disease, the following criteria also apply:

Urine red cell excretion of less than 50 cells per high power field (when no urinary catheter is in place) and protein excretion less than 500 mg/day.

Lack of improvement in renal function after volume expansion with intravenous albumin (1 g/kg of body weight per day up to 100 g/day) for at least two days and withdrawal of diuretics.
●As noted above, patients diagnosed with hepatorenal syndrome are classified as type 1 hepatorenal syndrome (more severe) or type 2 hepatorenal syndrome (less severe) based upon the rapidity of the acute kidney injury and the degree of renal impairment. Type 1 hepatorenal syndrome is present if the serum creatinine increases by at least twofold to a value greater than 2.5 mg/dL (221 micromol/L) during a period of less than two weeks. Less rapidly progressive disease is classified as type 2. (See 'Diagnosis' above.)

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مشاركةبواسطة دكتور كمال سيد » الأحد يناير 11, 2015 9:43 pm

●The diagnosis of the hepatorenal syndrome is one of exclusion, entertained only after other potential causes of acute or subacute kidney injury have been ruled out. Alternate etiologies include, but are not limited to, glomerulonephritis, prerenal disease, and ATN. (See 'Differential diagnosis' above.)
●The ideal therapy for hepatorenal syndrome is improvement of liver function from either recovery of alcoholic hepatitis, treatment of decompensated hepatitis B with effective antiviral therapy, recovery from acute hepatic failure, or liver transplantation. (See 'Approach to therapy' above and 'Improving hepatic function' above.)
●However, when improvement of liver function is not possible in the short term, medical therapy should be instituted in an attempt to reverse the acute kidney injury associated with hepatorenal syndrome. Our suggestions regarding the choice of medical therapy depend upon several factors, including: whether the patient is admitted to the intensive care unit; the availability of certain drugs, for which there is national and regional variability; and whether the patient is a candidate for liver transplantation. (See 'Approach to therapy' above.)
●In patients with hepatorenal syndrome who are admitted to the intensive care unit, we suggest initial treatment with norepinephrine in combination with albumin rather than other medical therapies (Grade 2B). Norepinephrine is given intravenously as a continuous infusion (0.5 to 3 mg/hr) with the goal of raising the mean arterial pressure by 10 mmHg, and albumin is given for at least two days as an intravenous bolus (1 g/kg per day [100 g maximum]). Intravenous vasopressin may also be effective, starting at 0.01 units/min. (See 'Norepinephrine for patients in the intensive care unit' above.)
●In patients with hepatorenal syndrome who are not admitted to the intensive care unit, our suggestions depend upon the availability of certain drugs:
•Where terlipressin therapy is available, we suggest initial treatment with terlipressin in combination with albumin rather than midodrine, octreotide, and albumin (Grade 2C). Terlipressin is given as an intravenous bolus (1 to 2 mg every four to six hours), and albumin is given for two days as an intravenous bolus (1 g/kg per day [100 g maximum]), followed by 25 to 50 grams per day until terlipressin therapy is discontinued. (See 'Terlipressin plus albumin where available' above.)
•Where terlipressin therapy is not available (principally the United States), we suggest initial treatment with a combination of midodrine, octreotide, and albumin (Grade 2C). Midodrine is given orally (7.5 to 15 mg by mouth three times daily), octreotide is either given as a continuous intravenous infusion (50 mcg/hr) or subcutaneously (100 to 200 mcg three times daily), and albumin is given for two days as an intravenous bolus (1 g/kg per day [100 g maximum]), followed by 25 to 50 grams per day until midodrine and octreotide therapy is discontinued. (See 'Midodrine, octreotide, and albumin where terlipressin is not available' above.)
●In highly selected patients who fail to respond to medical therapy with the above regimens, who are awaiting liver transplantation, and who are considered well enough to undergo the procedure, transjugular intrahepatic portosystemic shunt (TIPS) is sometimes successful; however the procedure is associated with numerous complications. (See 'Transjugular intrahepatic portosystemic shunt' above.)
●In patients who fail to respond to the above therapies, develop severely impaired renal function, are not considered candidates for TIPS, and either are candidates for liver transplantation or have a reversible form of liver injury and are expected to survive, we recommend dialysis as a bridge to liver transplantation or liver recovery (Grade 1B). Hemodialysis is frequently difficult to perform in patients with hepatorenal syndrome, and survival is generally limited by the severity of the hepatic failure, as well as concurrent respiratory failure. (See 'Dialysis' above.)
●The goal of medical therapy or TIPS in patients with hepatorenal syndrome is reversal of the acute kidney injury. In addition, when patients are treated with norepinephrine, terlipressin, or midodrine plus octreotide, an immediate goal of therapy is to raise the mean arterial pressure by approximately 10 to 15 mmHg. (See 'Approach to therapy' above.)
●In patients treated with norepinephrine, terlipressin, or octreotide, we usually treat for a total of two weeks. However, we and others occasionally treat for longer durations (up to one month or more) if there is some but not complete improvement in renal function after two weeks of therapy. In patients who respond to therapy, we occasionally treat indefinitely with midodrine to maintain a higher mean arterial pressure (or until liver transplantation or resolution of liver injury). In contrast, if a patient has no improvement in renal function after two weeks, therapy with these drugs can be considered futile. (See 'Approach to therapy' above.)
●The following therapies may prevent the development of hepatorenal syndrome in these patients (see 'Prevention' above):
•In patients with spontaneous bacterial peritonitis, we recommend the administration of intravenous albumin (1.5 g/kg) at the time of diagnosis of infection and another dose of albumin (1 g/kg) on day 3 of antibiotic treatment (Grade 1B). (See "Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis".)
•In selected patients with cirrhosis and ascites, we recommend chronic norfloxacin therapy (400 mg/day) (Grade 1B). A discussion of which patients should receive chronic norfloxacin therapy, as well as the evidence for this graded recommendation, are presented elsewhere. (See "Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis".)
●Without therapy, most patients with hepatorenal syndrome die within weeks of the onset of the renal impairment. The outcome of patients with hepatorenal syndrome, as well as recovery of kidney function, is strongly dependent upon reversal of the hepatic failure, whether spontaneous, following medical therapy, or following successful liver transplantation. (See 'Prognosis' above.)

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