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Hepatorenal Syndrome

Hepatorenal syndrome is the deterioration of kidney function in patients who have acute or chronic liver failure but otherwise healthy kidneys. This disorder may occur spontaneously but more often is the result of an infection, an episode of gastrointestinal bleeding, or overly aggressive use of diuretics. There are two types of hepatorenal syndrome: Type I conveys the highest risk of death and develops rapidly over a couple of weeks; Type II progresses more slowly, usually over several months. The diagnosis of hepatorenal syndrome requires fulfillment of all of the following criteria: deterioration of kidney function demonstrated by a concentration of creatinine in the blood of more than 1.5 mg/dl or a decrease in creatinine clearance to less than 40 milliliters per minute. No evidence of dehydration, no exposure to a drug or infection that causes kidney toxicity, and absence of severe low blood pressure. Failure to respond to discontinuation of diuretics or to treatment with 1.5 liters of saline solution to expand blood volume. No evidence of obstruction of urine flow or primary kidney disease, as demonstrated by ultrasound exam. Little or no protein in the urine.

The majority of patients who will develop hepatorenal syndrome will first develop diuretic-resistant ascites, usually with very low sodium in the urine. In general, among patients who have ascites, the risk of developing hepatorenal syndrome is 2 in 10 during the first year and 4 in 10 during the first 5 years. Among patients with Type I hepatorenal syndrome, the estimated mortality without appropriate therapy is 80 percent after 2 weeks and 90 percent after 10 weeks.

Hepatorenal syndrome is thought to result from a severe contraction of the artery that feeds the kidney, which may occur as a response to excessive relaxation of the vessels in the rest of the body and a relatively low volume of blood inside the vascular system. Thus, the first approach to treatment of this disorder is to try to expand vascular volume and then to increase the degree of contraction of vessels other than the kidney artery.

Several strategies have been used to reverse hepatorenal syndrome. The first involves intravenous infusions of albumin, followed by administration of ornipressin, a medication that increases the contraction of most of the vessels in the body. Similar effects with fewer complications have been obtained using intravenous albumin with terlipressin, which causes vessel contraction more safely.

In the United States, neither ornipressin nor terlipressin is available, and the most popular intervention for hepatorenal syndrome is to expand blood volume using intravenous albumin, then to administer midodrine and octreotide to regulate vascular contraction. For patients who cannot tolerate medication by mouth, intravenous albumin can be used, followed by continuous infusion of norepinephrine. With the latter two regimens, beneficial effects usually can be seen by day 10 of therapy and, if not successful, the treatment usually is discontinued after 15 days. Patients who do respond can complete at least 2 weeks of therapy, and after that, therapy can be discontinued, usually without deterioration of kidney function.

Other therapies are being used, including the transjugular intrahepatic portal systemic shunt, in which a long catheter is inserted via the jugular vein in the neck, advanced into a hepatic vein and then into a large branch of the portal vein in the liver. Using an inflatable balloon-tipped catheter tube, the section between the portal vein branch and the hepatic vein is widened and then kept open with a cylindrical wire-mesh stent. This helps to lower the increased pressure in the portal vein. In addition, hepatorenal syndrome has been treated using high doses of antioxidants. More recently, a system known as MARS (molecular absorbent recirculating system) has been used; with this treatment, a patient's blood is transported to a filter, where it is mixed with albumin, which carries the toxins out of the blood.

Although these treatments are available, hepatorenal syndrome will very likely recur, and patients should be moved quickly in the direction of possible liver transplantation.

Esophageal Varices

Cirrhosis causes an increase in pressure in the fine net of blood vessels inside the liver. This pressure is transmitted back to the portal vein and onto the veins that form it. Because of the high pressure on the veins forming the portal vein and the portal vein itself, blood tries to escape, forming new collateral veins (the increased pressure causes very small varices to grow larger). Many of these veins are localized superficially inside the esophagus and the upper part of the stomach. When these veins engorge because of increased pressure, they are called varices.

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