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PubMed1986

Effect of portacaval shunt on drug disposition in patients with cirrhosis.

To examine the consequences of liver blood flow variations on drug disposition in cirrhosis, we studied the effects of portacaval shunt on drug clearance in 35 cirrhotic patients. Lidocaine clearance and bioavailability, indocyanine green (ICG) clearance, aminopyrine breath test, and hepatic blood flow were measured before and 18 months after surgery. The patients were divided into two groups according to severity of disease: 14 patients (group 1) had slight liver dysfunction (ICG extraction ratio greater than 0.25) and 21 patients (group 2) had severe liver disease (ICG extraction ratio less than 0.25). After portacaval shunt the decrease in hepatic blood flow was similar for both groups (-65%). In group 1, ICG systemic clearance decreased from 9.10 +/- 0.68 to 4.40 +/- 0.34 ml/min . kg (p less than 0.05), whereas ICG intrinsic clearance remained unchanged; lidocaine systemic clearance decreased from 7.93 +/- 0.93 to 5.09 +/- 0.33 ml/min . kg (p less than 0.05), whereas lidocaine intrinsic clearance remained unchanged; bioavailability increased from 0.601 +/- 0.076 to 1, resulting in an abrupt reduction of oral clearance from 18.01 +/- 4.90 to 5.09 +/- 0.33 ml/min . kg (p less than 0.05). In group 2, ICG systemic clearance decreased slightly from 3.90 +/- 0.39 to 2.28 +/- 0.16 ml/min . kg (p less than 0.01) and ICG intrinsic clearance was not modified; lidocaine systemic and intrinsic clearance remained unchanged; and bioavailability increased from 0.779 +/- 0.229 to 1, resulting in a decrease of oral clearance from 7.68 +/- 1.65 to 4.23 +/- 0.37 ml/min X kg (p less than 0.05). The aminopyrine breath test was not affected by surgery in either group. We conclude that reduction of hepatic blood flow after portacaval shunt has only minimal effects on drug disposition in patients with severe liver disease, but results in a notable reduction in the clearance of high-extraction drugs in cirrhotics with mild liver disease.

Adult↗
PubMed1998

Prognostic value of serum procollagen III peptide and type IV collagen in patients with biliary atresia.

BACKGROUND/PURPOSE: Progressive hepatic fibrosis, in spite of a successful Kasai procedure, is a major problem in patients with biliary atresia (BA). Early identification of patients at risk would be of great value. N-terminal procollagen-III peptide (PIIIP) (which is a marker of fibrogenesis and, therefore, of on going inflammation), and type IV collagen (found in basement membrane extracellular matrix), were measured in patients with BA to determine their potential as prognostic markers. METHODS: Thirty-three postoperative BA patients (11.0+/-3.7 years old) and 20 normal controls (10.5+/-2.8 years old) were studied. The BA patients were classified on the basis of their current liver function test results into three outcome groups. Group I (n = 9) had severe liver dysfunction, group II (n = 13) had moderate, and group III (n = 11) had good liver function. Serum P-III-P and type IV collagen values were determined by radioimmunoassays and one step sandwich enzyme immunoassay. RESULTS: In group I, serum PIIIP (1.93+/-0.64 U/mL) and type IV collagen levels (363.5+/-69.5 ng/mL) were significantly higher than in group II (PIIIP [1.32+/-0.25 U/mL], type IV collagen [225.3+/-45.4 ng/mL]; P < .01). There were increased levels in serum PIIIP and serum type IV collagen in group II compared with group III (PIIIP [1.01+/-0.25 U/mL], type IV collagen [171.3+/-47.2 ng/mL]; P < .01). There were no significant differences in serum PIIIP and type IV collagen levels between group III and controls. CONCLUSION: The authors conclude that serum levels of PIIIP and type IV collagen may be useful in the long-term follow-up of BA patients after Kasai's portoenterostomy.

Biliary Atresia↗
PubMed2003

Hepatic function and physiology in the newborn.

The liver develops from progenitor cells into a well-differentiated organ in which bile secretion can be observed by 12 weeks' gestation. Full maturity takes up to two years after birth to be achieved, and involves the normal expression of signalling pathways such as that responsible for the JAG1 genes (aberrations occur in Alagille's syndrome), amino acid transport and insulin growth factors. At birth, hepatocytes are already specialized and have two surfaces: the sinusoidal side receives and absorbs a mixture of oxygenated blood and nutrients from the portal vein; the other surface delivers bile and other products of conjugation and metabolism (including drugs) to the canalicular network which joins up to the bile ductules. There is a rapid induction of functions such as transamination, glutamyl transferase, synthesis of coagulation factors, bile production and transport as soon as the umbilical supply is interrupted. Anatomical specialization can be observed across the hepatic acinus which has three distinct zones. Zone 1 borders the portal tracts (also known as periportal hepatocytes) and is noted for hepatocyte regeneration, bile duct proliferation and gluconeogenesis. Zone 3 borders the central vein and is associated with detoxification (e.g. paracetamol), aerobic metabolism, glycolysis and hydrolysis and zone 2 is an area of mixed function between the two zones. Preterm infants are at special risk of hepatic decompensation because their immaturity results in a delay in achieving normal detoxifying and synthetic function. Hypoxia and sepsis are also frequent and serious causes of liver dysfunction in neonates. Stem cell research has produced many answers to the questions about liver development and regeneration, and genetic studies including studies of susceptibility genes may yield further insights. The possibility that fatty liver (increasingly recognized as non-alcoholic steatohepatitis or NASH) may have roots in the neonatal period is a concept which may have important long-term implications.

Fatty Liver↗
PubMed1989

An evaluation of the potency of Osbeckia octandra and Melothria maderaspantana as antihepatotoxic agents.

Aqueous extracts of the aerial parts of Melothria maderasptana and the leaves of Osbeckia octandra have been compared with (+)-3-cyanidanol with regard to their abilities to alleviate carbon tetrachloride (CCl4)-induced liver dysfunction in albino rats by comparing the abilities of these drugs to protect the liver against CCl4-mediated alterations in the liver histopathology and serum levels of aspartate aminotransferase (GOT), alkaline amino-transferase (GPT), and alkaline phosphatase. In both pretreatment and post-treatment (administration of drugs before or after CCl4 treatment) experiments, the most marked rate of recovery of the liver was exhibited by the group of rats treated with Melothria maderaspatana extract. Although the protection offered by (+)-3-cyanidanol and Osbeckia octandra appears to be comparable in post-treatment, Osbeckia was significantly more effective in pre-treatment. From the overall results obtained it appears that the aqueous extracts of Melothria maderaspatana and Osbeckia octandra are both as potent or in some instances (in pretreatment experiments) more potent than (+)-3-cyanidanol. Of the two plants tested under the present experimental conditions used, Melothria maderaspatana appears to be marginally more effective than Osbeckia octandra in protecting the liver against CCl4-induced alterations.

Animals↗
PubMed1996

Significant elevation of serum human hepatocyte growth factor levels in patients with acute pancreatitis.

Serum levels of human hepatocyte growth factor (HGF) were determined in 38 patients with acute pancreatitis by an enzyme-linked immunosorbent assay. The mean value of serum HGF levels on admission in the 38 patients was 1.69 +/- 0.40 (SEM) ng/ml. In 35 patients, serum HGF levels were found to be positive (> 0.39 ng/ml), with an incidence of 92.1%. In 17 patients, they were > 1.0 ng/ml, which was the cutoff value for fulminant hepatic failure. Serum HGF levels in the patients with severe acute pancreatitis (2.30 +/- 0.61 ng/ml; mean +/- SEM) were significantly higher than those in the patients with mild and moderate acute pancreatitis (0.63 +/- 0.06 ng/ml). Sixteen of seventeen patients whose serum HGF levels were > 1.0 ng/ml were evaluated as severe acute pancreatitis. Serum HGF levels were significantly elevated in the patients with higher Ranson scores, higher APACHE II scores, or higher computed tomography grades. Serum HGF levels in the patients with organ dysfunction (liver, kidney, or lung) were significantly higher than those in the patients without organ dysfunction. Moreover, serum HGF levels on admission in the nonsurvivors (3.17 +/- 1.30 ng/ml) were significantly higher than those in the survivors (1.22 +/- 0.33 ng/ml). The mortality rate of the patients showing serum HGF levels > 2.0 ng/ml on admission was 50%. In the patients with a lethal outcome, the mean serum HGF level remained constantly > 2.50 ng/ml during hospitalization. The serum HGF level reflected the clinical course of the disease rapidly and distinctly. Serum HGF levels increased with complications such as organ failure, infected pancreatic necrosis, and sepsis and decreased with successful intensive and surgical treatments. These results suggest that serum human HGF levels may reflect the severity, organ dysfunction, and prognosis in acute pancreatitis.

Acute Disease↗
PubMed1985

The impact of renal transplantation on the course of hepatitis B liver disease.

To establish the impact of transplantation on the course of chronic hepatitis B liver disease we performed a prospective study of the clinical and pathological sequelae of hepatitis B disease in all 22 patients who had renal allografts that functioned for more than 1 year and who were hepatitis B surface antigen (HBsAg)-positive following transplantation. No patient converted to HBsAg-negative. During a mean follow-up of 83 months serial liver biopsies were performed in 20 patients and 1 liver biopsy was available in the remaining 2 patients. Eleven patients died of liver disease, 5 of whom died of hepatic failure, 3 with hepatoma, 2 of gastrointestinal hemorrhage, and 1 of ascites with pleuroperitoneal fistula. Aggressive liver disease was observed in the vast majority of patients: 12 ultimately developed cirrhosis, (mean follow-up 81 months), 6 chronic active hepatitis (mean follow-up 93 months), 3 chronic persistent hepatitis (mean follow-up 89 months), and in 1 patient the presence of HB virus in hepatocytes was the sole morphologic alteration (follow-up 42 months). There was a marked tendency to progression in that 82% of patients with virus only, reactive hepatitis, or chronic persistent hepatitis on initial biopsy subsequently developed chronic active hepatitis or cirrhosis. For comparison, 10 HBsAg-positive patients whose renal failure had been treated by hemodialysis were also studied over a comparable period. Four patients converted to the negative state. Biochemical evidence of persistent liver dysfunction occurred in only 1 patient and no patient has died from complications of liver disease. We conclude that in the immunosuppressed renal transplant patient HB infection often results in the development of cirrhosis, leading to death from hepatoma and hepatic failure. This course is worse than that in dialysis patients. Renal transplantation of HBsAg-positive patients with end-stage renal failure may be inadvisable.

Aspartate Aminotransferases↗
PubMed2000

Outcome of lamivudine resistant hepatitis B virus infection in the liver transplant recipient.

BACKGROUND: In many transplant centres lamivudine is an important component of prophylaxis against, and treatment of, hepatitis B virus (HBV) graft infection. Drug resistant HBV species with specific polymerase mutations may emerge during lamivudine treatment. AIMS: To examine the clinical consequences of graft infection by lamivudine resistant virus. METHODS: The clinical course of four liver transplant patients who developed graft infection with lamivudine resistant virus was reviewed. The response of HBV infection to reduction of immunosuppression and to manipulation of antiviral therapy was assessed. For each patient, serum viral titre was measured and the viral polymerase gene was sequenced at multiple time points. RESULTS: High serum titres were observed following emergence of the lamivudine resistant species. Wild type HBV re-emerged as the dominant serum species after lamivudine withdrawal. All patients developed liver failure, and onset of liver dysfunction was observed when resistant virus was the dominant serum species. In three patients, liver recovery was observed when immunosuppression was stopped and when alternative antivirals were given. Wild type virus appeared to respond to ganciclovir, and to reintroduction of lamivudine. For one patient, introduction of famciclovir was associated with clinical, virological, and histological response. CONCLUSIONS: Failure of lamivudine prophylaxis may identify patients at special risk for the development of severe graft infection. Treatment of graft reinfection should include reduction of immunosuppression, and systematic exposure to alternative antivirals. Viral quantitation and genetic sequencing are essential components of therapeutic monitoring.

Adult↗
PubMedDate not supplied

Isolated orthotopic liver transplantation for parenteral nutrition-associated liver injury.

BACKGROUND: Mild liver dysfunction is common after prolonged use of parenteral nutrition (PN), but end-stage liver failure occurs only rarely. Few treatment options other than combined liver-intestine transplantation exist for patients with liver failure associated with PN use, however. Herein, we report the results of a cohort of patients undergoing isolated orthotopic liver transplantation (OLT) for PN-associated liver injury. METHODS: A retrospective cohort study of 80 patients (73 pediatric patients and 7 adults) who have undergone isolated OLT for PN-associated liver injury as the primary indication for transplantation was performed. RESULTS: At the time of OLT, the mean total serum bilirubin was 19.5 mg/dL and the mean serum albumin level was 2.9 mg/dL. Severe hepatic encephalopathy was seen in 5%, spontaneous bacterial peritonitis was seen in 6.3%, and respiratory failure requiring mechanical ventilation was seen in 14% of patients at the time of OLT. Overall 1- and 5-year survival rates were 72% and 52%, respectively, with infection being the most common cause of death after OLT. Retransplantation was required in 25% of patients, and the 5-year posttransplant patient survival rate only reached 35% in these cases. CONCLUSIONS: Patients with end-stage liver disease associated with PN administration often have very severe liver disease, multiple comorbidities, and poor prognosis by the time they are listed for OLT. Nonetheless, isolated OLT is associated with good long-term survival and should be considered for selected patients with combined intestine-liver failure.

Adult↗
PubMed2005

Chemotherapy dosing with elevated liver function test results in acute leukemia.

OBJECTIVE: To report a case of massive blast infiltration of the liver by acute lymphoblastic leukemia (ALL) manifested by worsening liver function test (LFT) results and concern over how to dose chemotherapy in this patient. CASE SUMMARY: A 36-year-old male presenting with productive cough, abdominal pain, and lower back pain was diagnosed with pre-B cell ALL. Of note, the patient developed worsening LFT results within the first few days of diagnosis. Because of concern over increasing liver dysfunction and the need to administer vincristine and daunorubicin with induction therapy, a transvenous liver biopsy was performed, revealing massive lymphoblast infiltration. DISCUSSION: A short course of prednisone was given to determine whether the LFT abnormalities would reverse with treatment. Once a downward trend in the abnormalities was noted, full-dose induction chemotherapy was administered. CONCLUSIONS: It is important to discern the cause of elevated LFT values in patients with acute leukemia who require induction chemotherapy, as this may affect treatment decisions and patient outcomes.

Acute Disease↗
PubMed2004

Low bone mineral density in noncholestatic liver cirrhosis: prevalence, severity and prediction.

BACKGROUND: Metabolic bone disease has long been associated with cholestatic disorders. However, data in noncholestatic cirrhosis are relatively scant. AIMS: To determine prevalence and severity of low bone mineral density in noncholestatic cirrhosis and to investigate whether age, gender, etiology, severity of underlying liver disease, and/or laboratory tests are predictive of the diagnosis. PATIENTS/METHODS: Between March and September/1998, 89 patients with noncholestatic cirrhosis and 20 healthy controls were enrolled in a cross-sectional study. All subjects underwent standard laboratory tests and bone densitometry at lumbar spine and femoral neck by dual X-ray absorptiometry. RESULTS: Bone mass was significantly reduced at both sites in patients compared to controls. The prevalence of low bone mineral density in noncholestatic cirrhosis, defined by the World Health Organization criteria, was 78% at lumbar spine and 71% at femoral neck. Bone density significantly decreased with age at both sites, especially in patients older than 50 years. Bone density was significantly lower in post-menopausal women patients compared to pre-menopausal and men at both sites. There was no significant difference in bone mineral density among noncholestatic etiologies. Lumbar spine bone density significantly decreased with the progression of liver dysfunction. No biochemical variable was significantly associated with low bone mineral density. CONCLUSIONS: Low bone mineral density is highly prevalent in patients with noncholestatic cirrhosis. Older patients, post-menopausal women and patients with severe hepatic dysfunction experienced more advanced bone disease. The laboratory tests routinely determined in patients with liver disease did not reliably predict low bone mineral density.

Adult↗
PubMed1997

Hemolysis, elevated liver enzymes, and low platelets syndrome associated with primary anti-phospholipid antibody syndrome.

A 28-year-old woman with a history of a spontaneous abortion developed thrombocytopenia, Coombs-negative hemolytic anemia, and liver dysfunction at the sixteenth week of pregnancy. These findings were compatible with hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome (hemolysis, elevated liver enzymes, and low platelet counts). Moreover, serum anti-phospholipid antibodies were positive, suggesting the association of anti-phospholipid antibody syndrome. An artificial abortion, anti-coagulation therapy, and plasma exchange were performed concomitantly with corticosteroid therapy. She responded to the therapy, a remission was obtained. Anti-phospholipid antibodies may play a role in the pathogenesis of HELLP syndrome.

Abortion, Induced↗
PubMedDate not supplied

Studies on changes of thyroid hormones in various liver diseases: usefulness of free thyroid hormones as liver function test.

Various thyroid parameters in liver disease which were morphologically diagnosed were measured, and their relationship to liver function was mainly studied. Serum T4 levels were elevated in acute hepatitis (AH), chronic persistent hepatitis (CPH) and chronic aggressive hepatitis (CAH) compared with in normal controls (C). Serum T3 levels were elevated in CAH and reduced in liver cirrhosis (LC). Serum reverse T3 (rT3) levels were elevated in AH and chronic liver diseases (CLD). T3/T4 ratios decreased in AH, CPH and CAH. RT3/T3 ratios increased in AH and CLD. Serum Free T3 (FT3) levels reduced in CLD in order of CPH, CAH and LC, and were low levels in AH with the same degree as LC. Moreover, serum FT3 levels revealed negative correlation with ICG-R15 and positive correlation with prothrombin time (PT) and serum albumin levels (Alb). Therefore serum FT3 level was considered to become a sensitive index of liver damage. Serum free T4 (FT4) levels did not change significantly in AH with high levels of transaminases and reduced in only LC. Therefore serum FT4 may become an index of severity of liver dysfunction. On the other hand, T3/T4 ratios and rT3/T3 ratios showed less correlation with liver function tests compared with free thyroid hormones.

Adult↗
PubMed1992

CA 125 serum levels in patients with non-neoplastic liver diseases. A clinical and laboratory study.

CA 125 is a tumour marker usually used in the monitoring of ovarian carcinoma patients. This study was performed to evaluate the behaviour of CA 125 in 159 patients with benign diffuse hepatic diseases who underwent thorough clinical and laboratory evaluation. Abnormal serum levels of CA 125 were found in 40.3% of the 159 patients, 70.6% of the 85 cirrhotics and 5.4% of the 74 non-cirrhotics. There was a correlation between CA 125 and numerous biochemical parameters characteristic of liver diseases, the liver failure tests being the most relevant. Ascites was a determining factor of serum CA 125 levels (98.4% of the ascites patients and only 4.1% of the non-ascitic patients had abnormal levels), and CA 125 had excellent sensitivity, specificity, efficiency, predictive values and likelihood ratios to detect ascites. In the absence of ascites, liver dysfunction played a small but significant role in the increase of CA 125. In liver disease patients with ascites the threshold required to obtain only 10% of abnormal values was more than 50-fold the basal level. These findings invalidate CA 125 as a tumour marker in these patients.

Adolescent↗
PubMed1997

Endogenous nitric oxide in exhaled air from patients with liver cirrhosis.

BACKGROUND: The aim of this study was to investigate the potential effects of liver insufficiency on nitric oxide concentrations in exhaled air. METHODS: Nitric oxide concentrations in the exhaled air from 13 patients with liver cirrhosis and 11 healthy control subjects was examined by the single-breath technique. RESULTS: There was a clear correlation between Child-Pugh score and NO in exhaled air (peak after 15 sec of breathholding, R = 0.623, P = 0.023). Similarly, there were significant correlations in peak NO concentrations and alkaline phosphatase, bilirubin, aspartate and alanine aminotransferase, and albumin. The most severely ill patient in our study had the highest NO concentrations in her exhaled air. On recovery from her liver illness the concentration of NO in her exhaled air decreased. There was no correlation between circulating levels of the endogenous NO synthase inhibitors asymmetric and symmetric N(G), N(G)-dimethyl-arginine and exhaled NO concentrations. CONCLUSIONS: The present data show a correlation between endogenous NO formation in the respiratory system and liver dysfunction. This might contribute to the understanding of the pathophysiology in pulmonary vasodilatation in liver disease.

Breath Tests↗
PubMed2000

[Non-cirrhotic portal hypertension associated with autoimmune disease].

OBJECTIVE: To summarize the cases of non-cirrhotic portal hypertension associated with autoimmune disease, review the literature and introduce the clinical and pathological features of the syndrome. METHODS: Six female patients treated, between 1983 and 1998 had no history of hepatitis. Variceal bleeding occurred in 5 patients. One patient received sclerotherapy and operation was performed in 3 patients for variceal bleeding. Four patients were subjected to liver biopsy. RESULTS: Liver dysfunction of these patients remained normal and variceal bleeding didn't reccur after therapy. Liver biopsy showed nodular regenerative hyperplasia without fibrous septa. CONCLUSIONS: Non-cirrhotic portal hypertension associated with autoimmune disease is a rare syndrome, characterized by significant portal hypertension as well as histological evidence that cirrhosis is absent. Prevention and treatment of variceal bleeding is very important.

Adult↗
PubMed2002

[A case of fulminant acute poststreptococcal glomerulonephritis showing mesangiolysis and crescent formation preceded by erysipelas].

A 66-year-old man with erysipelas was admitted with complaints of oliguria and massive proteinuria/hematuria. He was diagnosed as having acute poststreptococcal glomerulonephritis(APSGN) due to erysipelas infected by group A streptococcus pyogenes. On admission, his white cell count increased to 31,000, and CRP was 27.3 mg/dl. Serum urea nitrogen and creatinine were increased to 90.1 mg/dl and 4.5 mg/dl, respectively. He had diabetes mellitus(HbA1c 7.9%) and liver dysfunction(total bilirubin 3.5 mg/dl, AST 76 IU, ALT 41 IU) caused by alcoholic liver cirrhosis. Hypocomplementemia was found in addition to ASO 216 U/ml and ASK 10,240 x. After antibiotics treatment was initiated, inflammation of the erysipelas began to improve. Disseminated intravascular coagulation syndrome, probably due to sepsis, occurred on the 5th hospital day. He died of gastrointestinal bleeding on the 18th hospital day. Renal autopsy revealed 37% formation of fibrocellular crescents, and marked mesangiolysis was noted by light microscopy. Granular deposition of C3 and IgG was seen along the capillary walls on immunofluorescence study. Intramembranous deposits were scattered on electron microscopy. This case illustrates a fulminant type of APSGN, which was in part attributed to the presence of diabetes and alcoholic liver cirrhosis. Histological findings of crescent formation and marked mesangiolysis may account for the fulminant clinical course.

Aged↗
PubMed2002

[Prevalence and risk factors of significant intrapulmonary shunt in cirrhotic patients awaiting liver transplantation].

BACKGROUND/AIMS: Hepatopulmonary syndrome is a condition of severe hypoxia with intrapulmonary shunt (IPS) in the setting of hepatic dysfunction. Liver transplantation has been suggested as a definite treatment for hepatopulmonary syndrome with reversal of IPS in some patients. Inconsistency of response and inability to predict reversibility, however, are significant problems. We performed this study to evaluate the prevalence of significant IPS in pretransplantation cirrhotic patients and to find any risk factors of IPS. METHODS: Fifty-seven patients (M:F = 38:19, median age 49 years (range 18-71)) with liver cirrhosis awaiting liver transplantation were serially included. Their IPS status was evaluated using contrast- enhanced echocardiography. Significant shunt was defined as a shunt of grade >or= 2. RESULTS: Significant IPS was detected in 30 (52.6%) among 57 patients. Significant shunt was found in 24 (63.2%) of 38 Child-Pugh class C patients and in 6 (31.6%) of 19 Child-Pugh class A or B patients (p < 0.05). No significant difference in prevalence of significant shunt was seen according to age, sex, presence or absence of hepatocellular carcinoma, ascites, hepatic encephalopathy, and gastroesophageal varix. CONCLUSION: Significant intrapulmonary shunt is a common finding in cirrhotic patients awaiting liver transplantation. Child-Pugh class C is the risk factor associated with high prevalence of significant shunt.

Adolescent↗
PubMed1994

Organ interactions in the hepatorenal syndrome.

An increasing number of patients with severe liver dysfunction are admitted to the ICU for stabilization and organ-specific support, including liver transplantation. Global impairment of hepatic performance frequently results in pathologic organ interactions that limit the potential for recovery. One of the most notable of these interactions is the hepatorenal syndrome, an otherwise uniformly fatal complication of end-stage liver disease characterized by the progressive development of oliguria and low urine sodium excretion. The syndrome can occur in the setting of either acute or chronic liver disease, and portal hypertension may be important in the pathogenesis. The patient with the hepatorenal syndrome also has a number of systemic circulatory abnormalities induced by liver disease and/or portal hypertension, but the exact pathologic role of these abnormalities in the development of oliguria is uncertain. It is reasonably well established that diminished systemic BP characteristic of liver failure is not the primary cause of renal insufficiency. Rather, intrarenal preglomerular vasoconstriction mediated by unknown stimuli is the major defect in the hepatorenal syndrome, manifested by relative ischemia. Current data point to abnormal renal sympathetic innervation as one of the more likely major causes of this vasoconstriction. After exclusion of systemic intravascular volume depletion and other causes of oliguria, dialytic therapy is indicated when liver transplantation or recovery of liver function is anticipated; terminal supportive care is appropriate when these outcomes are not options.

Hemodynamics↗