Morpho-functional study of the kidney in patients with kidney disease and liver disease with magnetic resonance

INTRODUCTION: We studied renal function and perfusion after the i.v. injection of Gd-DTPA-BMA, a nonionic paramagnetic contrast agent, to assess renal morphology and function in normal subjects, in renal insufficiency patients and in patients with hepatic failure and normal renal function. The latter were chosen because some patients with advanced hepatic failure may suffer from the hepatorenal syndrome, characterized by severe vasoconstriction in the renal cortical vessels. We investigated if dynamic MRI can detect early renal perfusion abnormalities in the patients who will eventually develop this syndrome. MATERIAL AND METHODS: Thirty MR examinations were carried out on 30 subjects after the i.v. injection of Gd-DTPA-BMA. Our series consisted of: 10 normal subjects; 10 renal insufficiency patients; 10 patients with hepatic failure and normal renal function. MR examinations were performed on a Philips ACS II scanner operating at 1.5 T. Two sequences were carried out in all cases: T1-weighted SE and T1-weighted TGE sequences after the bolus injection of .1 mmol/kg contrast agent. Renal longitudinal diameter and parenchymal thickness were measured in all cases and signal intensity time curves were always made. The signal intensity of the cortex, corticomedullary junction, medulla and pyelocaliceal system of each kidney was measured using a region of interest (ROI). The signal intensity curves were made considering quantitative parameters, including the area below the curve (ASC), the peak (P) and the time to peak (T-P). RESULTS: Longitudinal diameter and parenchymal thickness values were significantly lower in renal insufficiency patients than in normal subjects. Four phases were demonstrated after i.v. contrast agent injection in normal subjects, namely A) the cortical phase, B) the corticomedullary junction phase, C) the medullary phase, D) the pyelocaliceal phase. No signal intensity decrease in the medullary and pyelocaliceal curves was observed in renal insufficiency patients. Signal intensity curves values were lower in hepatic failure patients than in those with normal renal function. Hepatic failure patients could be divided into two groups: 5 patients had low P and ASC values and 4 had normal P and ASC values. The patients with lower P and ASC values developed the hepatorenal syndrome within a few months of the MR examination. DISCUSSION: Signal intensity decreased in the pyelocaliceal system phase in normal subjects because of the high paramagnetic contrast agent concentration. The lack of signal intensity decrease in renal insufficiency patients was caused by the reduced capability of concentrating Gd-DTPA-BMA. Lower signal intensity values in hepatic failure patients may be considered an early sign of the hepatorenal syndrome.     

Effects of chronic renal insufficiency and metabolic acidosis on glutamine metabolism in man

1. Arterial concentration and arterial-venous differences of glutamine across the kidney, forearm, hepato-splanchnic bed and brain were measured in patients with chronic renal insufficiency and in patients with normally functioning kidneys before and during chronic ammonium chloride acidosis. 2. In chronic renal insufficiency and in chronic metabolic acidosis there is a rise in glutamine release from the muscles and a suppression of glutamine uptake by the hepato-splanchnic bed and the brain. 3. In chronic renal insufficiency arterial glutamine concentrations is significantly increased in comparison with subjects with normal renal function and either normal acid-base balance or chronic metabolic acidosis. 4. In patients with chronic renal insufficiency the kidney extracts negligible amounts of glutamine, which cannot account for the renal ammonia production measured in the same patients.     

The binding of chloramphenicol to serum proteins in patients with chronic renal insufficiency

The binding (r) of chloramphenicol to serum proteins is significantly lower in patients with chronic renal failure than in normal subjects. Before hemodialysis, the mean r value in patients with chronic renal insufficiency was 0.165 mg/g (+/-0.003) versus 0.188 mg/g (+/-0.004) in healthy individuals. Hemodialysis produced a significant rise in r (to 0.182 mg/g, +/-0.004). Decrease in the serum concentration of albumin in patients with chronic renal insufficiency does not seem to be the sole factor responsible for decreased r.     

Peripheral elimination of growth hormone in chronic liver disease

Chronic liver disease is associated with raised basal and TRH-stimulated PRL and GH levels. In a recent study we found the kidney to be the main site of prolactin elimination in patients with liver disease. In order to determine whether this is specific for PRL or a more general mechanism for polypeptide removal, we studied the elimination of GH, which resembles PRL in molecular weight and primary amino acid sequence, in 5 patients with portal hypertension and hepatic cirrhosis and 5 patients with noncirrhotic portal hypertension. Plasma GH levels were measured before and after TRH in peripheral, hepatic and renal vein samples, taken during diagnostic hepatic vein catheterization. An excessive paradoxical increase of GH after THR stimulation was found in 4 out of 5 cirrhotic patients but in none of the noncirrhotic individuals (p less than 0.025). After TRH the mean hepatic venous levels were significantly lower than the peripheral venous levels in 4 out of 5 noncirrhotic patients but in only 1 of the 5 cirrhotic patients (p less than 0.05). The mean renal vein GH levels were significantly lower than the peripheral levels in 3 out of 5 noncirrhotic patients and in none of the cirrhotic patients. In 2 patients in whom renal and hepatic plasma flow was measured, renal extraction of GH was found to be 0 to 6.4 micrograms, while liver extraction amounted to 22.1 and 34.7 micrograms of GH during the same 60-min period. Despite the similarity in molecular weight and primary amino acid sequence between PRL and GH, GH appears to be mainly taken up by the liver while PRL is mainly eliminated by the kidney in this group of patients with portal hypertension. This suggests that the renal elimination of prolactin is not solely dependent on glomerular filtration. The selective hepatic removal of growth hormone is probably related to a specific action of growth hormone on liver metabolism.     

Sex differences and lateral specialization of hemispheric functioning

Acute renal failure developed in nine of 78 patients who were subjected to hepatic artery ligation for nonresectable and extensive malignant tumor of the liver. Of those nine, six had hepatomas, one cholangiocarcinoma, one metastatic islet-cell carcinoma and one metastatic melanoma. Preoperative renal function as reflected in blood-urea-nitrogen and serum creatinine values was within normal limits. There were marked elevations of serum glutamic-oxalacetic transaminase and lactic dehydrogenase levels after hepatic artery ligation, an indication of massive ischemic injury of the tumor and the liver. A diagnosis of acute renal failure was established within 14 to 70 hours after hepatic artery ligation. In five patients, oliguric renal failure developed, and in four, high urinary output renal failure. In only three patients did systemic hypotension and hypovolemia precede acute renal failure. Seven of the nine patients died. Postmortem examination was done in five patients, and in only two was there evidence of renal tubular necrosis. The factors contributing to acute renal failure appear to be extensive involvement of the liver by tumor, presence of ascites and jaundice, occlusion of the portal vein and hyperuricemia. The presence of any one of the foregoing contraindicates the procedure.     

Thyroid status in patients with chronic renal failure

Serum thyroid hormone concentrations have been measured in 21 patients with chronic renal failure, treated conservatively and compared with values from 19 control subjects. Many patients had serum total T3 and T4 concentrations below the reference ranges. The concentrations of free T4 and free T3 and the free thyroxine index were significantly lower in patients with abnormal total concentrations of the thyroid hormones than in the controls. Both the free and the total concentrations of T4 correlated inversely with the degree of renal failure. The concentration of thyroxine binding globulin (TBG), fell within the reference range in each of the patients, but was significantly lower in the patient group when compared with the controls. These TBG concentrations, however, were not sufficiently decreased to explain the low total thyroid hormone concentrations found in the patients. The affinity of TBG for T4 and T3 in the patient and control groups was not significantly different. The TSH response to TRH was diminished in many of the patients, but the measurement of other pituitary hormones indicated that pituitary function was normal in these patients. The possible mechanisms responsible for the changes observed in thyroid and pituitary hormones are discussed.     

Bacillus thermoamyloliquefaciens KP1071 alpha-glucosidase II is a thermostable M(r) 540,000 homohexameric alpha-glucosidase with both exo-alpha-1,4-glucosidase and oligo-1,6-glucosidase activities

The lethality of acute renal failure exceeds 50% due to multiorgan dysfunction. In such critically ill patients a reduction of thyroid hormone concentrations without clinical symptoms or laboratory evidence of hypothyroidism frequently occurs. Selenium has recently been shown to play a major role in thyroid hormone metabolism. The aim of this study was to investigate the possible influence of selenium on thyroid hormone metabolism in acute renal failure. Changes in thyroid metabolism were related to the severity of multiorgan failure and to the clinical course. Thyroxine (T4), tri-iodothyronine (T3), free-T4, free-T3, thyrotropin (TSH), serum creatinine, and plasma selenium concentrations in 28 patients (mean age 60 +/- 13) with acute renal failure and multiple-organ dysfunction syndrome were determined initially, and every 3 days after hospital admission. The plasma selenium concentration was found to be reduced compared to normal controls (32 +/- 14 vs. 70-120 micrograms/L). T4 (56 +/- 15 nmol/L, normal range 64-148), T3 (1.31 +/- 0.38 nmol/L, normal range 1.42-2.46), free-T3 (3.1 +/- 1.0 pmol/L, normal range 4.7-9.0), and free-T4 (10.8 +/- 4.0 pmol/L, normal range 10.3-25.8) values were low in 50-70% of the patients at the time of presentation. Plasma TSH concentrations were within the normal range (0.59 +/- 0.79 mU/L, normal range 0.25-3.1), and no clinical symptoms of hypothyroidism were observed. T4 concentration was higher in patients who survived acute renal failure compared to nonsurvivors (62 +/- 22 vs. 51 +/- 16 nmol/L, p < 0.05). Plasma selenium concentration was lower in patients with a severe organ dysfunction syndrome (36 +/- 10 vs. 29 +/- 19 micrograms/L) and correlated with the number of organ failures in these patients (r = -0.247, p < 0.05). T4 and free-T4 values paralleled decreasing selenium concentrations (r = 0.35, p < 0.05). Thyroid hormone levels were reduced in patients with acute renal failure without an increase in TSH. An increase in T4 concentrations became apparent during treatment and may be related to a favorable outcome in acute renal failure. Thyroid hormone concentrations paralleled plasma selenium levels, indicating a possible influence of selenium on thyroid function in acute renal failure.     

Thyroid dysfunction in uremia: evidence for thyroid and hypophyseal abnormalities

Disturbances in thyroid function and a high prevalence of goiter develop in patients on chronic hemodialysis. This study shows that in patients on dialysis, mean serum thyroxine and triiodothyronine levels are lower than normal. Patients with chronic renal failure not on dialysis, have mean serum thyroxine levels similar to normal subjects and low mean serum triiodothyronine levels. However, both serum thyroxine and triiodothyronine concentrations decrease as the renal failure worsens. In addition, both groups of patients with renal failure have a decreased serum thyroxine response to oxogenous thyrotrophin and a diminished serum thyrotrophin response to thyrotrophin-releasing hormone. These data suggest the presence of an intrathyroidal and an hypophyseal defect in uremic patients. Although serum iodide concentrations are elevated, there is no correlation between the level of serum iodide and the degree of renal failure. Therefore, we have no direct evidence that iodide excess is responsible for the abnormalities observed.     

Levels of cadmium in serum of patients with chronic renal failure

The aim of the study was obtain answers the following questions: 1. Are serum cadmium concentrations in patients with chronic renal failure (CRF) different from levels in healthy subjects? 2. Are serum concentrations of above mentioned metal different between haemodialysed and non-haemodialysed patients. 3. Are serum cadmium concentrations changing during haemodialysis? 66 patients with chronic renal failure (42 patients treated with haemodialysis and 24 non-haemodialysed patients) and 16 healthy subjects were observed. The blood samples in non-haemodialysed patients and healthy subjects were withdrawn only after cannula had been inserted into the antebrachial vein. The blood samples in haemodialysed patients were withdrawn four times: just before dialysis, during haemodialysis (in one hour of dialysis just in front of dialyser and just behind one) and after haemodialysis. Cadmium concentrations in serum in all examined group and cadmium concentrations in dialysis fluid and in demineralised water were measured by flame atomic absorption spectrophotometry. No significant changes were observed in serum cadmium concentration between patients with CRF and healthy subjects. Cadmium-concentration in non-haemodialysed patients was significantly higher than in haemodialysed patients. During haemodialysis a significant increase of serum cadmium level was observed. Conclusions: 1. Serum cadmium concentration in patients with CRF and in healthy subjects are not statistically different; 2. No significant changes in cadmium concentration between uraemic group patients were found; 3. Haemodialysis influences significantly on cadmium concentration.     

Malaria in the southern sanitary district of Dakar (Senegal). 2. Entomologic data]

This study aimed to investigate the cause of persistently increased serum gastrin concentration seen in some Graves' disease patients even when euthyroid during antithyroid drug treatment. The subjects studied consisted of three groups: 33 patients with a common-type of Graves' disease, 14 with triiodothyronine (T3)-predominant Graves' disease (characterized from previous studies as having potent immunologic abnormalities including greater concentrations of thyroid-stimulating antibodies together with larger goiter size), and a group of 20 normal subjects. Fasting serum gastrin concentrations in common Graves' disease patients were significantly higher than those of normal subjects (58.4 +/- 38.9 pmol/L vs. 37.8 +/- 18.9 pmol/L [mean +/- SD], p < 0.05). The serum gastrin concentrations were even greater in T3-predominant Graves' disease patients than common Graves' disease patients (162.9 +/- 224.0 pmol/L vs. 58.4 +/- 38.9 pmol/L, p < .05). Serum pepsinogen I (PGI) concentrations were significantly lower in the T3-predominant patient group than the common Graves' group (24.0 +/- 12.9 ng/mL vs. 39.7 +/- 19.6 ng/mL, p < .05). Serum ratios of PG I to PG II were significantly lower in the T3-predominant Graves' disease patients than normal subjects (3.59 +/- 2.66 vs. 5.97 +/- 1.56, p < .01). The ratios also had a significant (p < .05) inverse correlation with serum gastrin concentrations in T3-predominant Graves' disease patients. The results suggest that autoimmune gastritis is associated with Graves' disease, particularly in patients with potent thyroid-autoimmunity.     

Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2

To determine the relationship between quantitative Doppler parameters of portal, hepatic, and splanchnic circulation and hepatic venous pressure gradient (HVPG), variceal size, and Child-Pugh class in patients with alcoholic cirrhosis, we studied forty patients with proved alcoholic cirrhosis who underwent Doppler ultrasonography, hepatic vein catheterization, and esophagoscopy. The following Doppler parameters were recorded: time-averaged mean blood velocity, volume flow of the main portal vein flow, and resistance index (RI) of the hepatic and of the superior mesenteric artery. Doppler findings were compared with HVPG, presence and size of esophageal varices, and Child-Pugh class. There was a significant inverse correlation between portal velocity and HVPG (r = -.69), as well as between portal vein flow and HVPG (r = -.58). No correlation was found between RI in the hepatic artery or superior mesenteric artery and HVPG. No correlation was found between portal vein measurements and presence and size of varices. Severe liver failure was associated with lower portal velocity and flow. In patients with alcoholic cirrhosis, only portal vein blood velocity and flow, but neither hepatic nor mesenteric artery RI, are correlated to the severity of portal hypertension and to the severity of liver failure.     

T3, T4 and TSH serum levels in patients on long-term treatment for epilepsy

The serum T3, T4 and TSH concentrations were assessed by RIA method in 25 (14 females, 11 males) long-term treated (mean treatment duration 12.8 years) epileptic patients. The mean serum T3, T4 and TSH levels were lower than in control group according to clinical picture of epilepsy and treatment applied. The lowest mean serum TSH concentration was in patients with known aetiology of epilepsy. Patients with tonic-clonic seizures had lower serum levels of all hormones measured in comparison with the patients with partial seizures. Mean serum T3, T4 and TSH levels were low in patient group receiving valproic acid. The lowest mean TSH serum concentration as compared to control group was in the patients treated with phenytoin. None of the epileptic patients developed clinical symptoms of hypothyreoidism.     

Plasma aldosterone concentrations in chronic renal disease

The disagreement in the literature concerning the role of aldosterone in the maintenance of potassium homeostasis in chronic renal disease might be partially explained by differences in plasma renin activity (PRA) among individual patients. Therefore, a study was done in 28 selected patients with varying degrees of renal insufficiency whose serum potassium and PRA concentrations were within the normal range. The results indicate that at comparable serum potassium and PRA concentrations, plasma aldosterone is in most instances elevated when creatinine clearance is lower than 50% of normal.     

Hemodynamic changes in the lower limbs during treadmill walking in normal subjects and in patients with arteriosclerosis obliterans

The effects of arteriosclerosis obliterans on the hemodynamic changes that occur during walking are largely unknown. For this reason, the authors measured blood pressure by transducer from the posterior tibial artery and vein at both ankles in 23 patients with arteriosclerosis obliterans of different severity and at the left ankle in 8 normal subjects. Radial artery pressure was also measured, and the differences between mean radial and ankle arterial pressures (pressure gradient) and between mean arterial and venous ankle pressures (foot perfusion pressure) were calculated. All measurements were made simultaneously and continuously during standing, treadmill walking at five different speeds, and during recovery. Compared with the normal subjects, the patients exhibited a greater pressure gradient and lower ankle arterial pressure and foot perfusion pressure at rest. During walking and recovery these intergroup hemodynamic differences were markedly enhanced, and ankle venous pressure was lower in the patients than in the normal subjects. In the patients the hemodynamic pattern depended on disease severity at rest and on both disease severity and walking speed during walking and recovery.     

Changes in serum thyrotropin (TSH) in man during halofenate administration

Halofenate, a serum lipid-lowering agent which inhibits binding of thyroid hormone to thyroxine-binding globulin (TBG), was administered daily for 14 days to 8 hypothyroid subjects with elevated TSH concentrations as a result of incomplete thyroxine (T4) therapy. Drug administration resulted in mean increases in serum dialyzable fraction T4 (DFT4) of 52% over pretreatment levels (P less than 0.01) and in dialyzable fraction triiodothyronine (DFT3) of 26% in 7 subjects, (P less than 0.01). During halofenate treatment in these 7 subjects, serum TSH concentrations decreased significantly (mean = 39%, P less than 0.01) when DFT4 and DFT3 were increased by halofenate. In only two subjects was there a convincing temporal relationship between increased serum absolute free T4 (AFT4) and decreased serum TSH concentrations. Contrary to what would be predicted from the "free hormone hypothesis", changes in serum TSH concentration in these hypothyroid patients appeared to relate primarily to changes in the free fraction of circulating T4 and T3 (DFT4, DFT3), rather than to alterations in AFT4 or AFT3. Halofenate did not alter serum TBG binding capacity. An eighth subject did not show increased DFT4 and DFT3 during halofenate treatment despite achievement of therapeutic serum levels of the agent; in this patient, serum TSH levels rose progressively throughout the period of inadequate T4 replacement and halofenate administration. In hypothyroid patients, short-term halofenate use suggests that the pituitary-thyroid hormone feedback circuit can respond to increases in serum DFT4 and DFT3 in the absence of detactable increases in absolute free hormone concentrations.     

Cathepsin D serum mass concentrations in patients with hepatocellular carcinoma and/or liver cirrhosis

Cathepsin D serum mass concentrations were determined by enzyme immunoassay in patients with hepatocellular carcinoma (n = 51) and/or liver cirrhosis (n = 92) or benign steatosis (n = 16) and correlated with some biochemical and clinical properties of these diseases. Increased cathepsin D serum mass concentrations (P < 0.001) were observed in all these groups of patients as compared to normal subjects (n = 98). However, patients with steatosis had serum mass concentrations of this enzyme significantly lower (mean 2-3 fold) than those measured in cancer patients (P < 0.05) or cirrhotic patients (P < 0.001). Interestingly, significantly higher cathepsin D serum mass concentrations (mean + 62%) (P < 0.006) were determined in the cirrhosis group as compared to cancer patients. No correlation between cathepsin D and a number of clinical and biochemical properties examined, namely, alpha-foetoprotein, number of neoplastic lesions and tumour size in cancer patients or, Child-Pugh grade of severity of cirrhosis and other enzymes of liver function tests in the cirrhotic group was found. The present data and those from other studies which indicate that cathepsin D may be involved in carcinogenesis suggest that this enzyme may be potentially useful as an additional biochemical marker to identify cirrhotic patients who may develop precancerous hepatic nodules.     

Renal vein renin activity: a prospective study of sampling techniques and methods of interpretation

Seventy patients undergoing renal arteriography were studied prospectively to define optimal techniques of renal venous sampling and to establish the most appropriate methods for interpretation of renal vein renin and activity (RVRA). Plasma renin activity values from the aorta, the antecubital vein and the lower inferior vena cava were nearly identical. The relationship between renal vein renin activity in the two renal veins was not influenced by lack of simultaneous sampling or by contrast administration. Thirty-one patients with normal arteriograms had a mean RVRA ratio (right over left) of 1.12 +/- .11 (mean +/- SEM) but RVRA difference (right minus left) of only 0.02 +/- .11 ng/ml/hr. In contrast 16 patients with "significant" (greater than 70%) narrowing of the main renal artery had a mean RVRA ratio (involved over uninvolved) of 4.3 +/- 1.2 and a mean RVRA difference (involved minus uninvolved) of 3.9 +/- 1.4 ng/ml/hr. Seven patients (22%) with normal arteriograms had "abnormal" RVRA ratios (greater than or equal 1.5) but corresponding RVRA differences within one standard deviation of the group mean. Thus the difference inRVRA between both renal veins may more accurately reflect a patient's renovascular status than does the corresponding RVRA ratio. An "abnormal" RVRA ratio alone inadequately indicates the presence of renal ischemia.     

Determination of hepatic zinc content in chronic liver disease due to hepatitis B virus

BACKGROUND/AIMS: Zinc is an essential, mostly intracellular, trace element which participates in many physiologic mechanisms. Some liver functions like urea formation require the presence of zinc; thus the determination of hepatic zinc content may contribute to the understanding of probable zinc-related clinical consequences of chronic liver disease. In this study, we aimed to determine the hepatic zinc concentrations in patients with chronic liver disease due to the Hepatitis B virus and to ascertain the relationship between the severity of liver disease and hepatic zinc content, if one in fact exists. METHODOLOGY: A total of 99 HBsAg positive subjects were included in the study. We performed a liver biopsy on all subjects. Hepatic zinc concentrations were determined by atomic absorption spectrophotometry. RESULTS: The liver biopsies were normal in 25 subjects. There were 33 chronic active hepatitis (CAH), 34 cirrhosis and 7 chronic persistent hepatitis (CPH) patients in the study group. In the control group, CAH, cirrhosis and CPH groups, the mean liver zinc concentrations were 3.83 +/- 1.86, 1.86 +/- 0.92, 1.14 +/- 0.68 and 3.74 +/- 1.81 mumol/g dry weight, respectively. Hepatic zinc in the CAH and cirrhosis groups were lower than that of the control group (p < 0.05). We also found that liver zinc in the cirrhosis group was lower than in the CAH group (p < 0.05). CONCLUSION: According to these results, as the severity of liver damage increases, the hepatic zinc concentration decreases. Therefore, it can be suggested that zinc supplementation may improve hepatic encephalopathy by increasing the efficiency of the urea cycle.     

Founder effect at PGL1 in hereditary head and neck paraganglioma families from the Netherlands

After repeated exposure to inhaled anesthetics, the hepatic function and metabolism of anesthetics may change. The purpose of this study was to investigate inorganic fluoride (F-) kinetics and renal and hepatic function after repeated exposure to sevoflurane. Ten patients (aged 40-70 yr) who had received sevoflurane anesthesia with a gas flow of 6 L/min for neurosurgery twice in 30-90 days were studied. Serum and urine F- concentrations were measured up to 24 h after anesthesia. Blood urea nitrogen, serum creatinine, serum and urine beta2-microglobulin, urine N-acetyl-beta-D-glucosaminidase, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin concentrations were measured up to 7 days after anesthesia. The area under the curve (AUC) of serum and urine F- concentration and half-life of serum F concentration were calculated. Urine beta2-microglobulin, AST, and ALT increased to abnormal levels after both anesthesias, with no difference between anesthesias. No measured variables, AUC of serum and urine F- concentration, or half-life of serum F- concentration showed any differences between the first and second anesthesias. In conclusion, the second exposure to sevoflurane with a high gas flow of 6 L/min in 30-90 days did not change the hepatic and renal function or affect the metabolism of sevoflurane. Implications: We studied the changes of metabolism of sevoflurane and hepatic and renal function after repeated sevoflurane anesthesia in 30-90 days. There were changes indicative of mild liver and kidney injury after sevoflurane anesthesia, but repeated exposure to sevoflurane did not enhance these changes.     

Alveolar echinococcosis of the liver: sequelae of chronic inferior vena cava obstructions in the hepatic segment

BACKGROUND: The clinical pattern and long-term course of chronic inferior vena cava (IVC) obstructions are variable and depend on the underlying cause, the segment involved, and the extension of secondary thrombosis. Pertinent data on IVC obstructions in well-defined series of patients are lacking. We report the sequelae of chronic IVC obstructions in the hepatic segment in 11 consecutive patients derived from a cohort of 104 patients with alveolar echinococcosis of the liver. METHODS: Based on the results of computed tomography scans, 11 patients (7 men, 4 women; mean age, 53.4 years) with IVC obstructions were selected from an ongoing prospective long-term chemotherapy trial comprising 104 patients with alveolar echinococcosis studied at yearly intervals according to a protocol. Obstruction of the IVC in the 11 patients existed for a mean duration of 8.6 years. In these patients, magnetic resonance imaging was performed to assess the morphologic features and extension of the IVC obstruction, as well as the collateral venous pathways. Patency and valvular function of the femoropopliteal veins were analyzed by color-coded duplex ultrasonography. RESULTS: Total occlusions of the IVC were evident in 8 patients (73%) and subtotal stenoses in 3 patients (27%). Only 4 patients (36%) exhibited signs and symptoms of chronic venous insufficiency of the lower extremities; 2 (18%) of the 4 had a history of swelling in the lower extremity. Seven patients (64%) had no lower extremity symptoms. One patient had a history of pulmonary embolism. Abdominal collateral veins were documented in 5 patients (45%) by using magnetic resonance imaging; however, they were clinically evident in only 3 patients (27%). In the 8 patients with IVC occlusion, thrombosis ended at the confluence of the hepatic veins. Obstruction of the IVC was limited to the hepatic segment in 2 patients (18%) and extended to the distal IVC or the iliofemoral veins in 6 patients (54%). Chronic venous insufficiency was present only if the femoropopliteal veins had been involved in the thrombotic process, showing residual venous obstruction, valvular incompetence, or both. Bilateral renal vein thrombosis with moderate proteinuria was observed in 2 patients (18%). The main collateral drainage was achieved through the ascending lumbar, azygos, and hemiazygos veins. CONCLUSIONS: In patients with alveolar echinococcosis, obstruction of the IVC in the hepatic segment often develops asymptomatically and rarely leads to the impairment of renal function. The collateral circulation fully compensates for obstruction of the IVC. Thrombotic involvement and valvular incompetence of the femoropopliteal veins seems to determine the development of chronic venous insufficiency of the lower extremities.