Bridging Vessels Research Articles

Effect of coronary-caval shunt combined with partial pericardial devascularisation on oesophageal and gastric variceal bleeding caused by portal hypertension.

To investigate the effect of coronary-caval shunt combined with partial pericardial devascularisation on oesophageal and gastric variceal bleeding caused by portal hypertension. Between January 2005 and January 2015, coronary-caval shunt operations combined with partial pericardial devascularisation were performed electively on 15 cirrhotic patients with portal hypertension. All of these patients had a history of oesophageal and gastric variceal bleeding. The clinical and follow-up data of these patients were reviewed retrospectively. Another 15 patients receiving non-surgical treatments in a similar follow-up period were used as controls to compare the preventive effects of different treatment strategies on rebleeding. All of the 15 surgical procedures were performed successfully, and no severe complications occurred. Among these, autogenous splenic veins were used as bridge vessels in 6 cases, whereas the coronary vein and inferior vena cava were anastomosed directly in 9 cases. All surgical patients were followed up from 5 months to 10 years with an average of 63 months; 2 patients died due to liver failure induced by reactivation of hepatitis B virus and oesophageal/gastric variceal rebleeding, respectively. The rebleeding rates for surgical and non-surgical patients were 6.7% and 66.7% (p < 0.05), respectively, whereas the 5-year survival rates for the two groups were 85.7% and 33.3% (p < 0.05), respectively. Patients with oesophageal and gastric variceal bleeding caused by portal hypertension may benefit from a coronary-caval shunt combined with partial pericardial devascularisation due to decreased coronary vein pressure, unaffected hepatic blood inflow, and reduced incidence of rebleeding.

The placenta is the center of the chronic disease universe

Over the past quarter century it has become clear that adult onset chronic diseases like heart disease and type 2 diabetes have their roots in early development. The report by David Barker and colleagues showing an inverse relationship between birthweight and mortality from ischemic heart disease was the first clear-cut demonstration of fetal programming. Because fetal growth depends upon the placental capacity to transport nutrients from maternal blood, it has been a suspected causative agent since the original Barker reports. Epidemiological studies have shown that placental size and shape have powerful associations with offspring disease. More recent studies have shown that maternal phenotypic characteristics, such as body mass index and height, interact with placental size and shape to predict disease with much more precision than does birthweight alone. For example, among people in the Helsinki Birth Cohort, who were born during 1924–1944, the risk for acquiring colorectal cancer increased as the placental surface became longer and more oval. Among people in whom the difference between the length and breadth of the surface exceeded 6 cm, the hazard ratio for the cancer was 2.3 (95% CI 1.2–4.7, p=0.003) compared with those in whom there was no difference. Among Finnish men, the hazard ratio for coronary heart disease was 1.07 (1.02–1.13, P =0.01) per 1% increase in the placental weight/birthweight ratio. Thus, it appears that the ratio of birthweight to placental weight, known as placental efficiency, predicts cardiovascular risk as well. Babies born with placentas at the extremes of efficiency are more vulnerable for adult onset chronic diseases. Recent evidence suggests that placental growth patterns are sex specific. Boys’ placentas are, in general, more efficient than those made by girls. Another recent discovery is that the size, shape and efficiencies of the placenta can change over years of time with very narrow confidence limits. This suggests that the growth of the placenta within a population of women is strongly affected by their nutritional environment. Even though it is known that an individual placenta can expand to improve its nutrient acquisition capacity in the first 2/3rd of gestation, the mechanisms by which placentas grow in response to a specific nutritional environment are not known. Discovering those mechanisms is the task of the current generation of scientists. While it may seem obvious that good nutrition is highly important for women who are pregnant because it supports optimal placentation and fetal development, more research is needed to determine the mechanisms by which maternal nutrition, placenta growth and fetal health are related.

Evaluation of fetal congenital persistence of the left superior vena cava using fetal MR

Results The 58 cases of fetal LSVC detected by fetal MRI represents 1.23% of all fetal MRI examinations performed in our hospital (58/4726). All the 58 cases were correctly diagnosed by MR imaging but only 40 cases (69%) were correctly diagnosed by fetal ultrasound. Of the 18 cases which did not be correctly diagnosed by fetal ultrasound, 8 were sent to perform fetal MRI for head or chest malformation. Before fetal MRI they only did general fetal ultrasound and never did fetal echocardiography. 9 did fetal echocardiography before fetal MRI. But the doctors are from small hospital and no enough experience. Only one case which did not be correctly diagnosed was performed fetal echocardiography by experienced doctors and this case first time performed fetal echocardiography was at 34 weeks gestation. After the fetal cardiac MRI examination, all the 18 cases were performed fetal echocardiography again and all can find persistent LSVC. In the 40 cases correctly diagnosed by fetal ultrasound, two cases LSVC were correctly diagnosed using fetal echocardiography by experienced doctors but fetal MRI found bridging vessels which did not found by echocardiography. In another two cases (not include the 58 cases) LSVC was diagnosed by fetal echocardiography but fetal cardiac MRI found it was really a retroesophageal left brachiocephalic vein.

Ultrasound predictors of placental invasion: the Placenta Accreta Index

We sought to apply a standardized evaluation of ultrasound parameters for the prediction of placental invasion in a high-risk population. This was a retrospective review of gravidas with ≥1 prior cesarean delivery who received an ultrasound diagnosis of placenta previa or low-lying placenta in the third trimester at our institution from 1997 through 2011. Sonographic images were reviewed by an investigator blinded to pregnancy outcome and sonography reports. Parameters assessed included loss of retroplacental clear zone, irregularity and width of uterine-bladder interface, smallest myometrial thickness, presence of lacunar spaces, and bridging vessels. Diagnosis of placental invasion was based on histologic confirmation. Statistical analyses were performed using linear logistic regression and multiparametric analyses to generate a predictive equation evaluated using a receiver operating characteristic curve. Of 184 gravidas who met inclusion criteria, 54 (29%) had invasion confirmed on hysterectomy specimen. All sonographic parameters were associated with placental invasion (P < .001). Constructing a receiver operating characteristic curve, the combination of smallest sagittal myometrial thickness, lacunae, and bridging vessels, in addition to number of cesarean deliveries and placental location, yielded an area under the curve of 0.87 (95% confidence interval, 0.80-0.95). Using logistic regression, a predictive equation was generated, termed the "Placenta Accreta Index." Each parameter was weighted to create a 9-point scale in which a score of 0-9 provided a probability of invasion that ranged from 2-96%, respectively. Assignment of the Placenta Accreta Index may be helpful in predicting individual patient risk for morbidly adherent placenta.

Triphasic umbilical artery waveform: association with severe fetal growth restriction, fetal demise, and extreme velamentous cord insertion

Abstract Extreme Doppler abnormalities of the umbilical artery such as absent or reversed end diastolic velocity are associated with adverse perinatal outcomes. We present a case of a triphasic umbilical artery waveform identified at 24 weeks. The fetus was severely growth restricted with an estimated fetal weight of 314 g. A week later, fetal demise occurred. Placental pathology revealed a placental weight of 83 g, an extensive maternal floor infarction, and an extreme velamentous cord insertion 7 cm from the edge of the placental disc, with vessels entering at opposite poles of the placental disc and a single anastomotic bridging vessel on the chorionic plate connecting these two vascular poles. A triphasic umbilical artery waveform may be associated with a premorbid state and severe placental vascular abnormality. We hypothesize that the third and positive component in late diastole is present due to forward flow across the communicating bridging vessel into the contralateral entering vessel.

The establishment of bridge conduits model for artery grafts in coronary artery bypass grafting and experimental study for adenoviral-mediated gene transfection of endothelial nitric oxide synthase

Objective The experiment was designed.to establish the animal model of bridge conduits for artery grafts in coronary artery bypass grafting (CABG) and evaluate the efficacy of adenoviral-mediated gene transfection with endothelial nitric oxide synthase (eNOS).Methods Forty rabbits were divided into 4 groups (n =10) randomly.Establish the bridge conduits model by end-to-end anastomosis of the femoral artery to carotid artery:(1) eNOS group,the bridge graft was transferred with adenoviral-mediated eNOS; (2) zero load group,adenoviral-mediated zero load eNOS was transferred; (3) control group,only the bridge graft without gene transfection; (4) normal femoral artery group.Gene transfection was by the way of soaking method for adenoviral-mediated eNOS gene or zero load eNOS gene for 1 h.Three weeks later,the grafts were harvested and sent for measurement such as immunohistochemisty,NO content,efficacy of eNOS in the vessel wall and immunoblotting assay (Western blotting).Results There were no deaths in the rabbits.All of the bridge vessels in different groups got adaptive changes without obstruction.In the eNOS group,the smooth muscle were found thicked and the expression of eNOS increased obviously,while the vascular wall degeneration could be found in the other groups.Also there were no obvious expression of eNOS in the vessel walls in the three groups (P ＜ 0.05).The NO content and eNOS energy in eNOS goup were (8.83 ± 1.24) μmol/g and (0.987 ± 0.239) U/mg,different remarkably with other groups (P ＜ 0.05).The Western blot also show the same results.Conclusion The model we built is reliable and the adenoviral-mediated of eNOS gene transfection is successful,which can be used to increase the content of NO or the express efficacy of eNOS gene in the vessel wall of the artery bridge. Key words: Coronary artery bypass grafting; Bridge vessel; Spasm; Endothelial nitric oxide synthase; Gene transfection

The coronary collateral circulation revisited

The coronary collateral circulation revisited

Accessory anterior cerebral arteryと交通する異常血管に生じた破裂紡錘状脳動脈瘤の1例

Accessory anterior cerebral artery (accessory ACA) is a type of median artery of anomalous triplicate ACA. Aneurysmal formation at accessory ACA is extremely rare. We report a case of ruptured fusiform aneurysm at the anomalous bridging vessel connecting lt. A2 and accessory anterior cerebral artery. A 32-year-old female presented with severe headache. Neurological examination was normal. Computed tomography showed diffuse subarachnoid hemorrhage. Left carotid angiography demonstrated the aneurysm arising from the anomalous bridging vessel. The shape of the anomalous bridging vessel looked like an aneurysm originating from lt. A2 and the dome attaching to the accessory ACA. We performed trapping for the fusiform aneurysm at the anomalous bridging vessel. The patient was ambulatory on discharge.

Flow and anastomosis in vascular networks

We analyze the effect that the geometrical place of anastomosis in the circulatory tree has on blood flow. We introduce an idealized model that consists of a symmetric network for the arterial and venous vascular trees. We consider that the network contains a viscoelastic fluid with the rheological characteristics of blood, and analyze the network hydrodynamic response to a time-dependent periodic pressure gradient. This response is a measurement of the resistance to flow: the larger the response, the smaller the resistance to flow. We find that for networks whose vessels have the same radius and length, the outer the level of the branching tree in which anastomosis occurs, the larger the network response. Moreover, when anastomosis is incorporated in the form of bypasses that bridge vessels at different bifurcation levels, the further apart are the levels bridged by the bypass, the larger the response is. Furthermore, we apply the model to the available information for the dog circulatory system and find that the effect that anastomosis causes at different bifurcation levels is strongly determined by the structure of the underlying network without anastomosis. We rationalize our results by introducing two idealized models and approximated analytical expressions that allow us to argue that, to a large extent, the response of the network with anastomosis is determined locally. We have also considered the influence of the myogenic effect. This one has a large quantitative impact on the network response. However, the qualitative behavior of the network response with anastomosis is the same with or without consideration of the myogenic effect. That is, it depends on the structure that the underlying vessel network has in a small neighborhood around the place where anastomosis occurs. This implies that whenever there is an underlying tree-like network in an in vivo vasculature, our model is able to interpret the anastomotic effect.

Chronic subdural hematoma associated with the middle fossa arachnoid cyst: pathogenesis and review of its management

The pathogenesis of chronic subdural hematoma (CSDH) associated with an arachnoid cyst (AC) is still not clear. We propose an origin of initial bleeding of CSDH in patients with AC based on our experience and discuss the management of this disease. The total number of operations included in this study was 23. Eleven cases were indicated because of associated CSDH (group 1), and the other cases were due to different reasons (group 2). The relationship of the AC and dura was evaluated in patients who did not have CSDH (group 2) because patients with CSDH would have had structural changes of AC due to hematoma. In group 1, the age distribution was from 8 to 61years (mean 23.0). The development of CSDH was not related with Galassi types. The hematomas were located outside of the outer cyst membrane in six patients and both inside and outside in three patients. In two patients, the location could not be reviewed. After suspicion of the outer cyst membrane as the origin of the bleeding site, we found small bridging vessels between the dura and outer cyst membrane in three of five consecutive patients in group 2. Based on our surgical experience of AC cyst, we found small bridging vessels between the dura and outer membrane of the AC. We suggested that these small vessels are the source of initial bleeding leading to CSDH in AC.

Rare Anomaly of Great Arteries

A full-term male infant was transferred to our neonatal intensive care unit because of tachypnea and mild hypoxia. Right atrium and right ventricle enlargement were suspected in the prenatal examination. Echocardiography was performed, and a rare combination of anomalies was observed. The ascending aorta and the main pulmonary artery joined together at the level of the innominate artery over the bridging vessel. The branching patterns of the pulmonary artery and the aorta were normal. There was a very small perimembranous ventricular septal defect. Computed tomography was performed to confirm the diagnosis (Figs. 1, 2). The observed combination had not been reported previously. It was not truncus arteriosus because the orifices of the pulmonary artery and the aorta were separated (Fig. 3). Two diagnoses for this rare combination were considered. The first diagnosis defines it as a variant of the aortopulmonary window. This diagnosis is not correct because the bridging part is not a window but rather a large tube. The second diagnosis defines it as a variant of the right aortic arch and the left-side patent ductus arteriosus. This diagnosis is not appropriate because the innominate artery arises from the bridging vessel. If this vessel is patent ductus arteriosus, there should not be branching. Although the diagnosis was not clear, we thought the spontaneous improvement of pulmonary hypertension could lead to systemic collapse. Ligation of the bridging vessel was performed to avoid such a situation. However, the pulmonary hypertension did not improve after surgery. The ventricular septal defect was so small that the reason for pulmonary hypertension was not clear. Catheter examination showed that although the resistance of the pulmonary artery was high, it responded to oxygen inhalation. The patient was discharged with pulmonary hypertension therapy.

Restriction of placental vasculature in a non-human primate: A unique model to study placental plasticity

The limits of placental plasticity, i.e., the ability of the placenta to adapt and alter its growth trajectory in response to altered fetal requirements, are not known. We report fetal and placental hemodynamic adaptations in a novel non-human primate model in which the fetal inter-placental bridging vessels were surgically ligated. Doppler ultrasound studies showed that the rhesus placenta compensates for an approximate 40% reduction in functional capacity by increased growth and maintenance of umbilical volume blood flow. This unique experimental animal model has applications for mechanistic studies of placental plasticity and the impact on fetal development.

The Study of Residual Stress in Welded Specimens of Aluminium Alloy by Using Acoustic Emission Method

Welding is one of the most significant causes of residual stresses and typically produces large tensile stresses whose maximum value can be approximately equal to the yield strength of the materials being joined. These large tensile stresses are often responsible for premature component failure. Metallurgical welding joints are extensively used in the fabrication industry, including ships, offshore structures, steel bridge, and pressure vessels. In this study, residual stresses in welded specimens of AL–6061 were evaluated by using ACOUSTIC EMISSION method which is one of the nondestructive tests. In this work, AE signals formed during the tensile test of welded specimens were investigated. The results show that AE signals in specimens which have large amount of residual stress were detected in less load.

Overrepresentation of Males in Traumatic Brain Injury of Infancy and in Infants With Macrocephaly

Shaken baby syndrome (SBS) has been thought to be caused by violent shaking of an infant and is characterized by the triad of findings: subdural hematoma (SDH), retinal hemorrhages, and neurologic abnormalities. The triad is not specific for SBS and can be seen in accidental trauma and in certain medical conditions. Recent observations, however, question whether SBS exists. Herein, we review the gender differences in 3 groups of infants with traumatic brain injury: (1) neonates with SDH from birth trauma, (2) infants with SDH from accidental trauma, and (3) infants with SDH from SBS. Gender differences are also presented in a fourth group of infants with macrocephaly related to increased extra-axial fluid spaces (IEAFS). Compared with the expected male frequency of 51.4% in newborns, there was a statistically significant overrepresentation of males in each of the 4 groups-65.3%, 62.2%, 62.6%, and 68.8%, respectively. We believe that the most likely explanation for these findings relates to the larger head size of the male compared with the female which has several relevant consequences. First, the larger head circumference of a male newborn compared with a female newborn may increase the likelihood that a male newborn will incur a small SDH from the minor trauma of the birthing process that can later rebleed and present with a symptomatic SDH that could be misdiagnosed as SBS and child abuse. Second, a short fall would have a greater likelihood of causing a SDH in a male infant than a female infant who could subsequently become symptomatic from hours to weeks later and could thus present as an unexplained SDH. Third, infants with macrocephaly related to IEAFS may be at increased risk for developing a SDH from the larger head size and greater tautness of the bridging vessels in the extra-axial fluid spaces. We believe that many infants who have been diagnosed with SBS have been given incorrect diagnoses of child abuse. Rather, their SDH may occur as a result of a small SDH from the birthing process that enlarges during early infancy, a short fall, or from macrocephaly with IEAFS.

Posterior retinal breaks as a cause of vitreous hemorrhage in diabetes.

To describe posterior retinal breaks as a cause of vitreous hemorrhage in diabetic patients. In two institutional practices, six posterior retinal breaks were identified in five eyes of five diabetic patients with vitreous hemorrhage. All eyes underwent fundus photography and fluorescein angiography. Four eyes received barrier photocoagulation. The outcome measures included retinal nonperfusion, proximity to retinal vessels, and progression to retinal detachment. All six posterior breaks were in areas of retinal ischemia. No eyes had neovascularization. Three breaks had a bridging vessel, and three were in a paravascular location. One untreated eye had progression to a retinal detachment. The differential diagnosis for vitreous hemorrhage in diabetic patients should include posterior retinal breaks, particularly in the absence of proliferative disease. These breaks are paravascular, are located in areas of retinal ischemia, and may involve avulsed bridging vessels. We suggest treatment with barrier rather than panretinal photocoagulation.

Bridging Mucosal Vessels Associated with Rhythmically Oscillating Blood Flow in Murine Colitis

Oscillatory blood flow in the microcirculation is generally considered to be the result of cardiopulmonary influences or active vasomotion. In this report, we describe rhythmically oscillating blood flow in the bridging vessels of the mouse colon that appeared to be independent of known biological control mechanisms. Corrosion casting and scanning electron microscopy of the mouse colon demonstrated highly branched bridging vessels that connected the submucosal vessels with the mucosal plexus. Because of similar morphometric characteristics (19 +/- 11 microm vs. 28 +/- 16 microm), bridging arterioles and venules were distinguished by tracking fluorescent nanoparticles through the microcirculation using intravital fluorescence videomicroscopy. In control mice, the blood flow through the bridging vessels was typically continuous and unidirectional. In contrast, two models of chemically induced inflammation (trinitrobenzenesulfonic acid and dextran sodium sulfate) were associated with a twofold reduction in flow velocity and the prominence of rhythmically oscillating blood flow. The blood oscillation was characterized by tracking the bidirectional displacement of fluorescent nanoparticles. Space-time plots and particle tracking of the oscillating segments demonstrated an oscillation frequency between 0.2 and 5.1 cycles per second. Discrete Fourier transforms demonstrated a power spectrum composed of several base frequencies. These observations suggest that inflammation-inducible changes in blood flow patterns in the murine colon resulted in both reduced blood flow velocity and rhythmic oscillations within the bridging vessels of the mouse colon.

Giant bilateral perinephric tumour and overt proteinuria

Keywords: angiomyolipoma; computed tomography;focal segmental glomerulosclerosis; kidney cancer;liposarcoma; proteinuriaA 63-year-old man with type 2 diabetes mellitus andhypertension presented with increasing abdominalgirth and foamy urine for the previous 2 years.Impaired renal function (BUN 33mg/dl, serum crea-tinine 2.3mg/dl), hypoalbuminaemia (2.3g/dl), overtproteinuria (11.2g/day), microscopic haematuria(RBC 21-35/HPF) and bilateral perinephric tumourwere noted at a local hospital. Non-contrast enhancedcomputed tomography of the abdomen confirmedgiant bilateral perinephric tumour with fat component(Figure 1). The differential diagnosis included retro-peritoneal liposarcomas or bilateral angiomyolipomaarising from renal capsule. After referral, physicalexamination revealed distended abdomen withoutpalpable mass. Magnetic resonance imaging(T1-weighted) demonstrated a lipomatous tumour ofabout 10cm in size, in the bilateral perinephric space(Figure 2). There was absence of radiological featuresof angiomyolipoma, including linear or branchingappearance of intra-tumoural vessels with evidentcontrast enhancement, aneurysmal dilatation of intra-tumoural vessels, haemorrhage within and outside thetumour, and the bridging vessel or beak signs [1].Hence, bilateral perinephric liposarcoma was favoured.However, a sonography-guided needle biopsy of theleft tumour showed only fibroadipose tissue, withoutidentification of malignant cells. The simultaneousneedle biopsy of left kidney revealed focal segmentalglomerulosclerosis (FSGS). Considering the invasiveclinical course of the tumours, bilateral radicalnephrectomy, with excision of the retroperitonealtumours, was performed. The pathology disclosedwell-differentiated liposarcomas with encasement ofbilateral kidney and involvement of the renal sinus,and further confirmed FSGS. The patient thereafterunderwent regular uneventful haemodialysis. TheFSGS and liposarcomas may just be coincidental inthis patient. However, the probability of bilateralperinephric liposarcoma with secondary FSGS stillcannot be completely excluded.Around 12–40% of liposarcomas occur in theretroperitoneum [2,3], and of these, 35% originate inthe perirenal fat [2]. Although liposarcoma is the mostcommon retroperitoneal soft tissues sarcoma, retro-peritoneal liposarcoma comprises only about 0.1% ofall cancers [2,3]. Liposarcomas tend to grow slowly in

Pass the Salt

Sodium is the most abundant extracellular ion. Historically, therapy with hypertonic saline was widely used for a variety of conditions. Currently, there are 3 primary indications for its use in critical care: hyponatremia, volume resuscitation, and brain injury. SIADH and CSW syndrome may require sodium replacement, but most cases of hyponatremia can be managed without administration of hypertonic saline. Studies of use of hypertonic saline in hypovolemia and brain injury are promising, but additional research is needed to better define optimal dosing regimens and to determine the relative risks associated with hypertonic saline versus conventional treatment for the management of patients with head injuries and for volume resuscitation in shock states.

COMPUTERIZED TOMOGRAPHY CHARACTERISTICS THAT DIFFERENTIATE ANGIOMYOLIPOMAS FROM LIPOSARCOMAS IN THE PERINEPHRIC SPACE

We performed a retrospective study to determine computerized tomography (CT) findings associated with perinephric angiomyolipomas or perinephric liposarcomas. During the last 7 years 6 patients with perinephric angiomyolipoma and 12 with perinephric liposarcoma were seen at our hospital. Two radiologists who were blinded to the pathological diagnosis retrospectively evaluated the CT characteristics of perinephric angiomyolipoma and perinephric liposarcoma. The relationship of each CT characteristic with tumor type was compared using Fisher's exact test. The CT characteristics of perinephric angiomyolipoma were intratumoral linear vascularity (p = 0.001), aneurysmal dilatation (p = 0.025), bridging vessel sign (p = 0.005), hematoma (p = 0.025), beak sign (p = 0.001) and discrete intrarenal fatty tumors (p = 0.025). The CT characteristic of perinephric liposarcoma was a nonfatty soft tissue mass (p = 0.005). There was no significant difference in the presence of calcifications in both groups. This retrospective study suggests that analysis of CT characteristics (linear vascularity, aneurysmal dilatation, bridging vessel sign, hematoma, beak sign and discrete intrarenal fatty tumors) may help to differentiate perinephric angiomyolipoma from perinephric liposarcoma.

Computerized tomography characteristics that differentiate angiomyolipomas from liposarcomas in the perinephric space.

We performed a retrospective study to determine computerized tomography (CT) findings associated with perinephric angiomyolipomas or perinephric liposarcomas. During the last 7 years 6 patients with perinephric angiomyolipoma and 12 with perinephric liposarcoma were seen at our hospital. Two radiologists who were blinded to the pathological diagnosis retrospectively evaluated the CT characteristics of perinephric angiomyolipoma and perinephric liposarcoma. The relationship of each CT characteristic with tumor type was compared using Fisher's exact test. The CT characteristics of perinephric angiomyolipoma were intratumoral linear vascularity (p = 0.001), aneurysmal dilatation (p = 0.025), bridging vessel sign (p = 0.005), hematoma (p = 0.025), beak sign (p = 0.001) and discrete intrarenal fatty tumors (p = 0.025). The CT characteristic of perinephric liposarcoma was a nonfatty soft tissue mass (p = 0.005). There was no significant difference in the presence of calcifications in both groups. This retrospective study suggests that analysis of CT characteristics (linear vascularity, aneurysmal dilatation, bridging vessel sign, hematoma, beak sign and discrete intrarenal fatty tumors) may help to differentiate perinephric angiomyolipoma from perinephric liposarcoma.