renal cysts are the most common benign finding in the kidneys.

Renal cysts can be divided

in cortical and sinus cysts. Renal sinus cysts are benign. They can be subdivided into
parapelvic cysts that originate from the adjacent parenchyma and protrude into the
renal sinus and peripelvic cyst that originate within the sinus itself. If a renal cyst
demonstrates no contrast enhancement or a difference in attenuation < 10 UH from
NECT to CECT (on portal phase) it is considered as non enhancing simple cysts. If there
in an increase in density from 10 to 20 HU it is indeterminate, and psuedoenhacement
artifact should be considered. A difference in density > 20 HU is a major criterion to
classify it as a complex cyst. Bosniak classification is helpful in predicting a risk of
malignancy of a complex renal cyst. Simple cysts are well-defined with thin or
imperceptible wall, and they show water attenuation (<20 HU) on NECT. These types
of cysts are classified as Bosniak I. When a cyst presents itself with minimally
increased number of septa, but non- measurable c.e of a hairline-thin septa they are
classified as Bosniak II. Hyper attenuating cyst on NECT are well capsulated cysts with
thin or imperceptible hyper attenuating (60-90 HU) walls, categorized as Bosniak II F.
Strictly follow-up is mandatory in II F cysts. Indeterminate cysts show thick margins,
nodular multiple septa or wall with measurable enhancement, hyperdense on CT
(Bosniak III). Lesions of this type have a high probability to be malignant (50%) Clearly
malignant renal cysts are solid mass with a large cystic or a necrotic component
(Bosniak IV)

Renal non-cystic lesions: renal lesions that do not exhibit a cystic density such as
angiomolypoma with negative densitometric values on NECT and solid lesions that
frequently exhibit high UH values in NECT and contrast enhancement on CECT are also
considered as solid findings. Mostly common renal non-cystic lesions are renal
angiomolypoma, renal cell carcinoma, transitional cell carcinoma that will be discussed
below. Renal Angiomiolypoma: most lesions involve the cortex and demonstrate
macroscopic fat content (less than -20 HU). When small in size it can be difficult to
differentiate them from a small simple cyst. Fat containing lesions are not
pathognomonic of renal angiomyolipoma because lipid necrosis or osseous metaplasia
can be present also in renal cell carcinoma and metastasis. Multiple renal
angiomyolipomas can be observed in tuberous sclerosis Renal Cell Carcinoma: it is the
most common renal tumor that derived from tubular epithelium. The renal cell
carcinoma most frequently affects middle-aged or advance-aged patients and clinically
it may manifest with flank pain or hematuria. Renal cell carcinomas, mostly when
asymptomatic, are usually found as small incidental lesions during a radiological
examination (ultrasound in primis) performed for other causes. The recognized risk
factors for kidney cancer are cigarette smoking, obesity and dialysis cystic related
disease. Renal cell carcinoma shows soft tissue attenuation on NECT. Larger lesions
can frequently have areas of necrosis or fat and some calcification can be present. On
CECT they demonstrate variable enhancement, usually less than the normal cortex.
Large lesions have irregular enhancement due to areas of necrosis. When the renal
cell carcinoma is well capsulated and a pseudo capsule is present the differential
diagnosis with renal oncocytoma cannot be made. The clear cell subtype may show
much stronger enhancement.

Renal Cell Carcinoma: it is the most common renal tumor that derived from tubular
epithelium. The renal cell carcinoma most frequently affects middle-aged or advance-
aged patients and clinically it may manifest with flank pain or hematuria. Renal cell
carcinomas, mostly when asymptomatic, are usually found as small incidental lesions
during a radiological examination (ultrasound in primis) performed for other causes.
The recognized risk factors for kidney cancer are cigarette smoking, obesity and
dialysis cystic related disease. Renal cell carcinoma shows soft tissue attenuation on
NECT. Larger lesions can frequently have areas of necrosis or fat and some
calcification can be present. On CECT they demonstrate variable enhancement,
usually less than the normal cortex. Large lesions have irregular enhancement due to
areas of necrosis (Fig 21). When the renal cell carcinoma is well capsulated and a
pseudo capsule is present the differential diagnosis with renal oncocytoma cannot be
made.
Transitional cell carcinoma: it affects renal excretory pathways and may occur at the
level of calyx, pelvis, ureter and bladder. Transitional cell carcinoma may usually
appear as papillary lesions
that partly or completely occupy the excretory pathway with frond like appearance.
Another morphologic pattern of presentation is non-papillary type with nodule or
sessile tumors. When transitional cell carcinoma grows into the renal pelvis can
completely occupy the lumen and obliterate the renal sinus fat. Clinically, it occurs
more frequently with micro or macro hematuria and pain at the side that mimics a
renal colic when hydronephrosis is manifested as a result of obstruction. CT plays a
fundamental role in the differential diagnosis between urinary stones and a neoplastic
lesion. The diagnosis of obstructive renal calculus is already possible in the NECT
phase where the presence of a hyper attenuating calculus along the urinary pathways
can be observed. In addition to the usual image CT protocol, it is crucial to perform
scans between 5 and 10 minutes in which the contrast media is excreted by the renal
excretory system and fills the excretory pathways allowing the visualization any filling
defects. If a fill defect is present, it is necessary to evaluate whether this findings
demonstrates contrast enhancement between the NECT phase and the arterial phases
and portal. This simple measurement allows to differentiate between the presence of a
clot that has density close to the blood, around 50-60 HU in the NECT phase but no
contrast enhancement in the CECT phases can be observed and a transitional cell
lesion whose contrast enhancement is greater than 15 from the NECT phase to CECT
phases. To increase sensitivity in detecting transitional lesions it is necessary to use a
proper windowing by reducing the contrast and lowering the grayscale once delayed
scans are obtained.
If the lesion to be studied is in the bladder it is necessary to wait longer than 10
minutes after contrast medium injection to acquire the delayed phases. In this way we
try to fill as much as
possible the bladder with the contrast medium especially for suspected anterior wall
lesions. This is because the contrast media is positioned by gravity from the posterior
bladder wall to the side wall until the anterior wall. An anterior wall lesion can be
studied also by positioning the patient prone on the bed during the delayed phase.
Even when performing a study for the evaluation of a bladder lesion (observed by
ultrasound or with cystoscopy), it is necessary to pay great attention to all urinary
tract because transitional lesions often manifest themselves as multicentric lesions.

Cystic lesions
Renal cystic lesions are the most commonly encountered focal lesions of the kidney;
they include simple cysts containing clear fluid, complicated cysts with proteinaceous
or hemorrhagic content and complex cysts with thick walls, intracystic septations and
sometimes mural nodules. Simple renal cysts appear similar to other pure cysts found
in different anatomical sites; they are often multiple and can be very numerous in
renal cystic diseases. A particular type of renal cysts develops in the renal sinus and
can have a lymphatic origin (peripelvic cysts), or result from a renal parenchymal cyst
extending into the renal sinus (parapelvic cyst). Peripelvic cysts are frequently
bilateral and have elongated morphology that can mimic dilated renal calyces and
pelvis; contrast enhanced images acquired in delayed excretory phase allow to
differentiate hydronephrosis from peripelvic cysts that can cause stretching and
compression of renal calyces. Renal sinus cysts rarely complicate with hemorrhage or
infection.
Complicated cysts show characteristic signal abnormalities; besides hyperintensity on
T1- weighted images they can exhibit low signal on T2-weighted images. Less
frequently chronically complicated cysts can appear pseudosolid due to slightly signal
iperintensity on T1-weighted images and near isointensity to renal parenchyma on T2-
weighted images; contrast enhanced imaging can demonstrate the cystic nature of
the lesion. Bosniak classification adapted to MR imaging is commonly used to define
risk of malignancy and allow correct management of renal cystic lesions. Simple cyst,
cystic lesions with few hairline thin septa and small complicated cyst without contrast
enhancing mural or intracystic component are typically benign; some cysts with more
numerous or slightly thickened septa can require follow-up. Complex cysts with thick
enhancing walls and septations are considered to be at increased risk of malignancy,
as they may represent a cystic form of renal cell carcinoma, and are usually surgically
excised. About half of complex cysts are constituted by benign lesions such as
complicated inflammatory cysts with thick fibrous walls and septa and the rare
multilocular cystic renal tumors. Complex cystic masses with solid enhancing nodules
are very frequently malignant and require intervention. Hematomas and abscesses
manifest as fluid containing masses with imaging features similar to those seen in
other organs; both lesions may be found inside the kidney, intraparenchymal or
subcapsular in location, or involve the perirenal space.

Solid masses
The second most common variant of RCC, the papillary type, may be differentiated from
its clear cell counterpart because it frequently exhibits low signal intensity on T2-
weighted images and typically demonstrates a lesser degree of contrast enhancement
that sometimes requires assessment of subtraction images between precontrast and
postcontrast acquisitions to be recognized. Intratumoral cystic changes and
hemorrhage can also be found in papillary RCC.
Renal metastases appears as solid masses with variable enhancement depending on
the pathological features of primary tumor, and when solitary may resemble RCC in
several aspects; the frequent multifocality and bilateral renal involvement in
metastatic disease can suggest the correct diagnosis. Similarly, renal lymphoma
usually encountered as part of a disseminated lymphoproliferative disorder often
manifests as multiple bilateral masses that characteristically show poor contrast
enhancement; less frequently lymphoma presents as a solitary mass that may not be
distinguishable from other solid lesions. Other possible patterns of renal involvement
include direct invasion from retroperitoneal masses, diffuse renal enlargement and
perirenal soft tissue encasing the kidney.
Renal angiomyolipoma, the second most common benign renal focal lesion after cysts,
typically appears as a fat containing mass. Angiomyolipoma can be reliably diagnosed
when macroscopic fat is indentified in a renal lesion; while this imaging feature is
strongly suggestive of angyomyolipoma it is not patognomonic since in rare cases
RCCs may contain macroscopic fat, typically associated with foci of calcification or
ossification that can help in the differential diagnosis. While most angiomyolipomas
are composed predominantly of fat that can be associated with solid enhancing
component constituted by vessels and smooth muscle, some appear as lipid-poor
angiomyolipomas. This tumors may contain scant amounts of microscopic fat
identifiable by dual phase chemical shift imaging; in some cases no fat is detectable
and imaging appearance may overlap with other solid renal lesions. Small lipid-poor
angiomyolipomas can show low signal intensity on T2-weighted images due to the
predominant smooth muscle composition, which can be a useful distinguishing feature
compared to clear cell RCC that typically appears hyperintense.
Transitional cell carcinoma are malignant tumors derived from urothelium that may
arise in renal calyces al pelvis. These tumors may appears as vegetating lesions
located in excretory cavities or as solid masses that infiltrate renal parenchyma and
typically determine less deformation of kidney contours compared to renal cell
carcinomas.

Liver Benign lesions ­1 
Liver cysts are the most common liver lesions and they can be solitary or multiple. On NECT, cysts have a 
watery density (0­15 HU). Simple cysts do not show contrast enhancement after contact media injection. 
When multiple cysts with different size involve the kidney as well, the autosomal dominant polycystic 
kidney disease (ADPKD) should be considered in the differential diagnosis. 
Liver hemangiomas are benign vascular malformations and they are the most common incidental finding 
after cysts that can be detected in asymptomatic patients. Considering their frequent occurrence during 
radiological examinations (especially with ultrasound), the differential diagnosis with malignant hepatic 
lesions should be considered, especially in those patients who have a history of neoplasia. Liver 
hemangiomas can be mainly divided into cavernous hemangiomas and in flash filling hemangioma, that 
usually cannot be detectable on NECT. Large cavernous hemangiomas typically show early peripheral 
contrast enhancement in arterial phase with a progressive filling in portal phase and equilibrium phase, with 
a globular pattern. 
Lesions with complete arterial contrast enhancement and blood pool behavior on portal and equilibrium 
phase could be characterized as capillary hemangiomas. The blood pool behavior can be observed when a 
liver lesion has the same density of the portal veins on all dynamic phases. When present, blood pool is an 
important finding that suggests the hemangioma in the differential diagnosis. Capillary hemangiomas differ 
from transient hepatic attenuating difference (THAD) and from other lesions that exhibit hyper attenuation 
only in the arterial phase due to the presence of blood pool behavior. THAD are secondary to perfusion 
alterations in liver parenchyma that may occur isolated or in association with other liver pathologies. These 
pseudo lesions are appreciated only on arterial phase and they become isodense compared to surrounding 
liver parenchyma in the other CT phases. 

Liver Benign lesions ­ 2 
Focal nodular hyperplasia is a solitary regenerative hepatic lesion characterized by a malformed biliary 
draining system. It typically presents as a mass with sharp margins and it can be supplied by a hepatic artery 
with a dedicated hepatic venous drainage system. Focal nodular hyperplasia is the second most common 
benign solid hepatic lesion and it has female predilection, especially in young­middle age. The typical 
behavior of focal nodular hyperplasia on CECT is a bright homogenous complete arterial contrast 
enhancement without wash out phenomena (Fig 13.). On portal and equilibrium phase the lesion becomes 
isodense to the liver parenchyma. In 30% of cases focal nodular hyperplasia has a central scar that is hypo 
attenuating on NECT, arterial and portal phase and shows contrast enhancement in the equilibrium phase. 
Focal nodular hyperplasia is considered atypical when central scar and/or a central artery can’t be observed. 
When the features of a hyper vascular liver lesion do not completely suggest a focal nodular hyperplasia, 
especially in woman with a prior history of breast cancer (breast metastasis may also appear hyper 
attenuating on arterial phase), further examinations such as magnetic resonance imaging must be considered. 
Hepatic adenomas are uncommon benign liver lesions usually encountered in young and middle age women 
that have been taking oral contraceptive pill for a long time. These lesions are usually solitary and may 
frequently show hemorrhagic phenomena. Hepatic adenomas have a right lobe predilection in subscapular 
location and they usually present with well­defined margins. The attenuation of hepatic adenomas on NECT 
depends on the presence of fat tissue that makes the lesion hypo attenuating. Hemorrhagic phenomena can 
give to the lesion a hyper attenuating appearance, compared to liver parenchyma. On CECT, hepatic 
adenomas present a vivid arterial contrast enhancement, and a pseudo capsule can be frequently seen. The 
enhancement in adenomas typically does not persist due to the presence of arteriovenous shunting. 

 OOn 
Malignant lesions 

Primary liver lesions 
Hepatocellular carcinoma (HCC) is the most common primary hepatic tumor, usually associated with 
hepatic cirrhosis (from viral or alcoholic etiologies). The incidence of this lesion is strictly correlated to 
chronic HBV or HCV infection, especially in development countries, and to alcohol abuse that lead to 
hepatic cirrhosis on western country. The most important risk factor in HCC development is HCV infection 
that lead to an increase risk of 30% every 5 years. Also biliary atresia, biliary cirrhosis, food toxins like 
aflatoxin and inborn metabolism failures (hemochromatosis, Wilson disease and alpha­1­ antitrypsin 
deficiency are the most common) are considerable risk factors. The common clinical presentation includes 
jaundice, portal hypertension due to portal veins infiltration, hepatomegaly and possible hemorrhage from 
the lesion. Hepatocellular carcinoma usually develops on a liver whose parenchyma is altered by the 
presence of cirrhosis­related fibrosis. HCC can be a solitary, large mass with well­defined margins or 
multiple, with variable attenuation. Another possible presentation is the infiltrative or diffuse type. In this 
latter case the presence of nodular alterations of the parenchyma as regenerative nodules or dysplastic 
nodules may make the diagnosis of HCC very tricky. The typical HCC pattern of contrast enhancement 
consists in a hyper attenuation in arterial phase due to branch of hepatic artery vascularization supply. The 
pathognomonic sign of HCC is the early contrast enhancement with wash out phenomena in portal and 
equilibrium phases (Fig14). When an early hyper attenuation on arterial phase is seen into a regenerative 
nodule a small HCC with “nodule in nodule” appearance must be suspected. Nodular HCC presents in more 
than half of the cases (50­80%) with a peripheral pseudo capsule. Furthermore, HCCs may infiltrate the 
portal vein causing thrombosis (also related to coagulation alteration due to liver cirrhosis) and portal 
hypertension. In this case a cavernous transformation of the portal vein can be observed (tortuous venous 
channel that replace the portal vein). Other liver lesions like porto­sistemic venous shunts, THAD or focal 
segmental parenchymal area of fatty changes or sparing in diffuse fatty liver may be observed. 
Malignant lesions 

Primary liver lesions 
Dysplastic nodules enter in differential diagnosis with HCC nodules. On CECT they often exhibit early 
contrast enhancement on the arterial phase but, unlike HCC nodules, they do not show wash out phenomena. 
Regenerative nodules are liver lesions observed in liver cirrhosis and are classified according to the size in 
micronodules, macronodules and giant nodules. Nodules are characterized by the presence of a regular 
parenchymal architecture in which a certain amount of fibrotic tissue or iron deposits may be included. These
findings are responsible for the modest hyper attenuation on NECT. There is no difference in attenuation of 
regenerative nodules respect to liver parenchyma on CECT study. 
Fibrolamellar carcinoma is a variant of HCC that occurs in younger patients with no correlation with 
common HCC risk factors. This type of tumor is a well­circumscribed lesion with sharp margins and it 
contains a discrete portion of fibrotic tissue organized in lamellar bands usually forming a central scar. The 
central scar unfortunately is not pathognomonic of fibrolamellar carcinoma because can be observed also in 
focal nodular hyperplasia. On NECT it may demonstrate a central area of low density due to necrosis or 
fibrosis. Calcifications can be observed in central scar up to 30% of all cases. Fibrolamellar carcinomas 
commonly are heterogeneously hypervascular lesions in arterial and portal phases. 
Secondary liver lesions 
Liver metastases are usually asymptomatic and can be found occasionally during radiological examination or
in staging examinations. Liver metastases are the most common malignant liver lesions in non­cirrhotic liver 
and in most cases they are not appreciable on NECT. Metastases on CECT study can be hypervascular (most 
commonly from renal cell carcinoma, breast carcinoma, islet cell tumor, melanoma and sarcoma, 
pheochromocytoma, carcinoid and thyroid carcinoma) or hypovascular (most commonly from GI tract, 
breast, pancreas, lung and cervix) (Fig 15). In the detection of small liver metastases, arterial phase is useful 
in both types of lesions: in hypovascular metastases it can accurately demonstrate the peripheral rim and in 
hypervascular metastases it shows heterogeneous hyper attenuation (this type of metastasis are likely 
isoattenuating to liver parenchyma in portal phase). The portal and equilibrium phases are the most important
phases in detection of hypovascular metastases that typically show hypo attenuation compared to normal 
liver parenchyma. NECT is helpful to distinguish calcified metastases from colon mucinous tumor, stomach, 
adnexa, breast, thyroid, lung or kidney, carcinoid and melanoma. When the patient has concomitant fatty 
liver disease, liver metastases may demonstrate iso­ or slight hyper attenuating with respect to liver 
parenchyma in portal phase. 

Malignant lesions 

Biliary tree 
Gallbladder carcinoma is usually asymptomatic at the time of the diagnosis and it is often an incidental 
finding during an abdominal ultrasound or a CT exam performed for other reasons. Long­standing gall 
bladder stones are the major risk factor for the development of this condition. Others risk factors include 
chronic cholecystitis, familial adenomatous polyposis syndrome, gall bladder polyps (when > 10 mm), 
porcelain gallbladder and inflammatory bowel diseases. Gallbladder carcinoma shows a predominance for 
elderly women. Clinical presentation can be different depending from the location of the tumor: if the lesion 
affects the fundus of the gallbladder the tumor can infiltrate the adjacent liver parenchyma or the colon and 
the first symptom could be upper abdominal quadrant pain; if the lesion affects the gallbladder infundibulum 
the initial symptom may be the jaundice. On NECT, calcifications of gallbladder’s walls could be present; 
when the wall is completely calcified and retracted the gallbladder is called porcelain gallbladder. On CECT,
gallbladder carcinoma could be seen as a solid polypoid mass with a diameter > 10 mm, with diffuse wall 
thickening showing hyper attenuating pattern of contrast enhancement, or as solid tissue that completely 
replaces the gallbladder. The last type of presentation is the most frequent one: it appears as an infiltrating 
heterogeneous mass with slightly and patchy contrast enhancement in arterial and portal phases. Dilatation of
intrahepatic biliary ducts, lymphoadenopathies and ascites may be present as features of advanced disease. 

Malignant lesions 
Biliary tree 
Cholangiocarcinoma is the second most frequent malignant hepatic tumor and it originates from 
cholangiocytes. The major risk factors for the development of cholangiocarcinoma are primary sclerosing 
cholangitis (PSC), especially in western countries, recurrent pyogenic cholangitis, choledocholithiasis and 
clonorchis chiniensis infection in asian country. Cholangiocarcinomas can arise from intrahepatic bile ducts 
or extrahepatic bile duct epithelium. The intrahepatic form is divided into a peripheral type that is usually a 
hypodense mass on NECT with associated intrahepatic bile ducts dilatation (capsular retraction is often 
seen), and a central (hilar) type that is a mass at the level of hepatic duct confluence. Cholangiocarcinoma is 
considered peripheral if it originates peripherally from a secondary branch of a biliary hepatic duct and hilar 
when it originates from a biliary hepatic duct or common hepatic duct (Klatskin tumor). 
Cholangiocarcinomas may be classified also depending on the shape and biological behavior. It may be mass
forming, infiltrating, periductal or intraductal. The extrahepatic type of cholangiocarcinoma is typically 
infiltrative in association with common bile duct and intrahepatic bile ducts dilatation. Mass forming 
cholangiocarcinoma on CECT typically shows early complete rim enhancement with progressive, centripetal
non­globular pattern of enhancement in portal and equilibrium phase. Invasion of portal veins is not a rare 
occurrence, especially in hilar type. Infiltrative periductal cholangiocarcinoma is most common at hepatic 
hilum and it is often associated with narrowing or dilatation of peripheral bile ducts due to pathological 
thickening of periductal hepatic parenchyma. The intraductal infiltrative cholangiocarcinoma may show the 
presence on polypoid lesion into a duct that demonstrate contrast enhancement on portal phase compared to 
NECT. 

Liver diffuse parenchymal alterations 
The most frequently encountered disease that involve liver 
parenchyma in a diffuse fashion are represented by hepatic 
steatosis, acute inflammatory disease and chronic liver disease. 
Hepatic steatosis, also denominated fatty liver disease, is a very 
common pathologic condition consisting of a pathological 
increase in triglyceride molecules stored within intracellular 
vacuoles in hepatocytes. In most circumstances steatosis involves 
diffusely liver parenchyma although inhomogeneous distribution 
of fat accumulation with areas of parenchyma relatively spared is 
a frequent occurrence, sometimes resulting in a patchy 
“geographic“ appearance. Less common variants of liver steatosis 
are represented by preferential fat deposition in specific liver 
territories, typically in the right lobe and rarely in a subcapsular o 
perivascular distribution. Occasionally fatty liver disease may 
mimic a focal liver lesion either because steatosis presents as a 
circumscribed signal alteration, often as a single localization and 
rarely as a multifocal pseudonodular disease, or liver parenchyma 
is focally spared. Imaging findings in fat liver disease are 
consistent with the presence of intracellular fat in areas of 
parenchyma involved, readily detectable on dual phase chemical 
shift imaging. Focal fat deposition typically appears as a sharp 
defined area, often showing straight of wedge­shaped margins, 
with no mass effect on adjacent normal vascular and biliary 
structures. 

Acute inflammatory diseases of different etiology tend to show 
similar unspecific imaging findings and their diagnosis requires 
interpretation in the clinical context. In post contrast images 
acquired during the hepatic arterial phase heterogeneous 
parenchymal enhancement can be seen with areas of transitory 
enhancement that typically fade to isointensity compared to liver 
parenchyma in portal venous and equilibrium phases images. On 
T2­weighted images hyperperfused areas may demonstrate a 
slightly increased signal intensity that is attributable to 
parenchymal inflammatory infiltrates. In conditions characterized 
by diffuse liver inflammation as found in acute hepatitis a 
periportal edema pattern with expansion and high signal intensity 
of portal spaces on T2­weighted images is a common occurrence. 
In more focal processes like cholangitis wedge­shaped areas of 
parenchymal inflammation surrounding dilated intrahepatic biliary
ducts are typical findings. 
In chronic inflammatory diseases evolving towards liver 
cirrhosis imaging findings indicate the presence of parenchymal 
fibrosis. Cirrhotic liver shows nodular contours, irregular shape 
with variable involvement of different liver segments, often with 
relative hypertrophy of caudate an left lobes, and an 
inhomogeneous parenchyma due to fibrotic tissue deposition 
delineating regenerative nodules. Fibrosis is better detected in 
delayed contrast enhanced images acquired in equilibrium phase 
(3­5 minutes after contrast injection) when gadolinium based 
contrast agent diffuses in expanded interstitial space and 
accumulates in fibrous tissue resulting in high signal intensity 
compared to liver parenchyma. In cases of mild fibrosis liver 
parenchyma assumes a granular texture attributable to 
micronodular regenerative hyperplasia; with more severe 
involvement a coarser nodular pattern with linear strands of 
fibrosis and large regenerative nodules can be observed. In some 
circumstances fibrotic tissue completely substitutes areas of liver 
parenchyma and can appear as a focal lesion (so­called confluent 
fibrosis); useful imaging findings that can suggest a fibrous 
composition are wedge­shaped margins, preferential subcapsular 
location, typical delayed contrast enhancement and mildly to 
moderately increased signal intensity on T2­weighted compared to
parenchyma probably due to vascular congestion or edema.