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The Renal Sinus—Transitional Cell Carcinoma and its Mimickers on Computed Tomography

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Author's Accepted Manuscript The Renal Sinus- Transitional Cell Carcinoma and its Mimickers on CT Gabriela Gayer MD, Rivka Zissin MD PII: S0887-2171(14)00021-3 DOI: http://dx.doi.org/10.1053/j.sult.2014.02.004 Reference: YSULT578 To appear in: Semin Ultrasound CT MRI Cite this article as: Gabriela Gayer MD, Rivka Zissin MD, The Renal Sinus- Transitional Cell Carcinoma and its Mimickers on CT, Semin Ultrasound CT MRI , http://dx.doi.org/10.1053/j.sult.2014.02.004 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. www.elsevier.com/locate/enganabound
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Author's Accepted Manuscript

The Renal Sinus- Transitional Cell Carcinoma and itsMimickers on CT

Gabriela Gayer MD, Rivka Zissin MD

PII: S0887-2171(14)00021-3DOI: http://dx.doi.org/10.1053/j.sult.2014.02.004Reference: YSULT578

To appear in:Semin Ultrasound CT MRI

Cite this article as: Gabriela Gayer MD, Rivka Zissin MD, The Renal Sinus- TransitionalCell Carcinoma and its Mimickers on CT,Semin Ultrasound CT MRI , http://dx.doi.org/10.1053/j.sult.2014.02.004

This is a PDF file of an unedited manuscript that has been accepted for publication. As aservice to our customers we are providing this early version of the manuscript. Themanuscript will undergo copyediting, typesetting, and review of the resulting galley proofbefore it is published in its final citable form. Please note that during the production processerrors may be discovered which could affect the content, and all legal disclaimers that applyto the journal pertain.

www.elsevier.com/locate/enganabound

1

The Renal Sinus- Transitional Cell Carcinoma and its Mimickers

on CT

* Gabriela Gayer MD (1,2,3)

Rivka Zissin MD (3,4)

(1) Department of Diagnostic Imaging and Nuclear Medicine,

Sheba Medical Center, Ramat-Gan, Israel

(2) Department of Radiology, Stanford Medical Center, Stanford,

California

(3) Sackler Faculty of Medicine, Tel-Aviv University, Israel

(4) Department of Diagnostic Imaging, Meir Medical Center, Kfar

Saba, Israel

*Corresponding author:

Gabriela Gayer

Email: [email protected]

2

Abstract

The renal sinus is a deep recess located at the medial aspect of the kidney

surrounded by the renal parenchyma. It contains within it the collecting

system of the kidney, lymphatics, nerves, and renal blood vessels. The

remainder of the sinus is filled with adipose and fibrous tissue. A variety of

pathological conditions arise from the different tissues in this site. The aim of

this review is to explore and illustrate the common and less common

processes affecting the renal pelvis.

Introduction

A variety of both benign and malignant lesions may affect the renal sinus, the

most common ones being renal sinus cysts and renal sinus lipomatosis.

These, however, rarely pose a diagnostic challenge on CT because of the

typical density of fluid and fat, respectively. Many other conditions that affect

the renal sinus are of soft tissue density and have far less specific imaging

features. While transitional cell carcinoma (TCC) is a relatively common

neoplasm of the renal sinus, many other processes that affect this site have

overlapping imaging findings. Some of these lesions have been mistaken for

TCC, based mainly on their imaging findings, and have lead to unnecessary

nephrectomy.1 The purpose of this review is to highlight the spectrum of

imaging features of a wide array of lesions affecting the renal sinus and to

increase awareness of lesions simulating TCC in this location on CT.

Neoplastic lesions

Malignant tumors

3

The most frequent malignant tumors that involve the renal sinus are

transitional cell carcinoma, renal cell carcinoma, lymphoma and metastatic

disease. Superficially, these masses resemble one another on cross-sectional

imaging, but are quite different histologically and clinically. Awareness of

subtle imaging findings may be helpful in the preoperative differentiation of

these masses, which is particularly important since the treatment of each is

substantially different. Transitional cell carcinoma is treated by means of

nephroureterectomy, while infiltrative renal cell carcinoma by nephrectomy,

and lymphoma is treated by systemic chemotherapy. In addition, patients with

upper tract TCC require more intensive surveillance because they have a

lifelong increased risk of developing urothelial tumors in the contralateral

upper urinary tract or bladder.2

• Transitional cell carcinoma

Transitional cell carcinoma (TCC) is the most common tumor of the renal

pelvis (<10% of renal malignancies). TCC arises from the urothelium, the

lining surface epithelium of the renal collecting tubules, calyces, pelvis, ureter,

bladder, and urethra. Hematuria, either gross or microscopic, is the most

common symptom reported in up to 95% of patients.3

On CT, TCC of the renal pelvis may appear as a pelvic filling defect or as

circumferential urothelial wall thickening, distorting the collecting system (Figs.

1,2). The tumor sometimes has a mass-like appearance, similar to that of

renal cell carcinoma (RCC).2 A recent study proved that CT scan is accurate

in distinguishing between intrarenal TCC and centrally located RCC by using

the following six CT features: intrarenal TCC is centered on the collecting

system, appears as a focal filling defect in the pelvicalyceal system,

4

preservation of reniform contour is present, cystic or necrotic change is

absent, homogeneous but modest tumor enhancement, and presence of

extension of the tumor towards the ureteropelvic junction.4

It is crucial to differentiate it from other conditions that present as a filling

defect - a urinary calculus, blood clot, or sloughed papillae (Fig. 3). The

presence of contrast enhancement of the filling defect is helpful in correctly

diagnosing TCC.5 Biopsy of infiltrative transitional cell carcinoma should be

avoided if possible because of the propensity for seeding.6

• Renal cell carcinoma

RCC is the most common primary renal malignant neoplasm in adults,

accounting for approximately 90% of renal tumors and 2% of all adult

malignancies. In recent years tumors are being discovered at an earlier stage,

likely due to increased use of imaging. RCC is characterized by increased

neovascularization, relatively frequent vascular invasion and early

metastasis.7 RCC is multicentric only in 4%, and bilateral in 0.5–3%.2 Most

renal cell carcinomas grow by expansion and commonly extend into the renal

sinus, leading to focal hydronephrosis or caliceal displacement.1

On un-enhanced CT scans, RCC may appear as isoattenuating,

hypoattenuating, or hyperattenuating relative to the remainder of the kidney.

Calcifications may be present and are usually amorphous and internal. On

contrast-enhanced CT scans, RCC is usually solid, and decreased

attenuation suggestive of necrosis is often present (Fig. 4). RCC is

occasionally a predominantly cystic mass, with thick septa and wall nodularity.

RCC may also appear as a completely solid and highly enhancing mass.

5

Renal vein invasion is a feature much more suggestive of centrally located

RCC (Fig. 5), although rarely TCC can invade the renal vein or even the

inferior vena cava. Treatment is surgical and varies according to the size and

stage of the tumor. 4

• Lymphoma

Involvement of the renal sinus by malignant lymphoma usually occurs within

the context of disseminated disease. Renal involvement by lymphoma has

various radiological manifestations: a single renal mass, multiple bilateral

renal masses, a perirenal mass, diffuse infiltration of a kidney and a renal

sinus mass. When the renal sinus is involved by lymphoma, an important clue

to the correct diagnosis is associated retroperitoneal lymphadenopathy.5

Primary lymphomas of the renal sinus are very rare because lymphoid tissue

at this site is scarce. 8 The most common histology of primary renal

lymphoma is diffuse large-cell lymphoma.9 Primary renal lymphoma is

characterized by lymphomatous renal infiltration, unilateral or bilateral

kidney enlargement without ureteral obstruction, and no additional

extrarenal imaging findings. Most patients present with flank pain, and

hematuria, symptoms and signs that are indistinguishable from more

common RCC and TCC.8

Lymphoma affecting the renal sinus usually appears as a homogeneous

mass without hydronephrosis (Fig. 6), quite similar to that of TCC.5,8

Treatment consists of chemotherapy combined with involved-field

6

radiation therapy. 8 If the diagnosis of lymphoma is not considered

preoperatively, then the patient might undergo unnecessary

nephroureterectomy for suspected TCC.

• Metastases

Renal metastases are present in approximately 10% to 20% of cancer

patients depending on tumor type and most commonly seen in the setting of

other metastatic diseases. A renal metastasis is the most common malignant

neoplasm of the kidney found at autopsy.10 The most common primary sites

for renal metastases (except hematologic malignancies) are lung, colon and

breast carcinoma, melanoma and reproductive system malignancies.10,11

Spread of metastasis to the kidney is usually hematogenous or lymphatic.

They are usually asymptomatic and discovered incidentally on imaging

studies performed for other purposes. 10 The most common CT appearance of

renal metastases is bilateral, multifocal, small (< 3 cm), hypodense masses.

The nephrographic phase is ideal to detect and characterize renal masses

(Fig. 7). 11,12 The maximal and homogeneous parenchymal enhancement in

this phase facilitates detection of renal metastases, which typically do not

enhance to the same degree as the renal parenchyma. Renal metastases

usually do not change the treatment approach due to the advanced stage of

the disease.10

Benign lesions

• Renal sinus cysts

7

Renal sinus cysts are common, with a reported prevalence between of up to

1.5% at autopsy.13

Cysts in the renal pelvis are referred to as parapelvic and peripelvic cysts.

Parapelvic cysts originate in the renal parenchyma and extend into the renal

sinus. Peripelvic cysts originate in sinus structures which presumably

represent mostly lymphatic collections.14 Peripelvic cysts are usually small,

multiple, confluent cysts. They are rarely symptomatic. At US and un-

enhanced CT, these cysts may mimic hydronephrosis. At contrast-enhanced

CT performed during the excretory phase, differentiation of peripelvic cysts

and hydronephrosis is obvious because the enhanced collecting system is

displaced by the water-attenuation sinus cysts (Figs. 7,8). A parapelvic cyst is

usually a single, larger cyst occurring in the sinus and likely originates from

the adjacent parenchyma. Parapelvic cysts exhibit the same imaging features

as simple renal cortical cysts. Neither type of renal sinus cyst is of clinical

importance and does not warrant follow-up or treatment.1, 14

• Renal sinus Lipomatosis

Renal sinus lipomatosis is a benign proliferation of fat that occurs with

advanced age, obesity, and exposure to steroids. Simple renal sinus

lipomatosis is often bilateral. It is asymptomatic because the process does not

cause caliceal obstruction.15 Another form of this process is an advanced or

aggressive form termed replacement renal sinus lipomatosis that usually

occurs unilaterally. The main etiologies of this form include a calculus

disease, chronic hydronephrosis, or infection. Calculus disease is seen in

8

70% of cases. Replacement renal sinus lipomatosis results in enlargement of

the kidney with marked proliferation of fat in the sinus and atrophy of the renal

cortex with preservation of the reniform shape of the kidney.16 CT and MR

reveal the fatty nature of sinus lipomatosis (Fig. 9). The main differential

diagnosis is xanthogranulomatous pyelonephritis. 1

• Angiomyolipoma

Angiomyolipoma is the most common mesenchymal renal neoplasm, with a

prevalence of 0.13% in a healthy adult population without tuberous sclerosis

complex.17,18 Angiomyolipoma is a benign tumor that, as the name implies,

typically contains variable proportions of blood vessels, smooth muscle, and

adipose tissue. The presence of macroscopic adipose tissue usually allows

accurate diagnosis with CT or MRI. However, when such neoplasm contains

minimal or no fat, differentiation from renal cell carcinoma on imaging

becomes difficult. Epithelioid angiomyolipoma (EAML) is a rare subtype of

angiomyolipoma, which consists predominately of sheets of epithelioid cells

with granular eosinophilic cytoplasm. It is considered a potentially malignant

neoplasm. On CT EAML usually shows no or very little fat and no calcification.

Tumor enhancement is variable and may be mild, moderate or marked (Fig.

10). EAML can therefore easily be misdiagnosed as renal cell carcinoma

during histologic and imaging examinations. 18

Vascular lesions

9

• Renal artery aneurysm

Renal artery aneurysm (RAA) is rare with an incidence of up to 0.9%. RAA

has no gender predilection. The peak incidence occurs in the fifth and sixth

decade. It involves the right artery more frequently than the left and is bilateral

in 10% of cases. More than 90% of true RAAs are extrarenal, typically located

in the renal hilum. RAA is often asymptomatic but may present acutely with

flank/ back pain and hematuria due to spontaneous rupture. 19,20

On CT RAA presents as a well-defined rounded mass in the renal hilum. A

peripheral ring-like calcification is often present (Fig. 11A). On contrast-

enhanced CT the aneurysm undergoes variable enhancement occurs,

depending on technical parameters of the scan (volume of contrast material,

injection rate and phase of acquisition). On arterial phase the aneurysm

shows enhancement similar to that of the abdominal aorta, indicating its

arterial origin (Fig. 11B). 20

Treatment of renal aneurysms is controversial and includes surgery,

endovascular treatment (embolization or stenting) or observation. 21

• Renal arteriovenous malformation

Renal arteriovenous malformations (AVMs) are very rare benign lesions. They

may be congenital or acquired. Most AVMs are acquired, resulting from trauma,

inflammation or percutaneous procedures such as renal biopsy. They are more

common in women and usually affect young people. In some cases they

present with massive hematuria.

AVM may be mistaken for a renal pelvis tumor if the vascular channels do not

opacify densely at the time of scanning. The accurate diagnosis can however

10

be made on contrast-enhanced CT performed at the arterial phase. Treatment

consists of transcatheter selective arterial embolization, which leads to

resolution of the hematuria whilst preserving renal parenchyma. 22

Infiltrative lesions:

• Extramedullary hematopoiesis

Extramedullary hematopoiesis (EMH) is the development and growth of

hematopoietic tissue outside of the bone marrow. It is an essential process in

fetal life, but its occurrence after birth is usually considered abnormal and

represents a compensatory mechanism for failure of erythropoiesis. EMH

occurs most frequently in the liver and spleen but has been reported to

involve a myriad of other tissues and organs, mainly intraspinal or paraspinal

in the thoracic region. At one autopsy series lymph nodes were the most

common site of EMH (excluding the liver and spleen) followed by the kidneys.

Most patients with renal EMH are asymptomatic, but may present with

abdominal pain or renal failure due to parenchymal involvement or ureteral

compression. 23

Renal EMH usually affects both kidneys but may be unilateral. It may involve

the renal pelvis, perinephric space or both. Imaging findings on CT and MRI

correspond to the involved compartment. EMH affecting the renal pelvis

appears as soft-tissue infiltration with encasement of the pelvicalyceal

systems, that sometimes involves the proximal ureters (Fig. 12).24 At MRI,

signal intensity on T2-weighted images is typically low owing to the

hemosiderin content. At ultrasound, the perinephric lesions usually appear as

11

solid hypoechoic masses. Additional CT findings of hepatosplenomegaly and

paraspinal soft tissue can support the diagnosis of extramedullary

hematopoiesis (Fig. 12C). Treatment for symptomatic cases consists of low-

dose radiation therapy.23

• IgG4-related disease

Immunoglobulin (Ig) G4-related disease is a recently designated benign

clinical entity characterized histopathologically by an extensive IgG4-positive

plasma cells and lymphocyte infiltration. IgG4-related disease has been

described in virtually every organ system including the biliary tree, pancreas.

salivary glands, periorbital tissues, kidneys, lungs, lymph nodes, meninges,

aorta. breast, prostate, thyroid, pericardium, and the skin. 25,26

Renal involvement is quite common and predominantly involves the cortex of

the kidney and less frequently the renal pelvis. The renal lesions manifest as

multiple wedge-shaped or nodular cortical lesions in one or both kidneys.

When the disease affects the renal sinus it will appear as diffuse wall

thickening of the renal pelvis (Fig. 13). 27 Histologic specimen shows

tubulointerstitial nephritis with marked expansion of the interstitium with

fibrosis and an inflammatory cell infiltrate. 26

Most patients with renal IgG4-related disease have involvement of another

organ. The coexistence of similar infiltrative processes affecting other organs

(e.g. pancreas, bile ducts) can support the diagnosis of IgG4-related disease

and serves as an important clue for the differentiation of IgG4-related disease

from RCC or TCC. 28

Glucocorticoids are typically the first line of therapy. Aggressive treatment is

needed when vital organs are involved because IgG4-related disease can

12

lead to serious organ dysfunction and failure. However, not all manifestations

of the disease require immediate treatment and watchful waiting has also

been advocated. 25

• Erdheim-Chester Disease

Erdheim-Chester disease is a rare non–Langerhans cell histiocytosis of

unknown etiology that usually affects middle-aged adults with no sex

predilection. 29,30 Patients typically present with lower-extremity bone pain.

Skeletal imaging findings include bilateral symmetric metadiaphyseal cortical

thickening, and medullary sclerosis in the long bones of the appendicular

skeleton, with sparing of the epiphyses and axial skeleton. 31 Extraskeletal

manifestations include central nervous system, lungs, skin, kidneys,

retroperitoneum and heart. 32

Renal involvement is found in about 30% of patients and may be an isolated

site of disease. 33 This involvement is usually asymptomatic but may progress

and lead to renal failure. CT shows hypoattenuated homogeneous tissue

infiltration with weak contrast enhancement. The perirenal infiltration is often

bilateral and symmetric is highly suggestive of the diagnosis. 33,34 The

infiltration may also extend to the renal sinuses and to the proximal and cause

upper urinary tract obstruction (Fig. 14A). On MRI, the soft-tissue infiltration of

the pararenal and perirenal fat appears isointense to muscle on T1- and T2-

weighted spin-echo sequences, with a slight and homogeneous enhancement

in signal intensity after gadolinium injection (Fig. 14B).33

The prognosis for Erdheim-Chester disease is considered poor and depends

on the extent of extraskeletal, mainly pulmonary and cardiac, involvement.

13

Treatment usually consists of a combination of steroids, radiotherapy, and

chemotherapy.34

• Suburothelial hemorrhage

Hemorrhage into the suburothelial layer of the collecting system is rare and

occurs mainly secondary to anticoagulant therapy. Because of its rarity

suburothelial hemorrhage is often not clinically suspected, even in a patient

receiving anticoagulant therapy. It presents acutely with flank pain and

hematuria and patients undergo CT for evaluation, mainly to evaluate for renal

calculi or a neoplastic process such as transitional cell carcinoma. 35

Suburothelial hemorrhage appears on CT as mural thickening of the renal

pelvis and sometimes involves also the proximal ureter, sometimes narrowing

their lumen. The hemorrhage is best appreciated on un-enhanced scan, when

the typical high density of the hemorrhage is most conspicuous (Fig. 15 A,B).

35,36 This high density is not as conspicuous on either nephrographic or

pyelographic phases. On the pyelographic phase the mural thickening is the

main abnormality (Fig. 15 C,D). The CT findings mimic those of a neoplasm of

the collecting system. This similarity has resulted in multiple reports of

erroneous nephrectomy.37 It is therefore important to scrutinize the images

obtained prior to intravenous contrast administration and if needed manipulate

the images digitally to search for the linear hyperdensity outlining the

collecting system. In the absence of an un-enhanced scan, a follow-up 2-3

weeks later will usually demonstrate complete resolution of the hemorrhage. 35

14

Pitfalls

Excretion of contrast material from an imaging study performed several hours

prior to the current CT may result in errors in interpretation.

Gadolinium, similar to iodinated contrast material, is excreted by the kidneys.

The density of concentrated excreted gadolinium is higher than that of urine,

but lower than that of iodine (Fig. 16). In a patient undergoing an un-enhanced

CT of the abdomen within hours after a gadolinium-enhanced MR study, the

high density of excreted gadolinium may be mistaken for hemorrhage. Such

an error can result in unnecessary additional investigations and anxiety. This

misinterpretation is less likely to occur in a patient scanned after an earlier

contrast-enhanced CT study, because of the typical high density of excreted

iodine. However if the collecting system is dilated the excreted iodine will be

less dense, mixing with low density urine, and may be misinterpreted as a soft

tissue mass (Fig. 17). In both settings, correlation with recent imaging history

is important and helps confirm the diagnosis.

Summary

A wide spectrum of neoplastic and nonneoplastic conditions may involve the

renal sinus. Diagnostic differentiation of these entities can be radiologically

challenging, but distinction is important because management strategies

differ. Several of these lesions have characteristic imaging findings that allow

for a correct diagnosis, while others have overlapping radiologic features, and

a biopsy and histopathologic evaluation are required to establish a definitive

diagnosis.

15

Knowledge of clinical information and familiarity with the spectrum of imaging

features of conditions affecting the renal sinus can facilitate accurate

diagnosis and timely treatment.

Legends

Fig. 1

TCC affecting the renal pelves bilaterally.

63-year-old man with history of bladder cancer, status post cystectomy and

ileal neobladder reconstruction, undergoing routine CT follow-up.

A, B. Axial contrast-enhanced CT shows urothelial thickening affecting the

renal pelves bilaterally (arrows). This finding was assumed to represent an

infectious/inflammatory process and follow-up was recommended.

C,D,E. Follow-up contrast-enhanced CT 6 months later shows interval

progression of urothelial thickening.

C. Nephrographic phase at the level of the left renal sinus shows worsening of

circumferential urothelial thickening (long arrows). Note interval progression of

retroperitoneal lymphadenopathy (short arrows).

D. Nephrographic phase at the level of the right renal sinus shows worsening

of circumferential urothelial thickening (white arrow). The left ureteral wall is

now also infiltrated (black arrow, compare to B).

E. Pyelographic phase at the level of the left renal sinus shows an irregular,

narrowed, amputated collecting system resulting from the infiltrative lesion

(arrow).

Fig. 2

16

74-year-old man with left-sided centrally located poorly differentiated

transitional cell carcinoma.

A,B. Contrast-enhanced axial images show a heterogeneously enhancing

mass (arrows) in the renal pelvis infiltrating the left upper pole region with

preservation of renal shape. Perinephric fat stranding is present (arrowheads).

C. Coronal image at the pyelographic phase shows amputated collecting

system resulting from the infiltrative lesion (arrow).

Fig. 3.

Blood clot mimicking TCC. 40-year-old man presenting with hematuria for 3

days prior to admission and right flank pain day of admission. He has been on

Coumadin treatment for atrial fibrillation. INR was 3.6, above therapeutic level.

A. Un-enhanced CT scan shows a high-density focus in the upper calyx of the

right kidney (arrow).

B. Contrast-enhanced axial CT at the nephrographic phase at the same level.

The high density focus is much less conspicuous on this phase scan (arrow).

C. Contrast-enhanced axial CT at the pyelographic phase clearly shows the

filling defect in the upper calyx of the right kidney (arrow).

D. Follow up CT 6 weeks later. Contrast-enhanced axial CT at the

pyelographic phase at the same level shows complete resolution of the filling

defect.

Fig. 4

Clear cell RCC affecting the left renal sinus.

43-year-old man presented with hematuria.

17

Axial (A) and coronal (B) CT contrast-enhanced CT images at the

corticomedullary phase show a rounded well-defined hetergenously

enhancing mass at the renal pelvis (arrow).

Fig. 5

35-year-old woman with left-sided RCC infiltrating the renal sinus with left

renal vein invasion.

Axial contrast-enhanced CT a shows a large hypodense mass in the left

kidney (black arrow), marked dilatation of the left renal vein (white arrow) with

a large heterogenous filling defect, compatible with invasion of the tumor into

the renal vein, a feature suggestive of RCC.

Fig. 6.

Lymphoma involving the renal pelvis.75-year-old woman presented with left

flank pain and elevated Creatinine level. Ultrasonography showed left-sided

hydronephrosis.

A. Un-enhanced CT shows a round soft tissue mass (white arrow) at the renal

hilum, measuring 25 HU.

B. Contrast-enhanced CT shows mild enhancement of the soft tissue mass

(white arrow) to 57HU. Associated enlarged retroperitoneal and mesenteric

lymph nodes are present, suggestive of metastatic disease.

A percutaneous nephrostomy tube (black arrow) had been inserted and

alleviated the hydronephrosis seen at US.

Fig. 7

Metastatic melanoma of the right renal hilum in a 78-year-old woman with

known melanoma.

18

Contrast-enhanced axial CT images at the nephrographic (A) and

pyelographic (B) phases show a well-defined round mass at the right renal

sinus enhancing to a lesser degree than the renal parenchyma (black arrow).

Note additional round masses (arrowheads) in the perirenal fat, suggestive of

metastatic disease. Small nonenhancing fluid-density lesions are seen in the

left renal sinus (white arrow), with an appearance typical of peripelvic cysts.

Fig. 8

Bilateral peripelvic cysts in a 64 -year-old asymptomatic woman. Axial

images on un-enhanced (A), corticomedullary (B), nephrographic (C) and

pyelographic (D) contrast-enhanced phases show multiple small confluent

low-attenuation cystic lesions (arrows) in the renal sinus bilaterally. The

enhanced calices on the pyelographic phase are stretched and attenuated but

not obstructed by the cysts. The latter phase is helpful in differentiating

peripelvic cysts from hydronephrosis.

Fig. 9

Renal pelvic sinus lipomatosis. Abundant fatty tissue occupying the renal

pelvis bilaterally (arrows) in a 88-year-old man with COPD, undergoing CT to

evaluate anemia.

Fig. 10

Epithelioid angiomyolipoma of the renal sinus. 33-year-old male presenting

with intermittent right-sided spine pain. Ultrasound showed a 3 x 4 cm mass in

the interpolar region of the right kidney.

A. Un-enhanced axial CT scan shows a soft tissue mass infiltrating the right

renal pelvis (arrow). Its density is minimally higher than that of the renal

parenchyma and it does not appear to contain any fat.

19

B,C. Axial (B) and coronal (C) contrast-enhanced images at nephrographic

phase show mild homogeneous enhancement of the mass (arrow).

D. The mass (arrow) shows no signal loss on fat-saturated gadolinium-

enhanced T1-weighted MR image, because it contains only microscopic fat.

The patient underwent nephrectomy and histologic sections showed an

angiomyolipoma of the renal sinus with epithelioid differentiation and atypia.

Fig. 11

Renal artery aneurysm. 56-year-old woman presenting with microhematuria.

A. Un-enhanced axial CT scan shows a round soft-tissue mass, that is

isodense to the renal parenchyma, with a peripheral linear calcification

(arrow).

B. Contrast-enhanced image at the corticomedullary phase shows marked

enhancement of the lesion (arrow), similar to the enhancement of the adjacent

aorta, indicating the diagnosis of a renal artery aneurysm.

Fig. 12

Extramedullary hematopoiesis. 64-year-old man with myelofibrosis.

A. Contrast-enhanced axial CT image obtained during portal venous phase

shows hypodense, hypovascular mass (long arrow) infiltrating the left renal

sinus. Note also rind-like soft tissue in the perirenal space (short arrows).

B. On pyelographic phase the collecting system is encased but the infiltrative

process (arrow) does not obstruct the calyces.

C. Axial contrast-enhanced CT at the level of the chest shows bilateral

paraspinal and pleural (arrows) soft tissue masses, findings highly suggestive

of EMH.

20

Fig. 13

IgG4-related tubulointerstitial nephritis affecting the left kidney in a 63-year-old

man.

A. Un-enhanced axial CT shows an abnormally enlarged left kidney without a

distinct renal pelvis (arrow).

B. Pyelographic phase shows a persistent corticomedullary enhancement of

the left kidney, without excretion of contrast material. The entire left renal

collecting system and medulla appear uniformly infiltrated (arrow).

C. A repeat scan after an additional 30 minutes delay shows excretion of

contrast material from the left kidney. The infiltrative process markedly distorts

the collecting system.

The left perinephric fat is diffusely infiltrated (arrowheads, A-C). The right

kidney is unremarkable.

D. T2-weighted MR image shows the infiltrative process encasing the calyces

(arrow).

Fig. 14

Erdheim-Chester disease infiltrating the renal sinus.

A 69-year-old man presented with lower extremity bone pain, diabetes

insipidus, chronic renal disease, hyperlipidemia and hypertension.

A. Un-enhanced axial CT shows infiltrative process in the left renal sinus

(arrow) and bilateral homogeneous perirenal soft tissue infiltration

(arrowheads) with attenuation similar to that of muscle.

B. Coronal MR image shows bilateral soft-tissue infiltration of the perirenal

space (black arrows) encasing both kidneys. The infiltrative process involves

also the left renal sinus (white arrow).

21

Biopsy of the peri-renal tissue confirmed Erdheim-Chester disease.

Radiograph of the lower extremities (not shown) showed enlarged femora with

metadiaphyseal sclerosis.

Fig. 15

Suburothelial hemorrhage secondary to anticoagulant therapy.

A 60-year-old man presented to the emergency department with left sided

flank pain, right lower quadrant pain and hematuria. The patient had been on

Coumadin treatment due to prior deep venous thrombosis and pulmonary

embolism. An un-enhanced CT of the abdomen and pelvis was initially

obtained to rule out stones.

Un-enhanced CT (A,B) shows high density outlining the left renal pelvis and to

a lesser degree also the right renal pelvis (arrows).

Contrast-enhanced CT at pyelographic phase (C,D) shows marked thickening

of both renal (arrows), extending to the ureters (arrowheads B,D). The

nephrographic phase is prolonged on the left.

Laboratory results showed elevated INR. Patient was treated conservatively

with fresh frozen plasma and Vitamin K with prompt return of INR to

therapeutic levels and resolution of abdominal pain and hematuria.

Fig. 16

Excreted gadolinium from a single left kidney. Un-enhanced CT was

performed several hours after a gadolinium-enhances MR study. The density

of excreted gadolinium (arrow) is higher than that of urine and mimics that of

fresh blood and may therefore be misinterpreted as hemorrhage.

Fig. 17

22

Excreted iodinated contrast material in a dilated extra-renal pelvis. Current un-

enhanced CT was performed several hours after a contrast-enhanced CT.

A,B. Un-enhanced axial (A) and coronal (B) CT show homogeneous high

density within the right renal pelvis (arrows). Without a prior CT it is

impossible to establish whether this is a soft tissue lesion or an extra-renal

pelvis containing high-density fluid. Note similarity to figure 10 (epithelioid

angiomyolipoma of the renal sinus).

C. Un-enhanced axial image from a prior study shows a similar dilated extra-

renal pelvis but containing clear fluid density (arrow).

23

RFERENCES

1. Rha SE, Byun JY, Jung SE, et al. The renal sinus: pathologic spectrum and

multimodality imaging approach. Radiographics. 2004;24 Suppl 1:S117-31.

2. Bata P, Tarnoki DL, Tarnoki AD, et al. Transitional cell and clear cell renal

carcinoma: differentiation of distinct histological types with multiphase CT.

Acta Radiol. 2013 Nov 15

3. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2009. CA Cancer J Clin

2009;59:225–249.

4. Raza SA, Sohaib SA, Sahdev A, et al. Centrally infiltrating renal masses on

CT: differentiating intrarenal transitional cell carcinoma from centrally located

renal cell carcinoma. Am J Roentgenol 2012;198:846–853.

5. Zhang J, Israel GM, Krinsky GA, et al. Masses and pseudomasses of the

kidney: imaging spectrum on MR. J Comput Assist Tomogr. 2004;28(5):588-

95.

6. Israel GM, Silverman SG. The incidental renal mass. Radiol Clin North Am.

2011;49(2):369-83.

7. Ljungberg B, Hanbury DC, Kuczyk MA, et al. European Association of

Urology Guideline Group for renal cell carcinoma. Renal cell carcinoma

guideline. Eur Urol 2007;51:1502–1510.

8. Bozas G, Tassidou A, Moulopoulos LA, et al. Non-Hodgkin's lymphoma of

the renal pelvis. Clin Lymphoma Myeloma. 2006;6(5):404-6.

9. Dimopoulos MA, Moulopoulos LA, Costantinides C, et al. Primary renal

lymphoma: a clinical and radiological study. J Urol 1996; 155:1865-1867.

24

10. Aras M, Dede F, Ones T, et al. Is The Value of FDG PET/CT In Evaluating

Renal Metastasis Underestimated? A Case Report And Review of The

Literature. Mol Imaging Radionucl Ther. 2013;22(3):109-12.

11.Shimko MS, Jacobs SC, Phelan MW. Renal metastasis of malignant

melanoma with unknown primary. Urology. 2007;69(2):384.e9-10.

12. Israel GM, Bosniak MA. Pitfalls in renal mass evaluation and how to avoid

them. Radiographics. 2008;28:1325–1238.

13. Amis ES Jr. Cysts of the renal sinus. In: Pollack HM, McClennan BL, eds.

Clinical urography. 2nd ed. Philadelphia, Pa: Saunders, 2000; 1404– 1412

14. Nahm AM, Ritz E. The renal sinus cyst-the great imitator. Nephrol Dial

Transplant. 2000;15(6):913-4

15. Dogra VS, Bhatt S. Replacement renal sinus lipomatosis of the

kidney.Ultrasound Q. 2009 Jun;25(2):71-3. 16. Kocaoglu M, Bozlar U, Sanal

HT, Guvenc I. Replacement lipomatosis: CT and MRI findings of a rare renal

mass. Br J Radiol. 2007;80(959):e287-9.

17. Fujii Y, Komai Y, Saito K, et al. Incidence of benign pathologic lesions at

partial nephrectomy for presumed RCC renal masses: Japanese dual-center

experience with 176 consecutive patients. Urology 2008; 72:598–602

18. Froemming AT, Boland J, Cheville J, et al. Renal epithelioid

angiomyolipoma: imaging characteristics in nine cases with radiologic-

pathologic correlation and review of the literature. AJR Am J Roentgenol.

2013;200(2):W178-86

19. Bulbul MA, Farrow GA. Renal artery aneurysms. Urology. 1992;40(2):124-

6.

25

20. Gayer G, Zissin R, Rimon U et al. Vascular lesions of the renal sinus.

Emerg Radiol. 2003;10(3):135-41.

21 Klausner JQ, Harlander-Locke MP, Plotnik AN, et al. Current treatment of

renal artery aneurysms may be too aggressive. J Vasc Surg. 2014 Jan 22.

22. Sountoulides P, Zachos I, Paschalidis K, et al. Massive hematuria due to

a congenital renal arteriovenous malformation mimicking a renal pelvis tumor:

a case report. J Med Case Rep. 2008 May 5;2:144. doi: 10.1186/1752-1947-

2-144.;

23. Koch CA, Li CY, Mesa RA, et al. Nonhepatosplenic extramedullary

hematopoiesis: associated diseases, pathology, clinical course, and

treatment. Mayo Clin Proc. 2003;78(10):1223-33.

24. Galperin-Aizenberg M, Volchek Y, Even Sapir E, et al. Case report: Renal

extramedullary haematopoiesis mimicking renal lymphoma on computed

tomography. Clin Radiol. 2006;61(10):896-8.

25. Stone JH, Zen Y, Deshpande V. IgG4-related disease. N Engl J Med.

2012;366(6):539-51

26. Takahashi N, Kawashima A, Fletcher JG, et al. Renal involvement in

patients with autoimmune pancreatitis: CT and MR imaging findings.

Radiology. 2007;242(3):791-801

27. Triantopoulou C, Malachias G, Maniatis P, et al. Renal lesions associated

with autoimmune pancreatitis: CT findings. Acta Radiol. 2010;51(6):702-7.

28. Kawano M, Saeki T, Nakashima H, et al. Proposal for diagnostic criteria

for IgG4-related kidney disease. Clin Exp Nephrol. 2011;15(5):615-26

26

29. Yun EJ, Yeh BM, Yabes AP, et al. Erdheim-Chester disease: case report

and review of associated urological, radiological and histological features. J

Urol 2003;169:1470–1471.

30. Sheu SY, Wenzel RR, Kersting C, et al. Erdheim-Chester disease: case

report with multisystemic manifestations including testes, thyroid, and lymph

nodes, and a review of literature. J Clin Pathol 2004;57:1225–1228.

31. Bancroft LW, Berquist TH. Erdheim-Chester disease: radiographic

findings in five patients. Skeletal Radiol 1998;27:127–132.

32. Fortman BJ, Beall DP. Erdheim-Chester disease of the retroperitoneum: a

rare cause of ureteral obstruction. AJR Am J Roentgenol 2001;176:1330–

1331.

33. Dion E, Graef C, Haroche J, et al. Imaging of thoracoabdominal

involvement in Erdheim-Chester disease. AJR Am J Roentgenol 2004;183:

1253e60.

34. Chew HC, Lee CH, Cheah FK, et al. Cardiac tumor and renal involvement

in a nonsmoker with centrilobular pulmonary nodules. Chest.

2009;135(4):1102-6.

35. Gayer G, Desser TS, Hertz M, et al. Spontaneous suburothelial

hemorrhage in coagulopathic patients: CT diagnosis. AJR Am J Roentgenol.

2011;197(5):W887-90

36. Phinney A, Hanson J, Talner LB. Diagnosis of renal pelvis subepithelial

hemorrhage using un-enhanced helical CT. AJR 2000; 174:1023–1024

37. Eccher A, Brunelli M, Gobbo S, et al. Subepithelial pelvic hematoma

(Antopol—Goldman lesion) simulating renal neoplasm: report of a case and

review of the literature. Int J Surg Pathol. 2009;17(3):264-7.

27

Fig 1A

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Fig 1B

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Fig 1C

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Fig 1D

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Fig 1E

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Fig 2A

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Fig 2B

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Fig 2C

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Fig 3A

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Fig 3B

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Fig 3C

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Fig 3D

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Fig 4A

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Fig 4B

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Fig 5

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Fig 6A

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Fig 6B

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Fig 7A

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Fig 7B

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Fig 8

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Fig 9

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Fig 10A

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Fig 10B

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Fig 10C

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Fig 10D

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Fig 11A

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Fig 11B

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Fig 12A

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Fig 12B

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Fig 12C

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Fig 13A

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Fig 13B

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Fig 13C

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Fig 13D

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Fig 14A

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Fig 14B

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Fig 15

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Fig 16

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Fig 17A

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Fig 17B

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Fig 17C


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