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Renal adenocarcinoma (renal cell carcinoma) is a malignant neoplasm
that arises from the renal cortex (proximal convoluted tubular epithelial
cells). It accounts for over 90% of renal neoplasms. Renal cell
carcinoma has no racial predilection and has a slight male predominance
(1.6:1). Patients on chronic hemodialysis or peritoneal dialysis
have an overall incidence of renal cell carcinoma of approximately
7%. Patient’s with von Hippel-Lindau disease often develop
renal carcinomas that are smaller and frequently multiple and bilateral.
Only a minority of patients present with a classic presentation
of flank mass, pain and hematuria. Most patients first complain
of nonspecific symptoms such as weight loss, fatigue, or gastrointestinal
and neurologic symptoms. Renal cell carcinomas can secrete a variety
of hormones including renin, erythropoietin, prolaction, parathormone,
gonadotropin, ACTH, and ACTH 5 corticotropin that can lead to characteristic
clinical manifestations.
There are several histological subtypes of renal cell carcinoma,
including: clear cell (70-80% of renal cell carcinomas), papillary
(10-15%), chromophobe cell (5%), and sarcomatoid (spindle cell,
1.5%). The more common subtypes (clear cell, papillary, and chromophobe)
typically appear as well-defined masses and may form a capsule of
connective tissue and compressed renal parenchyma as the tumor grows.
Metastatic disease is primarily to the lung, as well as to the liver,
bone, brain and skin.
On imaging, renal cell carcinomas appear as a relatively well-marginated,
expansile, solitary mass. A focal contour bulge in the renal surface
is typical and in 5% of patients tumors are multiple. The less common
infiltrative growth pattern has an ill-defined tumor margin. Calcification
is evident in approximately 15-20% of renal cell carcinomas, and
may be rim-like or central.
Conventional MRI sequences may be used to evaluate large renal
tumors, asses the presence of tumor thrombus, or extension of tumor
into adjacent organs. However, intravenous gadolinium contrast enhanced
MRI imaging is necessary to demonstrate small tumors, distinguish
between cysts and tumors, and to clearly evaluate tumor thrombus
and metastases. Typically, renal cell carcinoma appears as an irregular
mass with ill-defined margins. Tumors generally appear slightly
hypointense on T1-weighted images and slightly hyperintense on T2-weighted
images relative to the normal renal parenchyma. However, renal cell
carcinomas can have heterogeneous signal intensity depending on
the vascularity of the tumor and the presence or absence of central
necrosis, calcification, hemorrhage, and iron deposits.
Intravenous contrast (Gd-DPTA) administration enhances the vascular
tumors on T1-weigthed spin-echo sequences. Tumors are frequently
hypervascular and demonstrate intense enhancement on immediate post-contrast
images. Hypervascular cancers also tend to wash out, whereas the
renal cortex remains high in signal intensity due to retention of
contrast in the renal tubules. Hypervascular cancers greater than
5 cm also commonly demonstrate central necrosis. Homogeneous enhancement
does occur and is typical of small, low-grade cancers. Delayed interstitial
phase images should be included in a renal MRI protocol. Diminished
enhancement on interstitial-phase images is observed for the great
majority of renal cell carcinomas.
Approximately 20% of renal cell carcinomas may be hypovascular.
Hypovascularity is most commonly related to a papillary renal cell
carcinoma subtype. These subtype of tumors are characterized by
a lower stage at presentation and slower growth. On imaging, these
tumors tend to be to be large, solid, well-demarcated lesions, commonly
have calcifications, and show hypovascularity or avasularity on
angiography. These hypovascular renal cancers enhance minimally
on post-contrast capillary-phase images and remain low in signal
intensity relative to cortex on interstitial-phase images. Diagnosis
of a hypovasular renal cell cancer requires identification of small,
short, curvilinear enhanced structures that are present on post-contrast
images but are not apparent on pre-contrast images. These tumors
are best detected with interstial-phase images with fat saturation.
Invasion of the renal vein, and sometimes the inferior vena cava
(IVC), is found in up to 16% of tumors. Tumor thrombus extends from
the renal vein, into the IVC, and grows superiorly with the direction
of blood flow toward, and in advanced cases, into the right atrium.
Direct coronal or sagittal plane MRI images are important for demonstrating
the superior extent of the thrombus to help guide surgical planning
for thrombus extraction. Contrast administration is also useful
for the evaluation of thrombus composition because tumor thrombus
almost always enhances with gadolinium. The distinction between
tumor thrombus and bland thrombus is important because the surgical
thrombus extraction technique is affected (i.e. tumor thrombus adheres
to the venous wall and can invade the vessel wall whereas a simple
blood clot does not). In addition, patient prognosis and the likelihood
of lung metastases are also affected. The presence of vascular invasion
conveys a poor prognosis.
The two most commonly used staging systems are the Robson system
and the TNM system. The Robson classification system provides
anatomic and prognostic information. The Robson system is defined
as follows:
Stage I: Tumor is confined to the kidney and does not
extend beyond the renal capsule.
Stage II: Tumor penetrates beyond the renal capsule but
remains within Gerota’s fascia. The ipsilateral adreal gland
may be involved.
Stage IIIA: Tumor extends into the renal vein and may progress
into the IVC and up to the right atrium.
Stage IIIB: There is tumor involvement of the regional
lymph nodes.
Stage IIIC: There is both venous extension and lymph node
involvement.
Stage IVA: There is tumor growth through Gerota’s
fascia into adjacent tissues.
Stage IVB: Distant metastases of tumor.
References:
- Semelka, Richard. Abdominal-Pelvic MRI. New York: Wiley-Liss
Inc, 2002. pp. 774-797.
- Dunnick NR, Sandler CM, Newhouse JH, and ES Amis. Textbook
of Uroradiology, 3rd Edition. Philadelphia: Lippincott Williams
& Wilkins, c2001. pp. 123-132.
- Rickhardt PJ, Lonergan GJ, Davis FJ, Kashitani N, and BJ Wagner.
Infiltrative Renal Lesions: Radiologic-Pathologic Correlation.
RadioGraphics. 2000; 20: 215-243.
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