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Genitourinary Case Report 5
Contributors: Jennifer Zhang, M.D. and Manmeen Kaur, M.D.
Date: July 2, 2003

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Patient History

   

  Images
 

 

(Download DICOM files)

Figure 1: Coronal T2-weighted HASTE.
Figure 2: Coronal HASTE through IVC and renal veins.

Figure 3: Axial subtracted image from T1-weighted 3D GRE (VIBE) during nephrogram phase (unenhanced image was subtracted from enhanced image).

Figure 4: Coronal MPR from subtracted contrast-enhanced 3D GRE (VIBE).

 

 

 

Findings

 

 

Figure 1: Coronal HASTE image demonstrates a large, slightly heterogeneous mass (5.3 x 5.6 cm) in the upper pole of the RIGHT kidney. There is diffuse signal abnormality of the renal parenchyma in the upper and middle portions of the LEFT kidney.

Figure 2: Coronal HASTE image through the IVC and renal veins demonstrates loss of normal flow void signal in the renal veins and IVC. The left renal vein and IVC are distended with slightly hyperintense material consistent with tumor thrombus. The superior extent of this thrombus can be delineated at the level of the diaphragm. Inferiorly, the thrombus extends to the level of the iliac veins. There is no extension of the tumor thrombus into the right renal vein.

Figure 3: Axial subtracted post-contrast VIBE image again demonstrates a large heterogeneous enhancing mass in the upper pole of the right kidney and diffuse abnormal enhancement of the parenchyma of the left kidney. The left renal vein is distended with enhancing material consistent with tumor thrombosis. This enhancing tumor thrombus extends into the IVC. There is a crescentic area of dark signal intensity (non-enhancing) within the IVC consistent with a bland thrombus.

Figure 4: Coronal MPR image of subtracted dataset again demonstrates enhancing tumor thrombus involving the left renal vein and the suprarenal IVC to the level of the hepatic veins. Below the levels of renal veins, the IVC is filled with non-enhancing bland thrombus to the level of the iliac veins bilaterally.

 

 

 

Diagnosis

 

 

Bilateral renal cell carcinoma (papillary) with vascular invasion on the left.

 

 

 

Discussion

 

 

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:

  1. Semelka, Richard. Abdominal-Pelvic MRI. New York: Wiley-Liss Inc, 2002. pp. 774-797.
  2. Dunnick NR, Sandler CM, Newhouse JH, and ES Amis. Textbook of Uroradiology, 3rd Edition. Philadelphia: Lippincott Williams & Wilkins, c2001. pp. 123-132.
  3. 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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