Published online before print February 29, 2008, 10.1148/radiol.2472061846
(Radiology 2008;247:331-343.)
© RSNA, 2008
Simplified Imaging Approach for Evaluation of the Solid Renal Mass in Adults1
Ray Dyer, MD,
David J. DiSantis, MD, and
Bruce L. McClennan, MD
1 From the Department of Radiology, Wake Forest University School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157 (R.D., D.J.D.); and Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, Conn (B.L.M.). Received October 27, 2006; revision requested January 8, 2007; revision received January 30; accepted April 16; final version accepted May 14.
Address correspondence to R.D. (e-mail: rdyer{at}wfubmc.edu).
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ABSTRACT
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Current patterns of imaging utilization lead to frequent serendipitous discovery of renal lesions. Today, the majority of solid renal masses that are ultimately proved to be renal cell carcinomas were incidental findings on imaging studies performed for non–urinary tract symptoms. While earlier discovery has led to treatment of smaller and earlier-stage malignancies, the percentage of benign lesions discovered has also increased. A strategy for characterization of solid masses in adults based on the lesion's growth pattern, the "ball" versus the "bean," is presented. Common and uncommon renal masses, in concert with clinical and other imaging clues, are reviewed within the context of a renal ball or bean.
© RSNA, 2008
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INTRODUCTION
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Computed tomography (CT) has become the imaging procedure of choice in the investigation of virtually all abdominal complaints. Because the kidneys, if present, are obligatorily depicted during these examinations, as the number of abdominal imaging procedures has risen, so too has the number of serendipitously discovered renal lesions. By applying published rules to optimally performed CT, most renal masses can be characterized as solid or cystic. The overwhelming majority of cystic masses will be benign (1–4). In the past, all enhancing solid renal masses were treated as instances of renal cell carcinoma (RCC), although proof generally was obtained only after radical nephrectomy (5).
Incidental discovery of asymptomatic solid renal masses has meant smaller, more difficult to characterize lesions are now routinely identified on cross-sectional imaging studies and, for RCC, a decrease in the stage at presentation. Coincidentally, as the tumors discovered have become smaller (<4 cm in diameter), the number of benign lesions encountered has also increased, and opportunities to use less radical therapies for those lesions requiring treatment are evolving (6,7).
An accurate imaging diagnosis is, therefore, key to the therapeutic decision-making process. While RCC remains the diagnosis of exclusion for most enhancing solid renal masses, assessment of the growth pattern and vascularity of a mass, in concert with other imaging characteristics and the clinical context, can serve to improve diagnostic accuracy.
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THE BALL VERSUS THE BEAN
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A useful strategy for the evaluation of renal masses is to divide them on the basis of their growth pattern into ball-type or bean-type masses (8,9), a concept developed at the Armed Forces Institute of Pathology by David S. Hartman, MD, and Pablo R. Ros, MD, MPH (oral communication, October, 2006) (Fig 1).
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Figure 1a: Illustration shows ball-versus-bean concept. (a) Ball-type mass grows exophytically, creating contour deformity in the renal margin. It compresses adjacent renal parenchyma and may displace regional collecting system elements. (b) Bean-type mass uses renal parenchyma as scaffolding for growth; while the mass may enlarge the kidney, the renal shape is maintained. Sinus fat and collecting system elements may be destroyed.
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Figure 1b: Illustration shows ball-versus-bean concept. (a) Ball-type mass grows exophytically, creating contour deformity in the renal margin. It compresses adjacent renal parenchyma and may displace regional collecting system elements. (b) Bean-type mass uses renal parenchyma as scaffolding for growth; while the mass may enlarge the kidney, the renal shape is maintained. Sinus fat and collecting system elements may be destroyed.
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Ball-type masses are more common and enlarge by means of additive expansion. As they grow, these spherical masses can deform the renal contour, producing a hump or bulge. Such contour alterations, though sometimes subtle, may be appreciated on unenhanced CT studies. After intravenous contrast material administration, lesion conspicuity rises sharply, with a distinct interface between the mass and the surrounding renal parenchyma. Ball-type masses may produce a pseudocapsule as they compress adjacent renal parenchyma. The highly vascular nature of some masses can obscure them during the corticomedullary phase of CT imaging. During the nephrographic phase, however, even very vascular lesions become more conspicuous against the background of normally enhanced renal parenchyma (3,10,11). Excretory-phase CT imaging can reveal distortion and displacement of the pyelocaliceal system by the adjacent mass (8,9).
In contrast to the enlarging sphere of a ball-type mass, bean-type lesions use the tissues of the renal parenchyma as scaffolding for infiltrative growth (8,9). While the process can enlarge the kidney, its reniform (bean) shape typically is maintained. Because there is no contour deformity, bean-type lesions may be invisible on unenhanced CT images. After contrast material administration, the infiltrative mass is usually most conspicuous on nephrographic-phase CT images. The border of the mass typically is ill defined, reflecting the infiltrative nature of the lesion. On excretory-phase CT images, collecting system elements may be encased or even obliterated, with resultant distortion of the local renal sinus anatomy if the lesion is centrally located.
While there can be overlap in the imaging appearances of solid renal masses, recognition of the ball- or bean-type growth pattern offers a starting point for lesion characterization (Table).
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RCC: THE PROTOTYPIC BALL-TYPE LESION
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RCC accounts for 90% of primary renal neoplasms and represents 3% of all adult malignancies (9,12). The incidence of RCC has risen steadily over the past several decades (12,13). The impact of imaging on the diagnosis of RCC is difficult to understate. The classic triad of RCC, hematuria, flank pain, and a palpable abdominal mass, is now seen in a very small minority of patients in whom the diagnosis is made, and, when present, portends widespread disease (14). Today, most newly diagnosed RCCs are discovered incidentally during imaging performed for nonurologic symptoms (12,15) (Fig 2). Consequently, the lesions are often smaller and of lower stage and histologic grade. This earlier detection may result in improved outcomes while allowing for less-invasive nephron-sparing therapies (15).
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Figure 2: RCC discovered incidentally in 83-year-old woman who underwent CT after a fall. Transverse contrast-enhanced CT image from corticomedullary phase shows brisk enhancement in 4-cm exophytic ball-type mass (arrows) at right upper pole. Because of the patient's advanced age, biopsy was performed and conventional RCC was found.
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The occurrence of RCC peaks in the 6th to 7th decades, with a male predominance (12). Conventional (clear cell) RCC, the most common histologic subtype, accounts for 70%–80% of all RCCs and is the archetypical ball-type tumor (12,16). The inherent vascularity of conventional RCC characteristically produces strong enhancement in the mass on corticomedullary-phase CT images (the change is often in excess of 100 HU from unenhanced to contrast-enhanced images) (17). Unfortunately, if the lesion is small and located primarily within the cortex, it may be difficult to identify against the background of normal cortical enhancement. Mass conspicuity increases on nephrographic-phase images, making these the most sensitive for RCC detection (10,11) (Fig 3). When a lesion is large, a renal contour abnormality may be obvious on unenhanced CT images; when the lesion is small, however, the marginal deformity may be absent or quite subtle. It should be emphasized that any renal contour abnormality detected on an unenhanced CT study should be interpreted with caution. This is especially true for the patient with hematuria, for whom unenhanced CT alone should not be considered an adequate evaluation.
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Figure 3a: Improved mass conspicuity during nephrographic phase in 43-year-old woman who underwent CT for abdominal pain. (a) Transverse contrast-enhanced image of the kidney during the corticomedullary phase shows very subtle defect (arrow) at corticomedullary interface of the interpolar region of the left kidney. (b) On transverse contrast-enhanced image obtained during the nephrographic phase, the 9-mm mass (arrow) is more conspicuous. Surgical extirpation revealed conventional RCC.
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Figure 3b: Improved mass conspicuity during nephrographic phase in 43-year-old woman who underwent CT for abdominal pain. (a) Transverse contrast-enhanced image of the kidney during the corticomedullary phase shows very subtle defect (arrow) at corticomedullary interface of the interpolar region of the left kidney. (b) On transverse contrast-enhanced image obtained during the nephrographic phase, the 9-mm mass (arrow) is more conspicuous. Surgical extirpation revealed conventional RCC.
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Calcification may be seen on unenhanced CT images in up to 30% of RCCs. Thin calcification in the periphery of a mass is more often associated with a benign cyst, while centrally located calcification is more characteristic of RCC (18,19). Brisk enhancement is seen in conventional RCC owing to the inherent vascularity, and while the enhancement may be homogeneous when the lesion is small, areas of necrosis are often evident, producing internal heterogeneity. Early enhancement and deenhancement on delayed images in the lesion after contrast material administration serve to distinguish the lesion from a simple cyst and normal renal parenchymal background (20). Approximately 15% of RCCs have a substantial cystic component, due either to extensive necrosis within the lesion or to a primarily cystic growth pattern (21). In these cases, rules relevant to complex cystic masses must be carefully applied to determine if a lesion is surgical or nonsurgical (1,3).
Papillary RCC, the second most common tumor subtype, accounts for 10%–15% of tumors, while chromophobe-type RCC represents just 5% (12,16). Although both of these tumor types typically manifest as ball-type lesions, papillary tumors deserve specific comment. Some papillary RCCs exhibit little contrast enhancement (an increase of only 10–20 HU between unenhanced and enhanced images), making differentiation from a renal cyst difficult (3,22). This further emphasizes the need for careful evaluation of any focal renal contour abnormality (Fig 4).
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Figure 4a: Incidental papillary RCC detected as renal hump at unenhanced CT performed for left flank pain in a 73-year-old man. (a) Transverse unenhanced CT image shows contour abnormality (arrow) in interpolar region of the left kidney. Attenuation in the bulge was 36 HU. Left ureterovesical junction stone was also present (not shown). (b) Transverse contrast-enhanced CT image obtained during late nephrographic phase confirms that bulge is due to well-defined ball-type lesion (arrow). Attenuation of the mass was 65 HU. Pathologic diagnosis after nephrectomy was papillary RCC. (Reprinted, with permission, from reference 25.)
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Figure 4b: Incidental papillary RCC detected as renal hump at unenhanced CT performed for left flank pain in a 73-year-old man. (a) Transverse unenhanced CT image shows contour abnormality (arrow) in interpolar region of the left kidney. Attenuation in the bulge was 36 HU. Left ureterovesical junction stone was also present (not shown). (b) Transverse contrast-enhanced CT image obtained during late nephrographic phase confirms that bulge is due to well-defined ball-type lesion (arrow). Attenuation of the mass was 65 HU. Pathologic diagnosis after nephrectomy was papillary RCC. (Reprinted, with permission, from reference 25.)
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A patient in whom RCC is a diagnostic consideration merits a diligent search for imaging evidence of extension of the disease process. Identification of invasion into the perinephric fat beyond the renal fascia, extension into the renal vein or inferior vena cava, regional lymphadenopathy, invasion into adjacent organs, or evidence of distant metastasis supports the diagnosis of malignancy. This information is key to proper tumor staging. Specific attention should be given to the most common sites of RCC metastasis, including the lungs, mediastinum, bones, and liver, as well as to less common sites such as the contralateral kidney, adrenal gland, brain, pancreas, mesentery, and abdominal wall (18).
In patients who undergo radical nephrectomy for sporadic RCC, the chance of development of an asynchronous tumor in the contralateral kidney is approximately 2% (23). The prevalence of bilateral RCC is also reported at about 2% (14), although our recent experience with optimally performed CT examinations suggests that this number may be an underestimate.
Multicentricity of RCC is reported to be present in up to 25% of radical nephrectomy specimens (14). Multifocal and bilateral tumors should also prompt consideration of the presence of a hereditary association, seen in 4% of RCC cases (24). While von Hippel–Lindau disease is perhaps the best known hereditary condition associated with development of multiple conventional RCCs, each RCC histologic subtype is represented in a hereditary association (21,24). RCC can also develop in patients with renal failure against the background of acquired cystic disease of dialysis (14) (Fig 5). While it is implicit that patients with a tendency for multiple tumor development require ongoing surveillance, the statistics also support this path for sporadic RCC treated with newer nephron-sparing techniques (25).
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Figure 5a: Development of conventional RCCs in context of acquired cystic disease of dialysis in 53-year-old woman intermittently maintained on hemodialysis for many years. (a) Unenhanced reconstructed coronal CT image reveals numerous masses bilaterally in atrophic kidneys. Calcification (arrowhead) is seen in cyst in interpolar region of right kidney. (b) Reconstructed coronal contrast-enhanced CT image reveals 2-cm enhancing mass (arrow) in lower pole of left kidney. Smaller masses were evident on other images. Biopsy of this lesion performed in anticipation of radiofrequency ablation revealed conventional RCC.
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Figure 5b: Development of conventional RCCs in context of acquired cystic disease of dialysis in 53-year-old woman intermittently maintained on hemodialysis for many years. (a) Unenhanced reconstructed coronal CT image reveals numerous masses bilaterally in atrophic kidneys. Calcification (arrowhead) is seen in cyst in interpolar region of right kidney. (b) Reconstructed coronal contrast-enhanced CT image reveals 2-cm enhancing mass (arrow) in lower pole of left kidney. Smaller masses were evident on other images. Biopsy of this lesion performed in anticipation of radiofrequency ablation revealed conventional RCC.
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TCC: THE PROTOTYPIC BEAN-TYPE LESION
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TCC is the most common urothelial neoplasm and the second most common primary renal malignancy, accounting for approximately 10% of upper urinary tract tumors (26). Renal TCC most frequently arises in the renal pelvis, followed by the infundibular and caliceal regions (27). The majority of these tumors are low-grade, superficial, papillary tumors, which produce a focal intraluminal mass in the renal collecting system (26,28,29). More aggressive tumors may spread by means of mucosal extension, resulting in mural thickening with luminal narrowing, or by means of direct hematogenous or lymphatic invasion. This aggressive form of TCC is seen in approximately 15% of tumors (26,30). From its urothelial source, infiltrative TCC spreads centrifugally, altering the regional architecture of the adjacent renal sinus and renal parenchyma but preserving the renal contour. This form of TCC represents the prototypic bean-type lesion.
Hematuria usually prompts evaluation, but flank pain, which prompts an unenhanced CT examination for evaluation of acute renal colic due to urolithiasis, is not uncommon (26). On unenhanced studies, the intraluminal portion of a lesion often shows increased attenuation with respect to surrounding urine. Because the tumor does not typically deform the renal contour, invasion of sinus structures with infiltration of the sinus fat or isolated dilatation or encasement of collecting system elements may be subtle indicators of a TCC's presence on unenhanced images. After contrast material administration, the mass typically enhances, although to a lesser degree than normal renal parenchyma (and characteristically less than conventional RCC) (26).
The central location of these masses may make differentiation from the unenhanced medulla nearly impossible on corticomedullary-phase CT images, underscoring the need for nephrographic-phase imaging. The interface between a TCC and adjacent normal renal parenchyma during the nephrographic phase is typically ill defined. Excretory-phase images, especially when coupled with multiplanar reformatting (CT urography), improves visualization of collecting system abnormalities such as localized hydrocalices or caliceal "amputation" due to encasement, calices distended by tumor ("oncocalices"), or unopacified ("phantom") calices due to larger areas of parenchymal infiltration and replacement (Fig 6). The parenchymal infiltration may be sufficient to replace large volumes of normal tissue or even the entire kidney, causing pronounced alterations of renal enhancement or even nonfunction (26,30).
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Figure 6a: CT images of TCC in right upper renal pole in an 83-year-old woman after needle biopsy of a lung nodule revealed TCC. (a) Transverse unenhanced image shows obliteration of the sinus fat in upper aspect of the right kidney. (b) Transverse contrast-enhanced nephrographic-phase image at same level as a reveals poorly defined parenchymal mass with no alteration of the renal contour. (c) Reconstructed coronal contrast-enhanced image of right kidney during excretory phase (CT urographic image) better illustrates alteration of parenchymal enhancement and shows obliteration of caliceal elements in the upper pole (phantom calyces) (arrow). TCC was confirmed at nephroscopic biopsy.
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Figure 6b: CT images of TCC in right upper renal pole in an 83-year-old woman after needle biopsy of a lung nodule revealed TCC. (a) Transverse unenhanced image shows obliteration of the sinus fat in upper aspect of the right kidney. (b) Transverse contrast-enhanced nephrographic-phase image at same level as a reveals poorly defined parenchymal mass with no alteration of the renal contour. (c) Reconstructed coronal contrast-enhanced image of right kidney during excretory phase (CT urographic image) better illustrates alteration of parenchymal enhancement and shows obliteration of caliceal elements in the upper pole (phantom calyces) (arrow). TCC was confirmed at nephroscopic biopsy.
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Figure 6c: CT images of TCC in right upper renal pole in an 83-year-old woman after needle biopsy of a lung nodule revealed TCC. (a) Transverse unenhanced image shows obliteration of the sinus fat in upper aspect of the right kidney. (b) Transverse contrast-enhanced nephrographic-phase image at same level as a reveals poorly defined parenchymal mass with no alteration of the renal contour. (c) Reconstructed coronal contrast-enhanced image of right kidney during excretory phase (CT urographic image) better illustrates alteration of parenchymal enhancement and shows obliteration of caliceal elements in the upper pole (phantom calyces) (arrow). TCC was confirmed at nephroscopic biopsy.
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Upper-tract TCC is more common in men and typically develops in the 6th–7th decades of life (26). Smoking, chemical carcinogens, cyclophosphamide therapy, and analgesic abuse all have been associated with development of TCC. Carcinogens concentrated in the urine bathe the entire urothelium, increasing the risk of neoplastic development. Consequently, TCC is often multifocal, with synchronous and metachronous tumors necessitating vigilant clinical and radiologic surveillance (26,31).
In addition to direct invasion by TCC from the kidney into the retroperitoneum, lymphatic invasion often leads to regional lymphadenopathy. Hematogenous invasion may result in distant metastasis to lungs and bone (26,28). While therapies for superficial and lower-grade TCC are evolving, removal of the involved kidney, the ipsilateral ureter, and a cuff of bladder tissue surrounding the ureter has been the traditional therapy for aggressive upper-tract TCC, with the intent of extirpating the entire at-risk urothelial field (26).
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OTHER BALL-TYPE LESIONS
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AML Lesions
When a ball-type renal lesion contains detectable fat at CT imaging, a nearly specific diagnosis of AML can be offered in most cases (32). An AML is a benign tumor composed of angiomatous, myomatous, and lipomatous tissues in varying amounts (33). Even when the mass is small, the fat content of an AML is often conspicuous on thin-section unenhanced CT images (Fig 7). If fat within a mass is not visually obvious, pixel mapping can be performed, which may reveal the fat as clustered pixels with negative CT numbers (defined as at least 3 adjacent pixels with attenuation 
–20 HU) (34) (Fig 8).
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Figure 7: Hyperechoic mass in right kidney of a 48-year-old woman was incidentally discovered at sonography (not shown) performed for right upper quadrant pain. Transverse unenhanced CT image reveals that 1.3-cm lesion (arrow) is composed primarily of fat (attenuation, –66 HU). Confident diagnosis of AML can be made, and no further work-up is necessary.
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Figure 8a: Indeterminate mass and use of pixel mapping in 53-year-old woman evaluated for microscopic hematuria. (a) Transverse unenhanced CT image through right lower renal pole reveals small ball-type lesion (arrow) projecting medially. No fat was evident visually, and internal attenuation was 16 HU. (b) On transverse contrast-enhanced nephrographic-phase CT image, the mass is more conspicuous (arrow) and attenuation of 65 HU was observed, indicative of enhancement. (c) Pixel map from a region of interest in tumor seen on a reveals clustering of pixels with negative CT numbers (shaded areas), indicative of intralesional fat. Another area of clustered negative CT numbers is in left upper aspect of map. Angiomyolipoma was diagnosed, and the mass has been monitored for 2 years without change.
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Figure 8b: Indeterminate mass and use of pixel mapping in 53-year-old woman evaluated for microscopic hematuria. (a) Transverse unenhanced CT image through right lower renal pole reveals small ball-type lesion (arrow) projecting medially. No fat was evident visually, and internal attenuation was 16 HU. (b) On transverse contrast-enhanced nephrographic-phase CT image, the mass is more conspicuous (arrow) and attenuation of 65 HU was observed, indicative of enhancement. (c) Pixel map from a region of interest in tumor seen on a reveals clustering of pixels with negative CT numbers (shaded areas), indicative of intralesional fat. Another area of clustered negative CT numbers is in left upper aspect of map. Angiomyolipoma was diagnosed, and the mass has been monitored for 2 years without change.
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Figure 8c: Indeterminate mass and use of pixel mapping in 53-year-old woman evaluated for microscopic hematuria. (a) Transverse unenhanced CT image through right lower renal pole reveals small ball-type lesion (arrow) projecting medially. No fat was evident visually, and internal attenuation was 16 HU. (b) On transverse contrast-enhanced nephrographic-phase CT image, the mass is more conspicuous (arrow) and attenuation of 65 HU was observed, indicative of enhancement. (c) Pixel map from a region of interest in tumor seen on a reveals clustering of pixels with negative CT numbers (shaded areas), indicative of intralesional fat. Another area of clustered negative CT numbers is in left upper aspect of map. Angiomyolipoma was diagnosed, and the mass has been monitored for 2 years without change.
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Clinical clues can also help distinguish AML from RCC. Sporadic AML, accounting for about 80% of the tumors, are typically small, asymptomatic, and an incidental finding in middle-aged women (while an older male predominance typifies RCC). The tumor is usually well defined, and calcification or necrosis within the tumor is rare (33). The vascular and smooth muscle portions of the tumor variably enhance after contrast material administration, although less intensely than is seen in RCC or normal renal parenchyma. The vessels in an AML lack a complete elastic layer and tend to be thick walled, irregular, tortuous, and aneurysmal (33,35). Consequently, AMLs are prone to spontaneous bleeding. This tendency increases in larger tumors (usually defined as an AML >4 cm in diameter). Spontaneous hemorrhage associated with an AML may cause acute flank pain. Because of the increased risk of bleeding associated with tumors larger than 4 cm, therapeutic intervention is recommended even in the asymptomatic patient. Angiographic ablation or treatment with nephron-sparing techniques have been successful (35–37).
Patients with tuberous sclerosis account for 20% of cases of AML. Tuberous sclerosis is an autosomal-dominant inherited phacomatosis whose clinical hallmarks include adenoma sebaceum, seizures, and mental retardation (33,38). AMLs are found in up to 80% of individuals with tuberous sclerosis, and while the tumors are histologically identical to the sporadic form, they are more often multiple, bilateral, and present in younger patients. In addition, the AMLs in patients with tuberous sclerosis are often larger at the time of presentation and are likely to grow, so it is not surprising that they are more frequently symptomatic (33,38) (Fig 9).
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Figure 9: Multiple AMLs in a 32-year-old man with tuberous sclerosis. Transverse unenhanced CT image reveals near-total replacement of the right kidney by multiple fat-containing AMLs. Left kidney (K) also harbors numerous smaller but similar-appearing masses.
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While CT identification of fatty elements within an AML can be definitive, it is not foolproof. Internal hemorrhage, for example, may obscure the fat. Also, about 5% of AMLs unfortunately have insufficient fat to allow an unequivocal diagnosis (so-called minimal fat AML) (39,40). Particularly disconcerting are the rare reports of RCC containing fat. The mechanisms offered for this uncommon finding include (a) osseous metaplasia of the stromal portion of an RCC, with development of fatty marrow elements and bone trabeculae; (b) cholesterol clefts and lipid vacuoles in an area of lipid necrosis; (c) a distinct nodule of mature well-circumscribed fat developing in a papillary RCC; and (d) engulfment of perirenal or sinus fat by a large RCC (41).
A subset of RCC may reveal intratumoral lipid on opposed-phase magnetic resonance (MR) images (42). This characteristic could be a concern when evaluating a mass primarily with MR imaging (Fig 10). Since the lipid is likely to be intracellular in a conventional (nonpapillary) RCC, it is unlikely to be evident on CT images.
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Figure 10a: Transverse (a) in- and (b) out-of-phase MR images show intracellular fat in conventional RCC incidentally detected at unenhanced CT (not shown) to evaluate for possible renal colic. Patient was allergic to iodinated contrast material. (a) T1-weighted MR image (repetition time msec/echo time msec, 175/4.637) shows large mass in lower pole of the right kidney. Areas of higher signal intensity can be seen in the mass (arrow). (b) Corresponding T1-weighted out-of-phase MR image (175/2.084) shows signal dropout (arrow) in areas of high signal intensity seen in a. In this case, the fat is intracellular. No large areas of fatty tissue were identified in this tumor at pathologic examination after radical nephrectomy.
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Figure 10b: Transverse (a) in- and (b) out-of-phase MR images show intracellular fat in conventional RCC incidentally detected at unenhanced CT (not shown) to evaluate for possible renal colic. Patient was allergic to iodinated contrast material. (a) T1-weighted MR image (repetition time msec/echo time msec, 175/4.637) shows large mass in lower pole of the right kidney. Areas of higher signal intensity can be seen in the mass (arrow). (b) Corresponding T1-weighted out-of-phase MR image (175/2.084) shows signal dropout (arrow) in areas of high signal intensity seen in a. In this case, the fat is intracellular. No large areas of fatty tissue were identified in this tumor at pathologic examination after radical nephrectomy.
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Oncocytoma
The oncocytoma is the most common, benign, solid, non–fat-containing renal mass, accounting for about 5% of renal cortical neoplasms (43). There was initial hope that imaging features such as a central stellate scar or "spoked-wheel" pattern of vascular supply to the tumor might allow a specific imaging diagnosis (44). Unfortunately, RCC and oncocytoma can be indistinguishable, especially when the tumor is small (45).
An oncocytoma is a ball-type mass. It occurs more often in male patients and in the same age group as RCC, and the two lesions occasionally coexist (43). Oncocytomas most often are discovered fortuitously, though they may be quite large (up to 25 cm) at the time of presentation (44). Even large oncocytomas enhance uniformly at CT, except for the central scar, if present (Fig 11). This is in contrast to the central necrosis typical of large RCCs. The central scar has been described with all types of cross-sectional imaging (44). Calcification in an oncocytoma is rare, and while the tumor is usually solitary, multifocal and bilateral tumors can occur (43,44).
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Figure 11: Incidental discovery at CT of oncocytoma in 52-year-old woman undergoing evaluation after trauma. Reconstructed sagittal contrast-enhanced corticomedullary-phase CT image shows ball-type mass with stellate central scar (arrow) arising from anterior interpolar region of left kidney. Note presence of pseudocapsule at posterior margin of the mass. Pathologic diagnosis of oncocytoma was made after laparoscopic nephrectomy. (Reprinted, with permission, from reference 25.)
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Because there are no imaging characteristics that distinguish a small oncocytoma from a small RCC, oncocytomas remain the most commonly excised benign solid renal mass (6,7,45). Even the much-sought central scar does not reliably separate a benign tumor from a malignant one.
Traditionally, percutaneous biopsy has played a limited role in evaluation of all solid renal tumors (46). Biopsy of oncocytoma was especially controversial, because it is hard to tell a truly benign oncocytoma (composed entirely of oncocytes without cellular atypia or pleomorphism) from an RCC that contains some oncocytic cells (13,46,47). As many as 20% of excised solid renal tumors 4 cm or smaller are benign, with oncocytoma accounting for most (6,7). Advancement in cytologic techniques may allow more definitive diagnosis on the basis of percutaneous biopsy findings. Biopsy could then play a larger role in the decision to use nephron-sparing therapies for small renal masses (46).
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UNUSUAL BEAN-TYPE LESIONS
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Infiltrative RCC
About 5% of conventional RCCs have an infiltrative growth pattern (48). In contrast to TCC, these lesions are aggressive and hypervascular. While the renal contour is maintained, the internal architecture is altered, as depicted at CT during the corticomedullary and nephrographic phases of enhancement. The infiltrative nature of these lesions can cause collecting system abnormalities similar to those seen with TCC. Even with small infiltrative RCCs, there is often tumor spread at the time of presentation (48) (Fig 12). While the infiltrative type represents only a small percentage of all RCCs, the prevalence of RCC means that this tumor is a prime differential diagnostic consideration for an infiltrative renal neoplasm (9).
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Figure 12a: Infiltrative RCC discovered in 70-year-old man undergoing CT for bilateral lower extremity swelling. (a) Transverse unenhanced CT image shows abnormal soft-tissue attenuation in retroperitoneum. Perinephric fat infiltration is seen on the left, but left kidney contour is maintained. (b) Transverse contrast-enhanced nephrographic-phase CT image at same level as a reveals that abnormal soft-tissue represents enlargement of left renal vein (large arrow) and inferior vena cava due to intravenous extension of tumor originating in the left kidney. Note abnormal pattern of parenchymal enhancement in anterior hilar lip on the left (small arrows) and abnormal retroperitoneal lymph nodes (arrowheads). Diagnosis of high-grade conventional RCC was made after biopsy of a right atrial mass, the upper extent of venous extension of tumor in this patient.
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Figure 12b: Infiltrative RCC discovered in 70-year-old man undergoing CT for bilateral lower extremity swelling. (a) Transverse unenhanced CT image shows abnormal soft-tissue attenuation in retroperitoneum. Perinephric fat infiltration is seen on the left, but left kidney contour is maintained. (b) Transverse contrast-enhanced nephrographic-phase CT image at same level as a reveals that abnormal soft-tissue represents enlargement of left renal vein (large arrow) and inferior vena cava due to intravenous extension of tumor originating in the left kidney. Note abnormal pattern of parenchymal enhancement in anterior hilar lip on the left (small arrows) and abnormal retroperitoneal lymph nodes (arrowheads). Diagnosis of high-grade conventional RCC was made after biopsy of a right atrial mass, the upper extent of venous extension of tumor in this patient.
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Renal Medullary Carcinoma and Collecting Duct Carcinoma
Renal medullary carcinoma (RMC) is a very rare histologic RCC subtype, accounting for fewer than 1% of all tumors. The clinical, pathologic, and imaging features of this tumor were first described in 1995 (49,50). RMC is thought to arise from caliceal epithelium in or near the renal papilla, from which it grows in an infiltrative (bean-type) pattern (49–51). Because of the tumor's central origin deep in the renal medulla, there is often caliectasis without pelviectasis. It encases or obliterates adjacent collecting system elements. The margins of an RMC are poorly defined at imaging, and most contain areas of hemorrhage and necrosis (50,51) (Fig 13).
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Figure 13a: Renal medullary carcinoma in 11-year-old boy with known sickle cell trait who presented with 2-week history of fever, malaise, and weight loss. (a) Reconstructed coronal contrast-enhanced corticomedullary-phase CT image reveals bean-type mass replacing lower two-thirds of the left kidney. Renal contour is undisturbed. (b) Reconstructed coronal contrast-enhanced corticomedullary-phase CT image obtained at a more ventral level reveals extensive left paraaortic lymphadenopathy (arrows). Diagnosis of RMC was confirmed at surgery. (Reprinted, with permission, from reference 25.)
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Figure 13b: Renal medullary carcinoma in 11-year-old boy with known sickle cell trait who presented with 2-week history of fever, malaise, and weight loss. (a) Reconstructed coronal contrast-enhanced corticomedullary-phase CT image reveals bean-type mass replacing lower two-thirds of the left kidney. Renal contour is undisturbed. (b) Reconstructed coronal contrast-enhanced corticomedullary-phase CT image obtained at a more ventral level reveals extensive left paraaortic lymphadenopathy (arrows). Diagnosis of RMC was confirmed at surgery. (Reprinted, with permission, from reference 25.)
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Patient history can be key in making this diagnosis, since RMC is found almost exclusively in patients with the sickle cell trait. Consequently, RMC develops in a much younger population than do RCC or TCC (with no patient over 40 years of age in the originally reported series) (49,50). Interestingly, the tumor more often involves the right kidney (51). There is a predilection for males, but only in patients 24 years of age or younger (49). Presenting symptoms include hematuria, which may be gross, flank or abdominal pain, and a palpable mass (49,50). Associated systemic symptoms are common and include nausea and vomiting, fever, and weight loss.
RMC is extraordinarily aggressive. Although the duration of symptoms leading to presentation is often short, most patients already have metastases. The tumor may invade locally into the regional lymph nodes (common), the renal vein and inferior vena cava, the adrenal gland, the liver, and the perinephric or retroperitoneal soft tissues (49,50). Distant sites of metastasis include the liver, the lung, and the nonregional lymph nodes, including those in omental, pulmonary hilar, and cervical sites (49–51). The rapidity of disease progression causes the mean survival to be measured in weeks (49,51).
Collecting duct carcinoma is also a very rare and aggressive histologic RCC subtype. The mean age of a patient with collecting duct carcinoma is the mid-50s, and the presentation with a flank mass and gross hematuria is common to all renal malignancies (52,53). Collecting duct carcinoma is thought to originate in the distal segment of the collecting duct in the renal medullary pyramids (52). Collecting duct carcinoma's growth pattern is initially infiltrative, and with its medullary source, it may be identified as a bean-type lesion when detected early in its course. As with TCC, imaging studies may depict abnormalities in the collecting system or renal sinus (Fig 14). However, the aggressive nature of collecting duct carcinoma frequently means that the lesion is large at the time of discovery. The resulting distortion of the renal anatomy makes differentiation from conventional RCC difficult (53). As with RMC, most collecting duct carcinomas have already metastasized at the time of diagnosis, and two-thirds of patients will succumb within 2 years (52).
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Figure 14: Collecting duct carcinoma in 24-year-old man who presented with a single episode of gross hematuria. Transverse contrast-enhanced nephrographic-phase CT image shows mass located deep in medulla of the right kidney, with associated dilatation of adjacent collecting system elements (arrowhead). Collecting system obstruction caused by the mass has produced a delay in nephrographic progression, with persistence of corticomedullary differentiation. Despite its relatively small size, mass contains areas of decreased attenuation consistent with necrosis (arrow). The portion of the mass exposed to the collecting system has calcification along its surface. Collecting duct carcinoma was confirmed after radical nephrectomy.
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Pathologic characterization of both RMC and collecting duct carcinoma is currently in evolution, as the tumors are rare and have only relatively recently been added to the classification of RCC (16,49,52).
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SECONDARY RENAL INVOLVEMENT
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Renal Metastasis
Although RCC is the most common primary renal malignancy, metastatic disease to the kidney is statistically the most common renal malignancy (54,55). The more frequent use of CT in the diagnosis, staging, and surveillance in patients with a known primary malignancy, along with improved survival rates, has led to more frequent antemortem diagnoses of renal metastasis (56). In autopsy series, up to 48% of patients who died of cancer had renal metastases, making the kidney the fifth most common site of hematogenous metastases (57,58). The primary tumors that metastasize to the kidney reflect the pattern of cancer occurrence in the general population, with lung, breast, and gastrointestinal tumors and melanoma representing the most common (57,58).
Renal metastatic disease usually occurs late in the course of known malignancy, often as a part of widespread disease. In patients with a history of malignancy, renal metastases outnumber RCCs by approximately four to one (56).
At CT, metastatic lesions are typically small, multifocal, and bilateral, exhibiting an infiltrative growth pattern. The contrast enhancement of renal metastases is much less than that of normal renal parenchyma, so the lesions can be readily identified on appropriately timed CT images (54) (Fig 15). Rarely, a renal metastasis may manifest as a solitary exophytic lesion, indistinguishable from RCC (54) (Fig 16). The diagnostic distinction between primary RCC and a renal metastasis has obvious implications for therapy and prognosis. Percutaneous renal biopsy has been useful in helping solve this clinical conundrum (46).
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Figure 15: Renal metastases from squamous cell lung carcinoma in 56-year-old man. Transverse contrast-enhanced CT image obtained in late nephrographic phase shows two poorly defined bean-type lesions (arrows) in upper pole of left kidney (arrows). Numerous other lesions were evident in both kidneys. Note extensive hepatic metastatic disease and abnormal retroperitoneal lymphadenopathy.
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Figure 16: Renal metastases from papillary thyroid carcinoma in 34-year-old man. Reconstructed coronal contrast-enhanced CT image reveals 2.5-cm ball-type lesion projecting from lateral aspect of left kidney (black arrow). Metastatic nature of the lesion was confirmed after percutaneous biopsy. Note liver metastases (white arrow), as well as numerous pulmonary nodules.
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Lymphoma
Because the kidney has no intrinsic lymphoid tissue, it is rarely the first or only site of lymphoproliferative disease (54,59). Still, the kidney is one of the most common extranodal sites of involvement by lymphoma (60). As with metastatic disease from other primary malignancies, however, renal lymphoma is usually clinically silent. The antemortem diagnosis of renal lymphoma was uncommon in the past, despite autopsy data indicating that up to one-third of patients dying of lymphoma had evidence of the disease in the kidney (60). Like RCC and metastatic disease, routine use of CT for staging and surveillance has led to more frequent antemortem diagnoses of renal lymphoma.
Kidney involvement by lymphoma typically occurs in the setting of widespread disease and usually with non-Hodgkin histologic types. Lymphoma may enter the kidney hematogenously or through sinus, perinephric, or capsular lymphatics. Several patterns of renal involvement have been described (54,60,61).
Multiple bilateral renal masses, with either a ball- or a bean-type growth pattern, are seen in 50%–60% of patients. Most have associated retroperitoneal lymphadenopathy (Fig 17). In up to 25% of patients, renal lymphoma represents contiguous spread from adjacent adenopathy into the kidney, usually showing a bean-type infiltrative pattern. Diffuse lymphomatous infiltration producing smooth generalized renal enlargement occurs in approximately 20% of patients, and it is almost always bilateral (Fig 18). Renal lymphoma as a solitary mass is the least common pattern of involvement, seen in fewer than 10% of patients (54,60).
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Figure 17a: Nodular renal lymphoma in 70-year-old woman being evaluated for malaise. (a) Transverse contrast-enhanced nephrographic-phase CT image shows multiple poorly defined masses (arrowheads) in left kidney. Note extensive retroperitoneal lymphadenopathy (arrows), as well as mesenteric lymphadenopathy, hepatosplenomegaly, ascites, and anasarca. (b) Transverse contrast-enhanced CT image through right kidney shows similar involvement with multiple masses (arrowheads). Diagnosis of large B-cell type non-Hodgkin lymphoma was made after cervical lymph node biopsy.
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Figure 17b: Nodular renal lymphoma in 70-year-old woman being evaluated for malaise. (a) Transverse contrast-enhanced nephrographic-phase CT image shows multiple poorly defined masses (arrowheads) in left kidney. Note extensive retroperitoneal lymphadenopathy (arrows), as well as mesenteric lymphadenopathy, hepatosplenomegaly, ascites, and anasarca. (b) Transverse contrast-enhanced CT image through right kidney shows similar involvement with multiple masses (arrowheads). Diagnosis of large B-cell type non-Hodgkin lymphoma was made after cervical lymph node biopsy.
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Figure 18: Infiltrative form of renal lymphoma. Transverse contrast-enhanced nephrographic-phase CT image shows bilateral bean-type renal involvement with non-Hodgkin lymphoma. In some areas, the infiltrative process in the kidneys has become coalescent. Note retroperitoneal lymphadenopathy and multiple splenic lesions (arrow). (Image courtesy of Neal Dalrymple, MD, San Antonio, Tex)
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At CT, renal lymphoma is a soft-tissue attenuation mass that enhances homogeneously but less intensely than normal renal parenchyma after contrast material administration (54,60,61). Nephrographic-phase CT imaging is essential, since lymphomatous deposits in the kidney may be small and medullary in location, making them inconspicuous on corticomedullary-phase images (61).
Patients with renal lymphoma nearly always have evidence of disease elsewhere. If the imaging findings are typical, then differentiation from RCC is usually not in question. In this situation, systemic therapy for lymphoma can be instituted, with the anticipation that the renal disease will respond in like fashion (3). On rare occasions, renal lymphoma occurs as a solitary mass or exhibits unusual imaging characteristics, making differentiation from RCC difficult. In these circumstances, image-guided biopsy results can be diagnostic (3,46).
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SUMMARY
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In current practice, most renal masses are discovered serendipitously. As the size of these newly discovered renal lesions decreases, the proportion of benign lesions increases. However, while great strides have been made in lesion detection, lesion characterization has lagged (62).
The ball-versus-bean strategy is a useful framework for analyzing the imaging characteristics of renal masses. Its basic principles apply not only to CT but also to MR and sonography. When faced with the bewildering array of pathologic conditions that can assail the kidney, ball versus bean offers a starting point.
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ESSENTIALS
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- Today, the majority of renal masses ultimately diagnosed as renal cell carcinoma were incidentally discovered at imaging performed for non–urinary tract complaints.
- The earlier discovery of smaller solid renal lesions represents a challenge with respect to lesion characterization.
- Assessment of the growth pattern at imaging (ball-type vs bean-type pattern) can be useful in this initial characterization.
- Familiarity with clinical findings and other imaging features related to the variety of renal masses that can be detected at imaging will assist with the diagnosis.
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FOOTNOTES
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Abbreviations: AML = angiomyolipoma • RCC = renal cell carcinoma • RMC = renal medullary carcinoma • TCC = transitional cell carcinoma
Authors stated no financial relationship to disclose.
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ABSTRACT
INTRODUCTION