Cystic renal cell carcinoma: CT findings simulating a benign hyperdense cyst.

Hartman, David S.; Weatherby, E.; Laskin, William B.; Brody, Jeffrey M.; Corse, William R.; Baluch, J D

doi:10.2214/ajr.159.6.1442390

Cited by 44 publications

(17 citation statements)

References 4 publications

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“…Renal cell carcinoma, which presents as cystic RCC, was frequently observed in the extremely enlarged kidneys. Cystic RCC was first described in 1986 and more cases have been reported since then [24], [25], [26], [27], [28], [29], [30], [31], [32]. Images of human cystic RCC are also available in the webpathology website (http://www.webpathology.com/image.aspcase66n8; http://www.webpathology.com/image.aspcase66n9).…”

Section: Resultsmentioning

confidence: 99%

Deficiency of FLCN in Mouse Kidney Led to Development of Polycystic Kidneys and Renal Neoplasia

et al. 2008

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The Birt–Hogg–Dubé (BHD) disease is a genetic cancer syndrome. The responsible gene, BHD, has been identified by positional cloning and thought to be a novel tumor suppressor gene. BHD mutations cause many types of diseases including renal cell carcinomas, fibrofolliculomas, spontaneous pneumothorax, lung cysts, and colonic polyps/cancers. By combining Gateway Technology with the Ksp-Cre gene knockout system, we have developed a kidney-specific BHD knockout mouse model. BHDflox/flox/Ksp-Cre mice developed enlarged kidneys characterized by polycystic kidneys, hyperplasia, and cystic renal cell carcinoma. The affected BHDflox/flox/Ksp-Cre mice died of renal failure at approximate three weeks of age, having blood urea nitrogen levels over tenfold higher than those of BHD flox/+/Ksp-Cre and wild-type littermate controls. We further demonstrated that these phenotypes were caused by inactivation of BHD and subsequent activation of the mTOR pathway. Application of rapamycin, which inhibits mTOR activity, to the affected mice led to extended survival and inhibited further progression of cystogenesis. These results provide a correlation of kidney-targeted gene inactivation with renal carcinoma, and they suggest that the BHD product FLCN, functioning as a cyst and tumor suppressor, like other hamartoma syndrome–related proteins such as PTEN, LKB1, and TSC1/2, is a component of the mTOR pathway, constituting a novel FLCN-mTOR signaling branch that regulates cell growth/proliferation.

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Section: Resultsmentioning

confidence: 99%

Deficiency of FLCN in Mouse Kidney Led to Development of Polycystic Kidneys and Renal Neoplasia

et al. 2008

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“…Israel and Bosniak (6) believe that to be considered nonsurgical, a hyperattenuating mass should measure less than 3 cm in diameter with at least one-quarter of the lesion extending outside of the renal parenchyma so a portion of its wall can be evaluated. We are aware of only one reported case that met these criteria yet had well-differentiated renal cell carcinoma in the cyst wall (22). .…”

Section: High Attenuation or High Signal Intensitymentioning

confidence: 99%

From the RSNA Refresher Courses

Hartman¹,

Choyke²,

Hartman³

2004

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The pathologic and imaging features of the renal cyst have been well described. A fluid-filled lesion is considered a cystic mass (ie, not a simple cyst) when it has any of the following features: calcification, high attenuation (>20 HU) at computed tomography, signal intensity not typical of water at magnetic resonance imaging, septations, multiple locules, enhancement, wall thickening, or nodularity. There are two important causes of a cystic renal mass: a complicated simple cyst (eg, one with hemorrhage, infection, or ischemia) and cystic renal cell carcinoma. At radiologic evaluation of such masses, it is imperative that optimal imaging techniques be used. Masses with calcification, high attenuation or high signal intensity, or septations can be categorized as benign (no further evaluation required), as requiring follow-up (probably benign), or as requiring surgery. Lesions requiring surgery can be benign or malignant at microscopic examination. Lesions that are multiloculated or demonstrate enhancement, wall thickening, or nodularity usually require surgery. When multiple features are present (eg, calcification and enhancement), the mass should be managed according to its most aggressive feature. Likewise, when there are conflicting findings at evaluation with different imaging modalities, the mass should be managed according to the most aggressive finding.

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“…The diagnostic accuracy of CT is reported to be close to 95%. Characterization of a renal mass on CT relies on several factors, among which the definite demonstration of enhancement is the most significant [2][3][4][5][8][9][10][11][12][13][14]. The standard accepted protocol for CT evaluation of renal masses consists of both plain and enhanced images, typically acquired during the tubular nephrographic phase of excretion of contrast material [2-4, 7, 10, 12, 14-18].…”

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confidence: 99%