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2% of sporadic renal cell carcinomas (RCCs) are bilateral, and 16-25% of sporadic RCCs are multicentric in same kidney
Exophytic: Projects from cortical surface, distinct from parenchyma
Most are hypervascular (not papillary RCC)
Rarely, small areas of fat attenuation (-80 to -120 HU)
Combination of fat and calcification suggests RCC, not renal angiomyolipoma (AML)
Renal venous (23%) and inferior vena cava (IVC) tumor extension (7%)
Metastases (most to least common): Lung, liver, bone, adrenal, opposite kidney, and brain
Cystic RCC: Enhancing, smooth or nodular septa
Multiphase CT
Mandatory: Nonenhanced and parenchymal phase
Optional: Corticomedullary, excretory phases
Multiphase MR
T1WI: Typically low signal intensity (SI)
T2WI: High to heterogeneous SI due to necrosis
Post contrast: Heterogeneous due to areas of viable, hypervascular tumor and necrosis
Renal oncocytoma
Renal AML
Renal transitional cell carcinoma
Renal metastases and lymphoma
Renal abscess
Complex renal cysts (Bosniak classification types II and III)
Clear cell (70%), papillary (10-15%), granular cell (7%), chromophobe cell (5%), sarcomatoid (1.5%), collecting duct (< 1%)
Marked variability among tumors by histopathology
Accurate distinction relies on molecular and cytogenetic markers
Renal cell carcinoma (RCC)
Malignant tumor arising from renal tubular epithelium
Location
2% of sporadic RCCs are bilateral; 16-25% of sporadic RCC are multicentric in same kidney
Renal cortex is most common location
Morphology
Usually solid mass, but occasionally cystic
Other general features
~ 50% found incidentally on imaging
NECT
Heterogeneous mass ± cystic components
High attenuation (hemorrhage)
Low attenuation (≤ 20 HU) due to necrosis or cystic component
Pseudocapsule may result from hyperattenuating rim
Contour deformity due to exophytic tumors
Rare calcifications (< 10% of cases)
Mostly amorphous & internal
Rare, small areas of fat attenuation (-80 to -120 HU)
Usually due to enveloping perirenal or sinus fat
Dedifferentiated renal cell carcinoma (RCC) → fat and calcification
Fat + calcification suggests RCC > angiomyolipoma (AML)
Cystic RCC
Uni- or multilocular cystic mass with thick wall
Calcification of septa or tumor capsule
CECT
Enhancement (attenuation value ↑ by ≥ 20 HU compared to NECT)
< renal parenchyma on nephrographic and pyelographic phases
Small mass may be missed on corticomedullary phase
Heterogeneous enhancement (necrosis)
Exophytic: Projects from cortical surface, distinct from parenchyma
± lucent zone surrounding mass (pseudocapsule)
± infiltrating mass may simulate urothelial carcinoma
± subcapsular or perinephric hemorrhage
± invasion of renal veins or inferior vena cava (IVC)
Direct extension to adjacent muscles (e.g., diaphragm, psoas, quadratus lumborum, erector spinae) & viscera (i.e., colon, liver, pancreas, spleen)
Metastases to local lymph nodes (≥ 1 cm) or viscera
Metastases (most to least common): Lung, liver, bone, adrenal, opposite kidney, and brain (often hypervascular)
Cystic RCC: Enhancing, smooth or nodular septa
T1WI
Typically isointense (~ 60%) to hypointense
↑ signal intensity (SI) if internal hemorrhage (methemoglobin)
T2WI
Clear cell RCC: Typically ↑ SI
Papillary RCC: Typically ↓ SI
Appears same as AML with minimal fat
Papillary RCCs often have pseudocapsule
T1WI C+ FS
Enhancement is usually < normal renal tissue
Hypointense band/rim on T1WI (25%) and T2WI (60%)
In/out of phase
Clear cell RCC can lose SI on out-of-phase images
Tumor cells may contain intracellular lipid
Loss of signal on out-of-phase sequence cannot be reliably used to differentiate RCC from AML
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