Genitourinary Imaging Flashcards
Retroperitoneal Anatomy
Anterior pararenal space - ascending colon, descending colon, (2nd and 3rd) duodenum,and pancreas
Perirenal space: surrounds each kidney - kidneys, proximal ureter, adrenals, and lots of fat.
Posterior perirenal space - potential space, contains only fat, may become secondarily involved in inflammatory processes.
The retroperitoneum can be separated into three compartments by the anterior and posterior renal fascia and the lateral conal fascia.
The adrenals and kidneys are locatedwithin the perirenal space of the retroperitoneum.
The ascending and descending colon, the second and third portions of the duodenum, and the pancreas are located in the anterior pararenal space of the retroperitoneum.
The third compartment of the retroperitoneum, the posterior pararenal space, is a potential space that is clinically important as a pathway for potential disease spread due to secondary involvement of inflammation or neoplasm.
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Liposarcoma
Liposarcomas are a diverse group of neoplasms that make up the most common primary retroperitoneal tumors. 10-15% of all liposarcomas arise from the retroperitoneum.
The most common type of liposarcoma is the well-differentiated group, which is composed of adiopocytic, sclerosing, and inflammatory subtypes. Adipocytic liposarcoma resembles a lipoma, predominantly composed of fat with strands of tissue representing collagen bands.
In order of increasing malignancy, liposarcomas may also be myxoid, round-cell, pleomorphic, or dedifferentiated. The more aggressive subtypes may have minimal or no areas of macroscopic fat and may be indistinguishable from other malignant soft-tissue masses.
Retroperitoneal fibrosis
Retroperitoneal fibrosis is a rare inflammatory disorder causing increased fibrotic deposition in the retroperitoneum, often leading to ureteral obstruction.
Unlike malignant retroperitoneal adenopathy, retroperitoneal fibrosis tends not to elevate the aorta off the spine.
Adrenal Glands Anatomy
The adrenal glands are inverted Y-shaped endocrine glands, which primarily mediate the stress response by releasing cortisol and catecholamines. The adrenals are also a site of secondary sex hormone synthesis and blood pressure regulation (with aldosterone).
The two distinct components to the adrenal glands are the cortex and the medulla, which are derived from completely different embryological origins (the cortex is derived from mesothelium; the medulla is derived from neural crest) and are susceptible to different diseases.
Adrenal cortex
The adrenal cortex synthesizes the steroid hormones aldosterone, glucocorticoids, and androgens, which are all biochemical derivatives of cholesterol.
Each of the three layers of the adrenal cortex synthesizes one type of hormone: Zona glomerulosa (most superficial): Produces aldosterone. Zona fasciculata: Produces glucocorticoids in response to pituitary adrenocorticotropic hormone (ACTH). Zona reticularis (deepest; closest to the adrenal medulla): Produces androgens.
Pathology of the adrenal cortex that can be diagnosed on imaging includes adrenal hyperplasia, adrenal adenoma, and adrenal cortical carcinoma.
Adrenal medulla
The adrenal medulla is the central portion of the adrenal gland and produces the catecholamines norepinephrine and epinephrine, which are derived from tyrosine.
Pathology of the adrenal medulla includes pheochromocytoma and the neuroblastic tumors (ganglioneuroma, ganglioneuroblastoma, and neuroblastoma). Neuroblastoma is the most common extracranial solid tumor of childhood and is discussed in the pediatric imaging section.
Adrenal hyperfunction
Cushing syndrome is excess cortisol production from non-pituitary disease, such as idiopathic adrenal hyperplasia, adrenal adenoma, or ectopic/paraneoplastic ACTH (e.g., from small cell lung cancer).
Cushing disease is excess cortisol production driven by excessive pituitary ACTH.
Conn syndrome is excess aldosterone production, most commonly from an adrenal adenoma, which causes hypertension and hypokalemia. The adenomas implicated in Conn syndrome are typically small and may be difficult to detect on CT. Localizing the side of excess hormone production with venous sampling may be a helpful diagnostic adjunct.
Adrenal Hypofunction
Significant destruction of the adrenals is required to produce adrenal insufficiency.
Although usually not an imaging diagnosis, Addison disease represents chronic adrenocortical insufficiency and may be caused by autoimmune destruction of the adrenal glands or as a sequela of infection.
Waterhouse-Friderichsen syndrome is post-hemorrhagic adrenal failure secondary to Neisseria meningitidis bacteremia.
Idiopathic adrenal hemorrhage is usually unilateral and rarely causes adrenal hypofunction.
Adrenal adenoma
Adrenal adenoma is a benign tumor of the adrenal cortex. Adenomas are usually incidental, but they may occasionally produce excess aldosterone to cause secondary hypertension (Conn syndrome). Non-contrast imaging of the adrenal glands is the best test to evaluate for the presence of an adrenal adenoma in the presence of suspicious clinical symptoms or lab values.
A common clinical scenario is the need to differentiate between an adrenal adenoma and an adrenal metastasis in the staging of a patient with known malignancy. The diagnosis of an adenoma is made by the detection of intracellular lipid.
An adrenal nodule attenuating = 10 Hounsfield units (HU) an be reilably diagnosed as an adenoma with no further imaging or follow-up needed. Most (80%) adenomas are lipid-rich and will attenuate below this cutoff. Up to 20% may be lipid-poor adenomas, which attenuate >10 HU and are not able to be diagnosed on a noncontrast CT. An indeterminate (>10 HU), small, homogenous adrenal lesion in a patient without a known malignancy is overwhelmingly likely to represent a lipid-poor adenoma, and advanced imaging is usually not required in such cases.
If the nodule in question attenuates > 10 HU and clinical confirmation of an adenoma is necessary for clinical management (for instance, in a patient with lung cancer and no evidence of metastatic disease but with an indeterminate adrenal nodule), then an adrenal washout CT or in- and out-of-phase MRI may be helpful to characterize the lesion.
A collision tumor represents metastasis into an adrenal gland with a pre-existing adenoma. If an “adenoma” appears heterogenous or has shown an interval icnrease in size, then a collision tumor should be considered in a patient with a known primary even if a region attenuates < 10 HU.
Adenomas contain intracytoplasmic lipid due to steroid production. MRI is able to detect even a small amount of intracystoplasmic lipid that may be undetectable on CT by taking advantage of the fact that protons resonate at different frequencies in fat and in water. Chemical shift imaging consists of images obtained both in-phase and out-of-phase. When fat and water are contained within the same voxel, out-of-phase images show fat drop-out of signal because fat protons are more shielded and resonate at a slower frequency. Chemical shift imaging is based on T1 images.
Adenomas suppress on out-of-phase images, while metastases generally do not.
A short list of malignancies do contain intractyoplasmic lipid and thus would also lose signal on out-of-phase images: Well-differentiated adrenocortical carcinoma (very rare). Clear cell renal cell carcinomas metastatic to the adrenal gland. Hepatocellular carcinoma metastatic to the adrenal gland. Liposarcoma (typically a predominantly fatty mass that is rarely confused with adrenal adenoma.)
CT Imaging: Adrenal Washout CT
Adrenal adenomas demonstrate more rapid contrast washout than metastases do. The more rapid contrast washout of benign adenomas appears to be true even compared to adrenal metastases of hypervascular primaries.
The timing of the washout phase remains controversial, with recent evidence suggesting 15-minute washout has greater sensitivity than 10 minutes.
> 60% absolute washout is diagnostic of adenoma
If unenhanced CTis not available or not performed due to concern for radiation exposure, >40% relative washout is diagnostic of adenoma.
In a patient with a known primary malignancy, lesions that do not demonstrate benign washout kinetics are suspicious for, but not diagnostic of, metastasis.
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Role of biopsy of an adrenal mass
Adrenal mass biopsy is indicated for an indeterminate adrenal mass after full imaging workup remains nondiagnostic.
Biopsy is safe and generally very accurate.
Myelolipoma
An adrenal myelolipoma is a benign neoplasm consisting of myeloid cells (i.e., erythrocyte precursors - not “myo” as in muscle) and fat cells.
An adrenal mass with any discrete focus of macroscopic fat is virtually diagnostic of a myelolipoma. Exceedingly rare cases of adrenocortical carcinoma and metastatic carcinoma have been reported to contain macroscopic fat. A retroperitoneal liposarcoma may mimic a myelolipoma, although liposarcoma typically presents as a large mass that may displace, rather than arise from, the adrenal.
An adrenal myelolipoma should not be confused with a renal angiomyolipoma (AML). These two entities are unrelated, although they do have similar names, are located in adjacent organs, and are both diagnosed by the presence of macroscopic fat.
Adrenal cyst
Adrenal cysts are uncommon but have imaging characteristics typical of cysts elsewhere (thin, smooth, nonenhancing wall, and water-attenuation internal contents).
Endothelial adrenal cysts are the most common (45%) type and may be lymphatic or angiomatous in origin.
Pseudocysts are rare, comprising only 9% of adrenal cysts.
Occasionally an adrenal cyst may have a complex appearance that may be difficult to differentiate from a cystic/necrotic neoplasm. In such a case, percutaneous aspiration or surgical resection may be considered.
Small, asymptomatic, simple cysts can be ignored. A cyst may rarely grow so large as to cause symptoms, such as dull pain or compression of the stomach/duodenum, in which case surgery may be indicated.
Very rarely, hydatid disease may affect the adrenal glands, typically producing a complex lesion with an internal membrane.
Pheocromocytoma: Potentially malignant
Pheochromocytoma is a neoplasm of chromaffin cells, usually arising from the adrenal medulla. Pheochromocytoma may cause hypertension and episodic headaches/diaphoresis.
The “rule of 10’s” is a general rule characterizing the features of pheochromocytoms: 10% are extra-adrenal. 10% are bilateral. 10% are malignant. 10% are familial or syndromic.
Pheochromocytoma is associated with several syndromes: Multiple endocrine neoplasia (MEN) 2A and 2B: Typically bilateral intra-adrenal pheochromocytomas. Von Hippel-Lindau. Neurofibromatosis type 1. Carney’s triad (gastric leiomyosarcoma, pulmonary chondroma, and extra-adrenal pheochromocytoma).
An extra-adrenal pheochromocytoma is a paraganglioma. The most common intra-abdominal location of a paranglioma is the organ of Zuckerkandl, located at the aortic bifurcation. A rare intra-abdominal location of a paraganglioma is the bladder, producing the distinctive clinical presentation of post-micturition syncompe (syncope after urination).
Paragangliomas occur in the head and neck in characteristic locations. Paragangliomas of the head and neck are generally called glomus tumors and may be associated with the tympanic membrane (glomus tympanicum), the jugular foramen (glomus jugulare), the carotid body (called a carotid body tumor), or the vagus nerve (glomus vagale).
Nuclear medicine studies can be used in the workup of pheochromocytoma. Of note, I-123 MIBG is used for metastatic workup of adrenal pheochromocytoma and Indium-111 pentetreotide (an analog of octreotide) is used as tracer for localization of a paraganglioma.
In theory, pheochromocytoma should be diagnosed by urine/plasma metanephrines before imaging is performed, with imaging used for localization and staging. In clinical practice, CT is often employed based on suspicious symptoms (such as episodic hypertension or other symptoms of catecholamine excess).
The classic MRI appearance of pheochromocytoma is a hyperintense mass on T2-weighted images. When large, pheochromocytoma may appear heterogenous on MRI and CT.
Adrenal cortical carcinoma
Adrenal cortical carcinoma is a very rare malignancy, with a prevalence of approximately 1/1,000,000. Approximately 66% are functional, producing a disordered array of hormones that may manifest as Cushing syndrome, hyperaldosteronism, and virilization
Adrenal cortical carcinoma usually presents on imaging as a large, heterogenous mass. Central necrosis and hemorrhage are typical.
Metastasis
Autopsy studies show adrenal metastases are present in > 25% of patients with a known primary. Lung cancer and melanoma are the most common adrenal metastases.
Lymphoma
Primary adrenal lymphoma is rare.
Adrenal hyperplasia
Adrenal hyperplasia is caused by prolonged stress response or ectopic ACTH secretion.
Adrenal hemorrhage
Adrenal hemorrhage can be spontaneous or due to anticoagulation. When secondary to anticoagulation, the hemorrhage typically occurs within the first few weeks of beginning anticoagulation. Hemorrhage involves the right adrenal gland more commonly than the left.
Hemorrhage may appear mass-like and is often of heterogenous attenuation on CT. The most important clue is a new adrenal mass within a short time interval if priors are available.
Hemorrhage does not enhance and decreases in size on follow-up studies.
Adrenal calcification
Adrenal calcification rarely causes adrenal hypofunction. Adrenal calcification can be due to Wegener granulomatosis, tuberculosis, histoplasmosis, or old hemorrhage.
Renal mass protocol multiphase CT
A renal mass protocol CT consists of at least three phases of data acquisition, with each phase providing important information to aid in the diagnosis of a renal mass.
Unenhanced phase: necessary as a baseline to quantify enhancement.
Nephrogenic phase (100 second delay): The nephrogenic phase is the critical phase for evaluating for enhancement, comparing to the unenhanced images.
Pyelographic phase (15 minute delay; also called the excretory phase): The pyelographic phase is helpful for problem solving and to diagnose potential mimics of cystic renal masses. The pyelographic phase can distinguish between hydronephosis (will show dense opacification in the pyelographic phase) and renal sinus cysts (will not opacify).
Reflux nephropathy may cause a dilated calyx that can simulate a cystic renal mass on the nephrogenic phase. The pyelographic phase would show opacification of the dilated calyx. The pyelographic phase is also useful to demonstrate a calyceal diverticulum and to show the relationship of a renal mass to the collecting system for surgical planning.
Optionally, a vascular phase can be performed for presurgical planning.
Evaluating enhancement (CT and MRI) (Renal Mass)
The presence of enhancement is the most important characteristic to distinguish between a benign and malignant non-fat-containing renal mass ( a lesion containing intralesional fat is almost always a benign angiomyolipoma, even if it enhances).
On CT, enhancement is quantified as the absolute increase in Hounsfield units on post-contrast images, compared to pre-contrast: <10 HU: No enhancement; 10-19 HU: Equivocal enhancement; >/= 20 HU Enhancement.
Lesions are considered “too small to characterize” if the lesion diameter is smaller than twice the slice thickness. For instance, using 3 mm slices, a lesions less than 6 mm cannot be accurately characterized based on attenuation or enhancement.
Renal Mass biopsy
After full imaging workup is complete, there are several well-accepted indications for percutaneous renal mass biopsy:
- To distinguish renal cell carcinoma from metastasis in a patient with a known primary.
- To distinguish between renal infection and cystic neoplasm.
- To definitevely diagnose a hyperdense, homogenously enhancing mass (after MRI has been performed), which may represent a benign angiomyolipoma with minimal fat versus a renal cell carcinoma.
- To definitively diagnose a suspicious renal mass in patient with multiple comorbidities for whom nephrectomy would be high risk.
- To ensure correct tissue diagnosis prior to renal mass ablation.
Renal Cell Carcinoma
Renal cell carcinoma (RCC) is a relatively uncommon tumor that arises from the renal tubular cells. It represents 2-3% of all cancers. Risk factors for development of RCC include smoking, acquired cystic kidney disease, von Hippel-Lindau (VHL), and tuberous sclerosis.
Clear cell is the most common RCC subtype (~75%), with approximately 55% 5-year survival.
- Clear cell RCC tends to enhance more avidly than the less common subtypes
- Clear cell can be sporadic or associated with von Hippel-Lindau
Papillary RCC is a hypovascular subtype, with a 5-year survival of 80-90%
- Papillary RCC tends to enhance only mildly due to its hypovascularity
- A renal “adenoma” is frequently seen on autopsy specimens and is a papillary carcinoma = 5 mm.
Chromophobe is the subtype with the best prognosis, featuring a 90% 5-year survival.
Collecting duct carcinoma is rare and has a poor prognosis.
Medullary carcinoma is also rare, but is known to affect mostly young adult males with sickle cell trait. Medullary carcinoma is an extremely aggressive neoplasm, with a mean survival of 15 months, not helped by chemotherapy.
Staging of renal cell carcinoma is based on the Robson system, which characterizes fascial extension and vascular/lymph node involvement. Stages I-III are usually resectable, although the surgical approach may need to be altered for venous invasion (stages IIIA and IIIC)
- Stage I: Tumor confined to within the renal capsule.
- Stage II: Tumor extends out of the renal capsule but remains confined within Gerota’s fascia.
- Stage III: Vascular and/or lymph node involvement. IIIA: Renal vein involvement or IVC involvement. IIIB: lymph node involvement. IIIC: Venous and lymph node involvement.
- Stage IVA: Tumor growth through Gerota’s fascia; Stage IVB: Distant metastasis.
Angiomyolipoma
Angiomyolipoma (AML) is the most common benign renal neoplasm, composed of fat, smooth muscle, and disorganized blood vessels. The majority are sporadic, but 40% are associated with tuberous sclerosis (where AMLs are bilateral, with multiple renal cysts).
AML has a risk of hemorrhage when large (>/= 4 cm), thought to be due to aneurysmal change of the vascular elements. Small, asymptomatic AMLs are not typically followed or resected.
An early pathognomonic imaging finding is the presence of macroscopic fat in a non-calcified renal lesion. The non fat-containing portion enhances avidly and homogenously. Calcification is almost never present.
On MRI, the fat component will follow retroperitoneal fat on all sequences and will saturate out on fat-saturated sequences. Intracytoplasmic lipid is not a feature of AML, so there should be no significant drop-out on dual-phase MRI.
Approximately 4% of AMLs will not contain visible macroscopic fat and will appear as a hyperdense enhancing mass. MRI is the next step, with the T2-weighted images the most useful to distinguish from renal cell carcinoma in some cases.
- A T2 hyperintense mass suggests RCC (clear cell subtype) and the patient can proceed to surgery.
- A T2 hypointense mass is nonspecific and can represent either RCC (papillary type) or AML with minimal fat. Although an AML typically would enhance more avidly than a papillary RCC, biopsy is warranted for defnitive diagnosis.
Oncocytoma
Oncocytoma is the most commonly resected benign renal mass and has overlapping imaging findings with renal cell carcinoma.
Imaging features can suggest oncocytoma, but imaging features are not specific and cannot be reliably differentiated from RCC. The imaging featrues suggestive of oncocytoma are homogenous enhancement and a central scar.
Complicating the pathologic diagnosis, oncocytic cells can sometimes be found in the rare chromophobe RCC subtype. The pathologist can usually distinguish oncocytoma from the more common clear cell and papillary renal cell carcinoma subtypes.
Renal Lymphoma
Primary renal lymphoma is rare, as the kidneys do not contain native lymphoid tissue. However, the kidneys may become involved from hematogenously disseminated disease or spread from the retroperitoneum.
Renal invovlement of lymphoma has several patterns of disease:
- Multiple lymphomatous masses (most common pattern; seen in 50% of cases of renal lymphoma).
- Solitary renal mass.
- Diffuse lymphomatous infiltration, causing nephromegaly.
- Direct extension of retroperitoneal disease.
Non-neoplastic solid renal mass
When evaluating a potential renal mass, it’s important to always consider that an apparent solid renal mass may represent a non-neoplastic lesion.
Infection, especially focal pyelonephritis, can masquerade as a solid renal mass. Renal abscess may be difficult to differentiate on imaging from a cystic renal cell carcinoma.
Renal arteriovenous malformation (AVM) will avidly enchance and can mimic a hypervascular renal mass. One clue to the presence of an AVM would be asymmetric enhancement of the renal vein on the affected side, due to early shunting of venous blood.
Renal Pseudotumors
Renal pseudotumors are normal variations of renal morphology that may mimic a renal mass.
Hypertrophied column of Bertin: The columns (septa) of Bertin are normal structures that anchor the renal cortex to the hilum and create the separations between the renal pyramids. When hypertrophied, the columns of Bertin may mimic a renal mass.
Persistant fetal lobation/lobulation: In normal fetal development, the fetal kidneys are divided into discrete lobes. Occasionally these lobulations persist in adulthood, producing an indentation of the renal cortex. This indentation can cause an adjacent focal bulge that simulates a renal mass. This pseudomass can usually be distinguished from a true mass by the present of septa of Bertin on either side.
von Hippel-Lindau (VHL with renal masses)
von Hippel-Lindau (VHL) is an autosomal dominant multiorgan syndrome caused by a mutation in the VHL tumor suppressor gene on chromosome 3, which leads to cysts and neoplasms in multiple organs.
The primary manifestation of VHL in the genitourinary system is bilateral or multifocal renal cell carcinomas, most commonly the clear-cell subtype.
Other genitourinary manifestations of VHL include multifocal pheochromoctyoma and renal cysts.
Central nervous system manifestations of VHL include hemangioblastoma of the brainstem, cerebellum, or spinal cord.
Pancreatic and hepatic manifestations include malignant neuroendocrine pancreatic tumor, pancreatic tumor, pancreatic serous cystadenoma ( a benign neoplasm), and pancreatic/hepatic cysts.
Birt-Hogg-Dube
Birt-Hogg-Dube is an autosomal dominant syndrome of dermatologic lesions, cystic lung disease, and multiple renal oncocytomas and renal cell carcinomas.
Tuberous sclerosis (TS)
Tuberous sclerosis is an autosomal dominant neurocutaneous disease caused by a tumor suppressor gene mutation. It manifests clinically with seizures, developmental delay, and (mostly) benign tumors in multiple organ systems.
The most common renal manifestations of tuberous sclerosis is multiple bilateral renal angiomyolipomas (AML). Approximately 50% of patients with TS will have at least one AML.
Renal cyst can be seen in ~25%.
The relative risk of renal cell carcinoma is increased in patients with TS, and occurs in approximately 2-3% of patients. Diagnosis of renal cell carcinoma is complicated by the abnormal kidneys that may have multiple cysts and/or AMLs.
The the heart, the most common neoplasm is a rhabdomyoma. A cardiac rhabdomyoma may be present during fetal life and can be detected by fetal ultrasound.
In the lung, a process of smooth muscle proliferation identical to lymphangioleiomyomatosis can occur, causing cystic replacement of lung parenchyma. It has been suggested that the abnormal smooth muscle in te lung in patients with TS represents genetically identical metastatic smooth muscle from a renal angiomyolipoma.
Approach to a cystic renal mass
- A cystic renal mass may be neoplastic or infectious; the most comon entities to cause a cystic renal mass are renal cell carcinoma and renal abscess
Neoplastic differential of a cystic renal mass
- Cystic renal cell carcinoma. Although renal cell carcinoma most commonly presents as a solid renal mass, it can also manifest as a cystic renal mass.
- Multilocular cystic nephroma is a benign cystic neoplasm with enhancing septa that occurs in a bimodal age distribution in baby boys and middle-aged women. A characteristic but nonspecific feature is the propensity to herniate into the renal pelvis, causing hydronephosis. (In adults, multilocular cystic nephroma can be indistinguishable from cystic renal cell carcinoma. In children, multilocular cystic nephroma can be indistinguishable from cystic Wilms tumor.)
- Mixed epithelial and stromal tumor (MEST) is a benign neoplasm composed of epithelial and mesenchymal elements, typically found in middle-aged women. MEST may appear as either a solid or cystic mass.
Non-neoplastic differential of a cystic renal mass
- Renal abscess is a contained purulent collection within the kidney.
- Hemorrhagic renal cyst, which will not have any enhancing component.
Role of MRI in evaluation of a complex cystic renal mass
- MRI has a limited role in the evaluation of a cystic renal mass. The key advantage of MRI is more accurate enhancement characterization, as MRI does not suffer from the CT phenomenon of pseudoenhancement due to beam hardening from adjacent, densely enhancing renal parenchyma. (The increased accuracy of MRI to characterize enhancement is most useful to distinguish a Bosniak IIF from a Bosniak III lesion. Thickening of a septation or cyst wall that shows measureable enhancement defines a Bosniak III lesion. The Bosniak classification is discussed on the following page.)
- MRI is more sensitive for detecting septations compared to CT.
- Calcifications are more difficult to detect with MRI.
Simple renal cyst
Simple renal cysts are extremely common, found in approximately 50% of patients over age 50. A simple renal cyst is an incidental lesion that requires no follow-up, even when large.
On CT a simple cyst must attenuate close to 0 Hounsfield units, not contain any enhancing components, and have a thin imperceptible wall.
On MRI, a simple cyst must be hypointense on T1-weighted images, hyperintense on T2-weighted images, and not contain any enhancing component.
Renal sinus cyst
Cysts in the renal sinus may be classified as parapelvic and peripelvic cysts. A parapelvic cyst is a renal cortical cyst that herniates into the renal sinus. These cysts are usually large but solitary. Peripelvic cysts, in contrast, are lymphatic in origin and usually small and multiple.
Hyperdense cyst
A homogenous renal cyst with an attenuation of >70 Hounsfield units on noncontrast imaging represents a benign hyperdense cyst, likely secondary to prior hemorrhage.
A hyperdense cyst cannot be diagnosed if only post-contrast imaging is available as there is no way to distinguish a hyperdense cyst from an enhancing renal mass.
Bosniak classification of cystic renal masses
The Bosniak classification risk-stratifies cystic renal masses, with increasing risk for cystic renal cell carcinoma with increasing Bosniak category. Classification is based on morphology, not size (except for hyperdense cysts in categories II and IIF).
Category I and II: No risk of malignancy. No follow-up necessary.
Category IIF: Small risk of malignancy. Imaging follow-up is needed.
Category III and IV: Surgical lesions, concerning for cystic renal cel carcinoma.
Bosniak Category I
Water-attenuation cyst, with a hairline wall and no areas of enhancement. Practically, this classification is never used as such a lesio is simply called a simple renal cyst.
Always benign. No folow up needed.
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Bosniak Category II
Water-attenuation cyst containing a few (3 or fewer) hairline epta. May contain fine septal calcificatio. No enhancement.
Also includes small (< 3 cm) hyperattenuating cysts without enhancement.
Essentially always benign. No follow-up needed.
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Bosniak Category IIF
Multiple septa, with minimal smooth thickening (3 mm or less). May have thick and nodular mural calcification.
Walls may slightly enhance.
Also includes large (> 3 cm) hyperattenuating cysts without enhancement.
Usually benign. Radiographic follow-up is recommended, where morphologic change or new enhacement would be concerning for malignancy.
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Bosniak Category III
Thickened, irregular walls or septa, with measurable enhancement.
Concern for malignancy, but may be benign (e.g., infection, multilocular cystic nephroma). Without comorbidities, treatment is surgical.
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Bosniak Category IV
Distinguishing features is enhancing nodular component separate from wall or septa.
Clearly malignant. Surgical lesion unless significant comorbidities.
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