Urinary: Cystic Disease

Question 1

Bosniak 1 renal cyst

Answer 1

Less than 15 HU with no enhancement

Question 2

Bosniak 2 renal cyst

Answer 2

Think calcifications or septations

OR

Hyperdense and <3 cm

Question 3

Bosniak 2F renal cyst

Answer 3

Minimally thickened calcifications

OR

Hyperdense and >3 cm

Note: These have a low enough risk (<5%) that you want to follow them.

Question 4

Bosniak 3 renal cyst

Answer 4

Thick septations

OR

Mural nodule

Note: These have a 50% change of cancer.

Question 5

Bosniak 4 renal cyst

Answer 5

Any enhancement (>15 HU difference)

Note: These have a near 100% chance of being cancer.

Question 6

When can you be comfortable calling a benign hyperdense renal cyst

Answer 6

If HU > 70

Note: These are hemorrhagic or proteinaceous cysts 99.9% of the time.

Question 7

Clinical manifestations of autosomal dominant polycystic kidney disease

Answer 7

• Renal cysts
• Liver cysts (70%)
• Seminal vesicle cysts (60%)
• Berry aneurysms

Question 8

Which polycystic kidney disease is associated with congenital hepatic fibrosis?

Answer 8

Autosomal recessive (100%)

Question 9

Prognosis of autosomal dominant polycystic kidney disease

Answer 9

Dialysis by the 5th decade of life

Question 10

Answer 10

Autosomal dominant polycystic kidney disease

Note: Also cysts in the liver.

Question 11

Pediatric renal scan

Answer 11

Autosomal recessive polycystic kidney disease

Note: Enlarged, echogenic kidney with loss of corticomedullary differentiation.

Question 12

History of bipolar disorder

Answer 12

Lithium nephropathy

Note: Small kidneys with innumerable microcysts.

Question 13

History of end stage renal disease

Answer 13

Uremic cystic kidney disease

Note: Numerous macrocysts in a pt with ESRD. This is seen in 90% of pts after 5 years of dialysis.

Question 14

Does dialysis increase or decrease the risk of renal malignancy?

Answer 14

Increase (3-6x)

Question 15

Are pts with autosomal dominant polycystic kidney disease at an increased risk for renal malignancy?

Answer 15

Not due to their disease directly, but once they get on dialysis their risk increases due to the dialysis

Question 16

Inheritance pattern of Von Hippel Lindau

Answer 16

Autosomal dominant

Question 17

Renal manifestations of Von Hippel Lindau

Answer 17

• Renal cysts (50-75%)
• Clear cell RCC (25-50%)

Question 18

Pancreatic manifestations of Von Hippel Lindau

Answer 18

• Cysts
• Serous microcytic adenomas
• Neuroendocrine (islet cell) tumors

Question 19

Adrenal manifestations of Von Hippel Lindau

Answer 19

Pheochromocytoma (often multiple)

Question 20

CNS manifestations of Von Hippel Lindau

Answer 20

• Hemangioblastomas of the cerebellum, brain stem, and spinal cord
• Endolymphatic sac tumors

Question 21

Urogenital manifestations of Von Hippel Lindau

Answer 21

• Epididymal cysts
• Cystadenomas

Question 22

Inheritance pattern of tuberous sclerosis

Answer 22

Autosomal dominant

Question 23

Renal manifestation sof tuberous sclerosis

Answer 23

• Hamartomas
• Bilateral angiomyolipomas
• Renal cysts
• RCC (same risk, but younger onset)

Question 24

Pulmonary manifestations of tuberous sclerosis

Answer 24

• Hamartomas
• LAM
• Chylothorax

Question 25

Cardiac manifestations of tuberous sclerosis

Answer 25

- Hamartomas - Rhabdomyosarcoma (classically involving the cardiac septum)

Question 26

CNS manifestations of tuberous sclerosis

Answer 26

- Hamartomas - Giant cell astrocytoma - Cortical and subcortical tubers - Subependymal nodules

Question 27

Bourneville Disease

Answer 27

Another name for tuberous sclerosis

Question 28

Answer 28

Calyceal diverticulum Note: Excretory phase image showing excreted contrast layering in the diverticulum.

Question 29

What is the hyper dense material layering in this calyces diverticulum?

Answer 29

Milk of calcium debris Note: This is a noncontrast image.

Question 30

Differential for a T2 dark renal cyst

Answer 30

- Lipid-poor angiomyolipoma - Hemorrhagic cyst - Papillary RCC

Question 31

Multiple lipid-poor angiomyolipomas...

Answer 31

Think tuberous sclerosis Note: About 30% of AMLs are lipid-poor in TS.

Question 32

How can you differentiate multi cystic dysplastic kidney from severe hydronephrosis if you can't show that the cysts connect with the renal pelvis?

Answer 32

Renal scintigraphy with MAG3 (multi cystic dysplastic kidneys have no functioning renal tissue and will not take up any radiotracer)

Question 33

Answer 33

Peripelvic cysts Note: This can mimic hydronephrosis (often needs excretory imaging to differentiate).

Question 34

Answer 34

Parapelvic cysts

Question 35

Parapelvic vs peripelvic renal cysts

Answer 35

Parapelvic cysts originate from the parenchyma and bulge into the renal pelvis (more round) Peripelvic cysts originate from the renal sinus and bulge into the renal pelvis (more oblong)