The document provides a comprehensive overview of cystic renal masses, detailing classifications such as the Bosniak classification and various types of renal cysts, including simple, complex, and inherited conditions. It discusses the role of different radiological modalities in evaluating these masses, highlighting ultrasound, CT, MRI, and the importance of identifying features that indicate malignancy. Additionally, it addresses the clinical implications and management of cystic renal masses, emphasizing the need for careful assessment to avoid misdiagnosis.

1. CYSTIC RENAL MASSES
PRESENTOR : DR NAVNI GARG

2. OVERVIEW
OLD CLASSIFICATION OF CYSTIC RENAL MASSES
BOSNIAK CLASSIFICATION
ROLE OFVARIOUS RADIOLOGICAL MODALITIES IN
EVALUATING CYSTIC RENAL MASSES
VARIOUS CYSTIC RENAL MASSES

3. CLASSIFICATION OF CYSTIC RENAL
MASSES
ELKIN & BERNSTEIN, 1969
RENAL DYSPLASIA
1. Multicystic kidney
2. Focal and segmental cystic dysplasia
3. Multiple cysts associated with lower urinary tract obstruction
POLYCYSTIC DISEASE
1. Childhood polycystic disease – AR
2. Adult polycystic disease –AD
CORTICAL CYSTS
1. Simple cyst
2. Multilocular cystic nephroma
3. Syndromes associated with cysts
4. Haemodialysis associated cysts (acquired)

4. MEDULLARY CYSTS
1. Calyceal cyst (diverticulum)
2. Pyelogenic cyst
3. Medullary sponge kidney
4. Papillary necrosis
5. Juvenile nephronophthisis (medullary cystic disease)
MISCELLANEOUS INTRARENAL CYSTS
1. Inflammatory
(a) Tuberculosis
(b) Calculus disease
(c) Hydatid
(d) Obliterative pyelonephritis
2. Neoplastic
cystic degeneration of parenchymal carcinoma
malignant changes in wall of simple cysts
cystadenoma
3. Traumatic – intrarenal haematoma
EXTRAPARENCHYMAL RENAL CYSTS
1. Parapelvic cyst
2. Peripelvic cyst

5. OTHER CLASSIFICATIONS

6. BOSNIAK CLASSIFICATION, 1986
DR MORTON A BOSNIAK

7. 1986 : BOSNIAK CLASSIFICATION , 4 CATEGORIES
1993 : MODIFIED BOSNIAK CLASSIFICATION ,ADDED
ADDITIONAL CATEGORY II F

8. CATEGORY I
 Benign lesions
 Thin wall
 Well defined interface with parenchyma
 No septations
 No calcification
 Density : 0 – 20 HU
 No enhancement
 Example – Simple renal cyst

9. CATEGORY II

 Cysts complicated by prior infection or haemorrhage
 Benign cystic lesion with hairline thin septa
 Fine calcification in walls/ septa
 Atleast one fourth of the lesion’s circumference should extend outside the
kidney so that the smoothness of the wall can be evaluated
 Minimal perceived post contrast enhancement
 Non enhancing high attenuation (40-100 HU) lesion < 3 cm in diameter

10. THIN SEPTA HEMORRAGIC CYST

11. CATEGORY II F
 F = Follow up
 More complex cyst
 Increase in number of septa
and calcifications
 Non enhancing high
attenuation lesions > 3 cm
 May advance to category III
with time and require 6
month follow up

12. CATEGORY III
 Indeterminate cystic masses
 Thick, irregular calcification in walls or septa
 Irregular borders
 Thickened or enhancing septa
 Uniform wall thickening or that contain small non enhancing nodules
 Examples –
multilocular cystic nephroma
lymphangioma
hydatid cyst
cystic renal cell carcinoma

14. CATEGORY IV
 Malignant cystic masses
 Shaggy thickened walls
 Thick septations
 Coarse calcifications
 Density > 20 HU
 Enhancing
 Example – Renal cell carcinoma

16. S
I II IIF III IV
DENSITY WATER Water
density or
40-100 HU
(<3 CM
SIZE)
40-100 HU
(>3CM)
WALL HAIRLINE
THIN
THIN MAY BE
THICKENED
THICKENED
SEPTA _ FEW
HAIRLINE
THIN
MULTIPLE
HAIRLINE
THIN,MAY BE
THICKENED
THICKENED
CALCIFICATION _ THIN
(<1MM) IN
WALL/
SEPTA
CAN BE
THICK/
NODULAR
NODULAR
THICK
SOLID
COMPONENT
_ _ _ +/- +
ENHANCEMENT _ _ _ WALL +
SEPTA+
SOLID -
ENHANCING
SOFT TISSUE
COMPONENT
RISK OF 1.7 18.5 > 18.5 33 92.5

18. WORKING INTERPRETATION OF BOSNIAK
CLASSIFICATION
CATEGORY I
We know it’s a cyst
CATEGORY II
We are still pretty certain it’s a cyst
CATEGORY III
We don’t know what it is
CATEGORY IV
Its probably a tumor

20. All the parameters should be assessed before classifying a lesion !

22. HOW USEFUL IS BOSNIAK
CLASSIFICATION?
It accurately identifies Category I & Category IV lesions
There are inter observer variations in Category II & Category III
lesions
Cannot efficiently characterize Category III lesions

23. INTERPRETATION PITFALLS
A small lesion with the same number and type of septa as a
large lesion will appear more complex.
Enhancement of hyperdense or heavily calcified lesions is
difficult to assess, especially when the lesion is small
Pseudoenhancement occurs when a cyst (generally < 2 cm)
is surrounded by enhancing parenchyma during peak
enhancement and artifactually appears to enhance. It should
be suspected when a lesion is homogeneous and measures
less than 10 HU on an unenhanced scan.
Rarely lymphoma, myomatous hamartoma , RCC and
metastasis measure greater than 20 HU on unenhanced scans.

24. ROLE OFVARIOUS RADIOLOGICAL
MODALITIES IN CYSTIC RENAL MASSES

25. MODALITIES
Ultrasound
Color Doppler
Computed tomography
Magnetic resonance imaging
USG/CT guided cyst aspiration
Angiography
Tc-99m DMSA Scintigraphy

26. ULTRASOUND
Differentiates between solid and cystic lesions
Features of cyst are
(a)Anechoic
(b) Posterior acoustic enhancement
(c) Sharply marginated smooth walls
Cyst septations yield strong back
echoes and may create reverberation
artifacts within the cyst.
Calcification within the cyst may cause
shadowing.

27. COLOR DOPPLER
To assess the vascularity
Vascularity within a nodule or septum greatly increases the
likelihood of malignancy.

28. TISSUE HARMONIC IMAGING
Hemorragic or proteinaceous cysts may contain low level
echoes or even layers of echoes.
THI helps in confirming this by eliminating dirty echoes
within an otherwise pristine cyst.
USG CAN BE EMPLOYEDTO DIRECT PERCUTANEOUS
THERAPIES SUCH AS RFA AND CRYOTHERAPY OF
COMPLEX RENAL LESIONS.

29. CONTRAST ENHANCED USG

30. CONTRAST ENHANCED USG MAY BE
HELPFUL IN PATIENTSWHO REQUIRE
FOLLOW UPTO REDUCETHE RADIATION
EXPOSURE
CEUSG IS APPROPRIATE IN THE BOSNIAK CLASSIFICATION OF
RENAL CYSTS

31. PITFALLS OF USG
Can miss carcinoma within a cluster of cysts
Vascular malformations may mimic cysts
Artifactual echoes
Complex cyst require further evaluation

32. COMPUTED TOMOGRAPHY
TECHNIQUE
Pre and post contrast images
2.5 to 5 mm thick slides
Images acquired :
Unenhanced CT
Corticomedullary phase ( 20-30 seconds)
Nephrographic phase ( 80-100 seconds)
Delayed ( 10 minutes )

33. CHANGE IN ATTENUATION INTERPRETATION
< 10 HU TYPICAL OF BENIGN CYST
VERY RARELY RENAL CYSTIC TUMOR
10-15 HU SUSPICIOUS FOR MALIGNANCY
COULD BE DUE TO VOLUME AVERAGING,
IMPERFECT PLACEMENT OF REGION OF
INTEREST, MOTION ARTIFACT
>15 HU PATHOLOGICAL PROCESS : MALIGNANCY,
CYSTIC ANGIOMYOLIPOMA , ONCOCYTOMA ,
INFECTIONS

34. ROLE OF DUAL ENERGY CT SCAN
DECT has ability to identify presence of iodine in body
tissues
We can generate virtual noncontrast images to reproduce the
baseline unenhanced attenuation, this allows reduction in
radiation doses.
It is also possible to produce an “iodine overlay,” in which the
presence of iodine in the tissues is indicated by a
superimposed color map
In this we do not rely on increase in attenuation to measure
enhancement instead,we directly visualise the presence of
iodine in lesion.

35. Since renal cysts do not have blood flow,an iodine-overlay
image should show a cyst as devoid of iodine signal
This method may prove beneficial beyond the current
practice of determining enhancement in a renal mass because
it has potential to reduce the effect of renal cyst
pseudoenhancement.

36. EVALUATION OF RENAL CYST
True unenhanced
Contrast enhanced
Virtual unenhanced
Iodine overlay

37. MAGNETIC RESONANCE IMAGING
TECHNIQUE
T1W Gradient echo : high signal protein ,hemorrage , fat
T2W HASTE : septa or nodules within the cystic fluid
POST CONTRASTT1W Serial images at 5,10,20 minutes

38. MAGNETIC RESONANCE IMAGING
ADVANTAGES :Demonstrates
 additional septa
 wall/septal thickening
Enhancement
Superior contrast resolution
Enhancement within a calcified cystic lesion : calcification is usually less
apparent on MRI thus making enhancement more apparent.
Substraction imaging : hemorragic cysts appear hyperintense on bothT1 and
T2 and don’t enhance after contrast administration. Substraction imaging can
help in identifying presence of enhancement in these high signal lesions.
DISADVANTAGES
Poor in demonstrating calcifications

40. RENAL CYST PUNCTURE AND ASPIRATION
Ultrasound or CT guided
Of doubtful utility
INDICATIONS
Infected cyst – diagnostic or therapeutic
Indeterminate cyst on USG/CT
Decompression
DISADVANTAGES
Though if positive confirms malignancy but
a negative aspirate doesn’t rule out
malignancy
Multiloculated cyst
Risk of needle track seeding

41. NUCLEAR MEDICINE
Tc 99m scintigram
Cyst and solid tumor appear as cold defect

42. CYSTIC RENAL MASSES

43. SIMPLE RENAL CYSTS
MC renal masses
ETIOLOGY
Probably secondary to
tubular obstruction
IVU
Radiolucent mass
Pencil thin wall
Claw or beak sign
USG
Anechoic with posterior
acoustic enhancement

44. CT CRITERIA MRI CRITERIA
Sharp margination and
demarcation from
surrounding renal
parenchyma
Smooth thin wall
Homogenous water density
content (0-20 HU)
No contrast enhancement
Sharp margination and
demarcation from
surrounding renal
parenchyma
Smooth thin wall
Homogeneous contents
with signal characteristics
of water
No contrast enhancement

45. OCCASIONALLY A, SOLID RENALTUMORS MAY
OBSTRUCTTHETUBULES OF ADJACENT NORMAL
RENAL PARENCHYMA RESULTING INTUBULAR
DILATATION AND SECONDARY CYST FORMATION
( SENTINEL CYST ). THEREFOREWHENEVER A SIMPLE
CYST IS DETECTED,THE ADJACENT PARENCHYMA
SHOULD BE CAREFULLY EVALUATED FORTHE
PRESENCE OF AN ADJACENT SOLID MASS.

46. COMPLEX CYSTS
Anything which is not a simple cyst
RADIOLOGICAL FINDINGS
 Thick wall
 Irregularity at the base of the cyst
 Septations
 Calcifications
 High attenuation values
 Contrast enhancement

47. HEMORRHAGIC CYST
Cyst containing blood
Common in
 polycystic renal disease
 malignant cysts
 trauma
Presentation - acute or insidious
Most hemorrhagic cysts < 3 cm are benign
RADIOLOGICAL FINDINGS
1. Hyperdense cyst
2. Settling debris
3. MRI – most commonly hyperintense onT1 andT2 weighted
sequences.They may show fluid-iron levels because of dependant
settling of methemoglobin containing sediments.

48. POLYCYSTIC KIDNEYS
If you can count the number of cysts, they are simple
cysts ; if you can’t, it’s polycystic
CHILDHOOD POLYCYSTIC DISEASE
 AR
 Ectasia of renal collecting ducts
 Subtypes :
Perinatal
Neonatal
Infantile
Juvenile
 Associations –
 Oligohydramnios
 Potter’s syndrome
 Respiratory failure
 Periportal fibrosis (sequelae) causing PHTN

49. Tubular ectasia is confined mainly to the renal medulla with
only occasional macrocysts
Renal cortex is less severely affected
Severity of disease is inversely related to age of the patient
Hepatic and renal involvement are inversely proportional to
each other.

50. IVU : striated
nephrogram due to
accumulation of
contrast in dilated
tubules
USG: Diffusely
echogenic kidneys

51. NCCT – smooth, enlarged kidneys, low in attenuation due to
large fluid volume in dilated ducts
CECT – Striated nephrogram, hepatic fibrosis and features of
portal hypertension

52. ADULT POLYCYSTIC KIDNEYS
AD
Pathology : cysts of varying size gradually replace renal
parenchyma
C/F :
 Presents between 20 and 39 years
 Hypertension
 Renal insufficiency
 Hematuria
 Renal stones
 Complications of multiple cysts

53. Associated with cysts in liver > pancreas > brain> spleen >
ovaries > testes
Associated with cardiac valvular disorders , abdominal and
inguinal hernias, aneurysm of cerebral and coronary arteries
Colonic diverticula : 80%

54. SPIDERY COLLECTING
SYSTEM WITH STRETCHED
CALYCES
NUMEROUS SMOOTHLY
MARGINATED
RADIOLUCENCIES
THROUGHOUT THE CORTEX
AND MEDULLA (SWISS
CHEESE APPEARNCE).

55. ADULT POLYCYSTIC KIDNEYS
CT/ MRI : multiple renal cysts of varying size
There may be features of complex cyst

56. The risk of renal cancer in patients with
ADPKD who are not undergoing dialysis is
not increased.However patients undergoing
dialysis are at greater risk for development
of renal malignancy relative to general
population.

57. 3 MAIN CRITERIA : FAMILY HISTORY, AGE, TYPE/NUMBER OF CYSTS

62. D/D
 Multiple simple cysts (less diffuse, no family history)
 Von Hippel-Lindau disease (cerebellar hemangioblastoma,
retinal hemangiomas, occasionally pheochromocytomas)
 Acquired uremic cystic disease (kidneys small, no renal
function, transplant)
Infantile PCKD (usually microscopic cysts)

63. MULTICYSTIC DYSPLASTIC
KIDNEYS
MC cystic disease in infants
M > F
Females have higher chances of bilateral
disease
May be associated with contralateral
abnormalities like obstruction of the
ureteropelvic junction,renal agenesis,renal
hypoplasia,VUR
May be associated with cleft palate, ductal
plate malformation of the liver,cardiac
abnormalities

64. MECHANISM :
In utero failure of ureteric
bud to connect with the
nephrons in the metanephric
blastaema
PATHOLOGY :
Kidney – non functioning and
converted into a multicystic
dysplastic mass
Ureter – atretic
Renal artery – hypoplastic/
atretic

65. TYPES
Pelvoinfundibular atresia : no discernible renal pelvis is seen.
Kidney may be small/normal or enlarged. Contains multiple
non communicating cysts.No exretion of contrast by kidneys.
No perfusion on renal scintigraphy.
Hydronephrotic type : Dilatation of renal pelvis and calyces
with parenchymal cysts that donot communicate with the
collecting system

66. Newborn shows no normal renal parenchyma and the
right renal fossa filled with multiple simple appearing
cystic structures c/w MCDK. The cysts did NOT
communicate thereby excluding hydronephrosis

67. MECKEL GRUBER SYNDROME : occipital encephalocele,
polydactyly, cystic dysplastic kidneys

68. MULTILOCULAR CYSTIC NEPHROMA
Tumor of primitive renal tissue
originating from metanephric
blastaema
Pathology – cyst with septa that
contain renal tissue of variable
maturity
Bimodal age distribution.
 Under the age of 5 years, cystic
nephroma occurs most frequently in
males, whereas the adult group has a
female predominance (91%) and
mean age of 55 years

69. Septate cystic mass with
multiple loculations,
hairlike septa,peripheral
and curvilinear
calcifications,irregular
borders, and minimal
contrast enhancement.
Extension into the
central sinus and into the
renal pelvis can also be
found

70. IVU – Multiple non enhancing areas bulging into renal pelvis
USG/CT/MRI –
Well defined multiloculated mass with an apparent capsule
Little or no enhancement
Calcification is usually not a feature

73. D/D : OTHER MULTILOCULAR CYSTIC LESIONS
DIFFERENTIALS
Septated renal cyst
Inflammatory – renal abscess
focal xanthogranulomatous pyelonephritis
hydatid disease
Segmental multicystic kidneys
Tumors – cystic renal cell carcinoma
Wilm’s tumor

74. UNILATERAL/LOCALISED RENAL CYSTIC
DISEASE
One kidney is replaced by renal cysts and other kidney is
normal.
Represents dilated ducts and tubules
No liver cysts, No renal failure, normal excretion of contrast

75.  Cysts are seen to be
separated by enhancing
bands of normal renal
parenchyma.
Individual smaller cysts are
often present in the renal
parenchyma adjacent to
main loculated mass.

77. LOCALIZED CYSTIC
DISEASE CYSTIC NEOPLASM
Unencapsulated : no
capsule between cluster of
cysts and renal parenchyma
Several small parenchymal
cysts not contained within
the main cluster of cysts
No mural irregularities
Encapsulated
Mural irregularities may be
present

78. Localized cystic disease
of kidney with multiple
simple cysts separated by
attenuated enhancing
renal tissue (arrow).
Well-encapsulated mass in
middle portion of left
kidney with multiple
enhancing septae (solid
arrow). Mass of cystic
locules is encompassed in
single large encapsulated
mass (open arrow).
Enhancing tissue seen in
lesion represents tumor
tissue.

79. ACQUIRED CYSTIC DISEASE OF KIDNEY
INCIDENCE :
Upto 80% of patients on chronic hemodialysis or peritoneal
dialysis develop renal cysts
Usually after 5-10 years of HD
8-16% develop neoplasm

80. CT is modality of choice
 Multiple small or
moderate size cysts
Affected kidneys are
small
Atleast 3 cysts in each
kidney who has CRF not
due to hereditary renal
cystic disease
Cysts both in cortex and
medulla

81. There is increased incidence of RCC in patients undergoing
dialysis.
Small RCC is more common than large masses
More in males as compared to females

82. CYSTS SECONDARY TO NON MALIGNANT RENAL
PATHOLOGY
OBLITERATIVE PYELONEPHRITIS
Constriction of major or minor calyx produces
cyst like structures
 Similar appearance seen in tuberculosis

83. HYDATID CYST
ETIOLOGY :
Echinococcus granulosis
E multilocularis
Three types :
Closed cyst
Pseudoclosed cyst
Open cyst

84. CLOSED CYST
Have an intact cyst lining and
adventitia and do not
communicate with the renal
collecting system
Rounded mass (with or without
calcification) causing elongation
and splaying of the infundibula
and calyces and, occasionally,
obliteration of one or more
calyces from pressure.

85. PSEUDOCLOSED CYST
 Exposed cyst with absence
of pericyst; the cyst is in
close contact with urine.
Contrast media can
interpose itself in crescent-
like fashion in the space
between the laminated
ectocyst and the pericyst,
producing the "goblet" or
"wine-glass" sign
(Surraco's sign)

86. OPEN TYPE
 Resulting from rupture
and discharge of daughter
cysts
Communicating with the
renal collecting system,
contrast medium from
either an intravenous or
retrograde urogram can
spread around the cyst or
fill it

87. In this open type of hydatid cyst, an intermittent or permanent
communication exists between the hydatid and the
pyelocalyceal system so that contrast medium flows directly
into the cyst. Usually there is a typical mottled appearance of
contrast, insinuating itself among a mass of daughter cysts
but, occasionally, if the cyst contents are tightly packed, the
contrast will be compressed between the contents and cyst
wall to produce an extensive false crescent sign.

89. MILK OF CALCIUM RENAL CYST
Not a true cyst
Communicating or closed off calyceal diverticulum
Lined with trasitional epithelium
Contains particulate colloidal suspension of various calcium salts
Plain X ray
Supine position – full moon sign
Horizontal beam – half moon
US/CT/MRI
Half moon shift

90. Echogenic debris layering at the dependent part of a small cyst. There
is change in the fluid-debris interphase with change in position. There
is minimal acoustic shadowing due to a relatively large amount of
calcium debris.

91. PSEUDOCYST
URINOMA (Uriniferous Perirenal Pseudocyst)
Any obstructive process may cause extravasation into perirenal spaces
Wall is formed by the fibrous capsule
May cause secondary ureteral obstrction

92. CALYCEAL CYST (DIVERTICULUM)
An intraparenchymal cavity lined by transitional
epithelium which communicates with a minor
calyx, either centrally or at fornix
Do not receive any drainage from nephrons
IVU – well defined opaque rounded area adjacent
but peripheral to a minor calyx
D/D – small cyst & hydrocalyx
RISK – calculus, infection & hematuria

94. PYEL0GENIC CYST
Similar to calyceal diverticulum but connect to pelvis proper
D/D - Hydropelvis

95. RENAL SINUS CYSTS/
EXTRAPARENCHYMAL
PARAPELVIC CYST – simple renal cyst originating from the
renal parenchyma, which are primarily expanding within the renal
sinus
PERIPELVIC CYST – cysts originating from the sinus
structures. Most likely lymphatic in origin

96. PARAPELVIC CYST
Usually single or few
Resemble simple renal cortical cyst in morphology
May cause compression of the pelvicalyceal system resulting
in hydronephrosis

97. PERIPELVIC CYST
Usually bilateral
Lymphatic in origin
Multilocular or unilocular
Water attenuation cysts closely abutting pelvis and
infundibuli
Don’t communicate with renal collecting system

98. Differentiation from
hydronephrosis/dilated
renal pelvis is made on
CECT scan ( surrounding
halo of renal sinus fat) and
delayed images.

99. D/D
 Renal sinus lipomatosis (fat attenuation )
Lymphoma or invasive transitional cell carcinoma (soft tissue
attenuation)

100. CYSTS ASSOCIATED WITH
MALIGNANCY

101. 3 MAIN AREAS
ACQUIRED CYSTIC RENAL DISEASE
VHL
TUBEROUS SCLEROSIS

102. CYSTIC RENAL CELL CARCINOMA
About 10% of RCC mainfest as fluid filled cystic mass
FOUR PATTERNS
Intrinsic unilocular cystic growth
 Intrinsic multilocular cystic growth
 Origin in the epithelium of a simple cyst
Cystic necrotic tumor

103. Cystic RCC is seen on MRI and CT as a water-attenuation
mass with an enhancing thick wall or septa sometimes with
associated soft-tissue nodules
 Nodular and septal enhancement is the most sensitive
finding to discriminate cystic RCC from complex benign
lesions .

105. MULTILOCULAR CYSTIC RCC
20-76 years of age
Low grade tumor
Characterized by septate variably sized cysts separated from
the kidney by a fibrous capsule.The cyst fluid may be serous
or hemorrhagic and thus can be of water attenuation or
higher.
Asymmetric septal thickening may be seen
May show septal or wall calcification

106. Cystic clear cell carcinoma is distinguished from multilocular
cystic RCC by the presence of fewer loculations,thicker and
more nodular septa, and expansile
enhancing mural nodules.

107. MIXED EPITHELIAL AND STROMAL
TUMOR
Benign neoplasm
Characterized by a biphasic proliferation of epithelium and
stroma and admixed solid and cystic regions that have
variable cellularity and growth patterns.
Tumor nearly always occurs in women (≈ 7:33 male-to-
female ratio), especially in perimenopausal women (median
age, 52 years
Bosniak III or IV lesion with septa, curvilinear calcifications,
and a delayed enhancing solid component.Areas ofT2
hypointensity suggesting fibrotic component may be seen.

109. SYNDROMES ASSOCIATED WITH RENAL CYSTS
LAURENCE MOON BIEDL SYNDROME
 Obesity
 MR
 Retinitis pigmentosa
 Hypogonadism
TUBEROUS SCLEROSIS
 MR
 Renal AML
 Renal cysts
 Hamartomas
VON HIPPEL LINDAU DISEASE
 Cerebellar hemangioblastomas
 Retinal angiomas
 Pancreatic cysts
 Islet cell tumors
 Phaeochromocytoma
 Endolymphatic sac tumors
 Cystadenomas of epididymis
 Multifocal renal carcinomas and renal cysts

110. A CHECK LIST FOR CYSTS
 Age
 Chief symptom
 Size
 Shape
 Number
 Location
 Margins
 Contents
 Walls
 Septa
 Calcification
 Solid areas
 Vascularity
 Enhancement
 Relation to Pelvis, Renal artery and vein
 USG
 Hyper/Iso/Hypoechoic
Complex
Through transmission
 CT
Hyper/Iso/Hypodense
Complex
HU
 MRI
Hyper/Iso/Hypointense
Complex
Apperances onT1,T2,VIBE

111. APPROACH TO AN INCIDENTAL RENAL MASS

112. THANK YOU ALL