Transcript SURGICAL PATHOLOGY

SURGICAL PATHOLOGY
RENAL DISEASES
ROBERTO D. PADUA JR., MD, DPSP
DEPARTMENT OF PATHOLOGY
FATIMA COLLEGE OF MEDICINE
Glomerular lesions associated with the nephrotic syndrome
Disease
Light Microscopy
Minimal change
glomerulopathy
Minimal or no mesangial prominence
Diffuse mesangial hypercellularity with nephrotic
syndrome
Mild mesangial hypercellularity
Focal and segmental
glomerulosclerosis
Focal and segmental mesangial sclerosis
Membranous
glomerulonephritis
Uniform capillary wall thickening, sometimes
with spiked dome pattern
Diabetic nephropathy
Nodular and diffuse mesangial sclerosis,
insudative lesions
Amyloidosis
Mesangial and vascular deposits of Congo redpositive material with green birefringence
Light chain deposition
disease
Mesangial widening and deposition of PAS
positive material
Fibrillary glomerulonephritis
Mesangial widening and ocassional
hypercellularity, capillary wall thickening
Glomerular lesions associated with the nephrotic syndrome
Disease
Light Microscopy
Fibrillary glomerulonephritis
Mesangial widening and occasional
hypercellularity,
Capillary wall thickening
Immunotactoid
glomerulopathy
Mesangial widening and occasional
hypercellularity,
Capillary wall thickening
Mesangial widening
Congenital nephrotic
syndrome
1.
Finnish type
2.
Diffuse Mesangial
sclerosis
Tubular ectasia, microcysts, glomerular
sclerosis
Diffuse mesangial sclerosis
WHO Classification of Lupus nephritis and clinicopathologic classification
Class
Pathology findings
Clinical renal
manifestations
1. Normal or
minimal
abnormality
Kidney is normal by light, electron,
and immunofluorescence
microscopy
Usually
asymptomatic
2. Pure mesangial
alterations
Mesangial expansion but mostly
patent capillaries
Mesangial immune deposits
Low-grade
proteinuria with or
without hematuria
Normal renal
function
3. Focal
proliferative GN
Focal and segmental proliferative
intra- and/or extracapillary
necrotizing and/or sclerosing lesions
in <50% of glomeruli
Predominantly mesangial and
subendothelial immune deposits
Nephritic urinary
sediment
Variable but usually
non-nephrotic
proteinuria
WHO classification of Lupus nephritis with clinicopathologic classification
Class
Pathology findings
Clinical renal
manifestations
4. Diffuse
proliferative GN
Predominantly global proliferative
lesions, necrosis, crescents in >50%
of glomeruli
Variable sclerosis, prominent
inflammatory interstitial infiltrate
Predominantly mesangial and
subendothelial immune deposits
Nephritic and
nephrotic
syndromes,
hypertension,
variable degree of
renal insufficiency
5. Membranous
GN
Diffuse thickening of capillary walls
subepithelial (and mesangial)
immune deposits
Nephrotic syndrome
or severe proteinuria
6. Advanced
sclerosing GN
Glomerular obsolescence and
Chronic renal failure
segemntal glomerulosclerosis, tubular
atrophy, and interstitial fibrosis
Few, if any, immune deposits
Dysplastic lesions of the renal artery
Diagnosis
Age
Sex
Freq
Lesion
Intimal fibroplasia
1-50
M=F
1-2%
Narrowing by intimal proliferation
without lipid
Medial fibroplasia
30-60
F>M
60-70%
“String of beads”, alterating
stenosis and mural thinning
Medial hyperplasia
30-60
F>M
5-15%
Smooth muscle hyperpalsia and
thickening
Perimedial fibroplasia
30-60
F>M
15-24%
Fibrosis of outer media,
occasionally aneurysms
Medial dissection
30-60
F>M
5-15%
Fibrosis of media with dissecting
aneurysms
Periarterial fibroplasia
15-50
F>M
1%
Perivascular fibrosis and
inflammation
Cystic diseases of the kidney

Multicystic renal dysplasia
 Anomalous
differentiation of the mesonephros
 Most common form of cystic disease in
children
 Most common cause of abdominal masses in
newborns
 Dysplasia is usually unilateral
Cystic diseases of the kidney
Multicystic renal dysplasia
Dysplastic kidney of an infant.
Cystic diseases of the kidney
Multicystic renal dysplasia
Section of kidney showing embryonic-like connective
tissue and tubules
Cystic diseases of the kidney

Autosomal dominant (adult) polycystic
kidney disease
 Hereditary
condition char by expanding cysts
that progressively destroy the renal
parenchyma of both kidneys  renal failure
 1 or 2 per 1000 live births
 10% of cases requires dialysis or renal
transplantation
 Transmitted as autosomal dominant with
complete penetrance
Cystic diseases of the kidney
Adult polycystic kidney diseases
 Mutation
in PKD1 (16p13.3) – 85 to 90%
 Mutation in PKD2 (4q13-23)
 PKD3 – seen in ADPKD not linked to PKD1 & 2
 Male=Females
 Symptomatic in 4th-5th decade of life with
gradual onset of renal failure
 Clinical manifestations – flank pain, flank
mass, hematuria, HPN, renal failure
 20% develop nephrolithiasis
Cystic diseases of the kidney
Adult polycystic kidney diseases
 Diagnosis
– UTZ, CT-scan
 Bilateral involvement of kidneys
 Markedly enlarged kidneys with bosselated
outer cortical surface
 Cysts develop in all segments of the renal
tubule and glomerular capsule
 Light microscopy – cysts are lined by
cuboidal, flattened epithelium, and
hyperplastic polypoid foci also seen
Cystic diseases of the kidney
Adult polycystic kidney diseases
External and cut surface of a nephrectomy specimen from a patient
with ADPKD.
Cystic diseases of the kidney

Autosomal recessive (infantile) polycystic
kidney disease
 Rare
disorder – 1 per 20,000 live births
 Genetic defect localized in the short arm of
chromosome 6
 Liver and both kidneys are affected
 Neonatal period – renal symptoms
 Later in life – hepatic disease
Cystic diseases of the kidney
Infantile polycystic kidney disease
 Present
with large abdominal masses at birth
 “Potter” phenotype – char facies due to
oligohydramios, joint deformities, pulmonary
hypoplasia
 Death is due to respiratory failure
 Beyond perinatal period – renal failure, HPN,
and portal HPN
 Estimated perinatal mortality is 30-50%
 5-year survival rate after first month of life is
80-95%
Cystic diseases of the kidney
Infantile polycystic kidney disease
 Kidneys
markedly enlarge bilaterally but retain
their reniform configuration
 Cysts tend to be linear and radiate from the
medulla to the outer cortex
 Microscopcally, cysts appear as dilated tubular
structures lined by cuboidal or flattened
epithelium, intervenning tissue may contain
uninvolved nephron
Cystic diseases of the kidney

Medullary sponge kidney
Char by dilated medullary and papillary collecting
ducts which give the medulla a sponge-like
appearance
 True incidence is unknown (1 per 5000 pop)
 Asymptomatic unless complicated by nephrolithiasis,
hematuria, or infections
 Symptoms start in the 4th-5th decades of life
 Male=Female
 25% of cases have associated hemihypertrophy of
the body

Cystic diseases of the kidney

Nephronophthisis-medullary cystic kidney
disease complex

2 major groups

Nephrolithiasis – autosomal recessive mode of inheritance


3 forms
 Juvenile (NPH1) = 13 years  ESRD
 Infantile (NPH2 = 1-3 years
 Adolescent (NPH3) = 19 years
MCKD – autosomal dominant trait

2 variants
 MCKD1 = 62 years
 MCKD2 = 32 years
Cystic diseases of the kidney
Nephronophthisis-MCKD complex
 Juvenile
 Most
NPH
common genetic cause of ESRD in children
 Both sexes are equally affected
 Clinical presentation = polydipsia, polyuria,
anuresis, dec. in urinary concentration, severe
anemia, growth retardation
 12% of cases assoc with retinitis pigmentosa
(Senior-Loken syndrome)
 Other assoc conditions = hepatic fibrosis, skeletal
malformations, defects in the CNS
 NPHP1 identified on chromosome 2q13
nephrocystin
Cystic diseases of the kidney
Nephronophthisis-MCKD complex
 MCKD
 Symptoms
occur in the 3rd and 4th decades of life
 Similar to NPH1 minus the growth retardation and
severe anemia + extrarenal disorders
 Associated with huperuricemia and gout
 MCKD1 = 1q21; MCKD2 = 16p13
Cystic diseases of the kidney
Nephronophthisis-MCKD complex
Kidneys
are normal or slightly reduced in size with
a granular surface
Renal involvement is always bilateral
Cut section – cortex and medulla both thinned
Cysts arise from the loop of Henle, DCT, and CD
Tubulointerstitial fibrosis with lymphocytic
inflammatory infiltrate, tubular atrophy and cysts
formation seen histologically
Cystic diseases of the kidney

Acquired renal cystic disease






7-22% of patients with renal failure who are not on dialysis
40% of patients on dialysis for 3 years
80-90% of patients on dialysis for 10 years
Theory – cysts results from obstruction of the renal tubules,
by local fibrosis, oxalate deposition, or epithelial hyperplasia
Usually asymptomatic but the cysts may bleed, rupture or
become infected
Most serious complication is development of renal
adenocarcinoma (50X in patients on dialysis)
Cystic diseases of the kidney

Simple cysts
 Most
common cystic abnormality seen in the
kidneys
 Incidence increases with age
 Usually asymptomatic and found incidentally on
autopsy
 May cause pain as a result of hemorrhage or
infection
 Occur more commonly in the renal cortex derived
from pre-existing tubules
 Usually unilocular less than 5cm in diameter
Pediatric tumors and tumor-like
conditions

Wilm’s tumor
 Also
known as nephroblastoma, embryoma,
carcinosarcoma, adenosarcoma,
adenomyosarcoma
 Primarily seen in infants – 50% occurring
before 3 y/o; 90% before the age of 6 years
 Both kidneys are equally affected
 Incidence of synchronous or metachronous
bilateral involvement is 5-10%
 Extrarenal sites have been reported
Pediatric tumors and tumor-like
conditions

Wilm’s tumor



Expression of WT1 gene
Conditions associated with definite increased risk :
WAGR syndrome, omphalocoele-macroglossia
(Beckwith-Wiedemann syndrome), hemihypertrophy,
Denys-Drash syndrome
Conditions associated with possible increased risk :
renal and genital malformations, cutaneous nevi and
angiomas, trisomy 18, Klippel-Trenaunay syndrome,
neurofibromatosis, Bloom syndrome, and cerebral
gigantism
Pediatric tumors and tumor-like
conditions

Wilm’s tumor


Clinical presentation – abdominal mass, HPN,
proteinuria
Diagnosis





IVP – shows intrarenal mass that displaces and distorts the
pelvis
UTZ
CT-scan
MRI
Potential tumor markers – inc hyaluronic acid, acquired Von
Willebrand’s factor, inactive renin, inc eryhtropoietin
Pediatric tumors and tumor-like
conditions

Wilm’s tumor
 Gross
 Solitary,
well-circumscribed, rounded, and soft
 Cut section is solid, pale gray or tan often exhibits
areas of cystic change, necrosis, and hemorrhage
 A lobular pattern results from fibrous septation
Wilm’s tumor - Gross
Tumors show a variegated appearance
Tumor is homogenous and
nodular
Tumor has extensive areas
of infarct-like necrosis
Wilm’s tumor

Microscopic = has 3 major components
 Undifferentiated
blastema – cellular, composed of
small round-to-oval primitive cells
 Mesenchymal (stromal) tissue – spindle cell
fibroblast-like configuration; exhibit differentiation
toward various cell types particularly smooth
muscle and skeletal muscle
 Epithelial tissue – characterized by the formation
of embryonic tubular (sometimes glomerular)
structures that closely recapitulate the appearance
of normal developing metanephric tubules (and
glomeruli)
Wilm’s tumor
 Histochemical
features
 Blastematous
and Immunohistochemical
elements – (+) for vimentin, keratin,
EMA
 Mesenchymal – (+) for myogenin and desmin,
NSE, S-100, glial fibrillary acidic protein
 Type I insulin-growth factor receptors –
responsible for increased proliferation and
inhibition of differentiation
 Electron
 Closely
microscopic features
resembles developing metanephros
Wilm’s tumor
 Spread
and metastasis
 Local
spread in perirenal soft tissues  adrenal
glands, bowel, liver, vertebrae, paraspinal region
 Renal vein invasion is common
 15% of cases involves regional LN
 Distant metastasis – lungs, liver, and peritoneum
 Therapy
 Stage
I and II – nephrectomy and 2 agent chemo
Wilm’s tumor

Prognosis
Overall cure rate for unilateral Wilm’s tumor is 8090%
 Age – less than 2y/o – good
 Stage – most important prognostic determinator;
increased rate of relapse: presence of inflammatory
pseudocapsule, invasion of the renal sinus, extensive
infiltration of the renal capsule, and tumor infiltration
of intrarenal vessels
 Size – bigger tumor – poor
 Anaplasia - poor

Wilm’s tumor

Prognosis
 Extensive
tubular differentiation – good
prognosis
 Skeletal muscle differentiation – good
prognosis
 Mucin production – poor prognosis
 P53 mutation – poor prognosis
Pediatric tumors and
tumor-like lesions

Mesoblastic nephroma



Also known as fetal, mesenchymal, or leiomyomatous
hamartoma
A congenital renal neoplasm that is usually discovered
before the patient reaches 6 months of age
Gross
Solid, yellowish gray to tan, with a whorledconfiguration
 Most are centered near the hilus of the kidney
 Well-circumscribed but may infiltrate the renal parenchyma and
perirenal fat
 Areas of necrosis and hemorrhage are usually absent

Gross appearance. The tumor is well-circumscribed with a fibrous
cut surface.
Mesoblastic nephroma

Microscopic
Cellular growth of spindle cells
 Proliferating cells have features of fibroblast,
myofibroblasts, and smooth muscle cells
 Tubules and glomeruli may be seen surrounded by
spindle cells with some exhibiting hyperplastic and
metaplastic changes
 Small islands of hyaline cartilage and foci of
extramedullary hematopoiesis may be present
 There is no capsule separating the tumor from rhe
uninvolved parenchyma
 Areas of necrosis and hemorrhage may be seen

Microscopic appearance showing a monotonous proliferation of
spindle cells with bland nuclei and abundant fibrillary acidophilic
cytoplasm.
Mesoblastic nephroma
Contain the t(12;15)(p13;q25)
translocation, which results to gene fusion
 Definitive treatment is nephrectomy

Pediatric tumors
and tumor-like lesions

Multicystic nephroma
 Also
called multilocular cystic nephroma;
multilocular cyst
 Arises in early infancy but may present
clinically at any age
 Clinical presentations result from the presence
of a mass or ureteral obstruction by one of
the daughter locules
Multicystic nephroma

Gross




Lesion is usually solitary, unilateral and sharply
delineated from the uninvolved renal parenchyma
Cut surface shows a multilocular appearance,
individual cyst measures 1 mm to 3 cm or more
The cysts do not communicate with each other or
with the pelvis
Extension of the lesion beyond the renal capsule may
occur
Gross appearance of muticystic nephroma involving most of the
kidney.
Multicystic nephroma

Microscopic
 Cysts
are lined by tubular epithelium ranges
in height from columnar to flat resembling
endothelium and simulating the appearance
of lymphangioma
 A “hobnail” pattern is common
LPO. Shows multiple cysts lined by flattened epithelium and
separated by a cellular spindle cell stroma.
The epithelial lining of the cyst
shows a “hobnail” pattern.
The cyst lining is flat, simulating
endothelium.
Pediatric tumors
and tumor-like lesions

Nephroblastomatosis and nephrogenic rests


Congenital dysontogenetic rather than neoplastic
disorders
Can be associated with Wilm’s tumor


They share the same mutation of WT1
Single or multifocal, unilateral or bilateral subcapsular
aggregates of primitive metanephric tissue


Microscopic in size – called nephrogenic rests
Massive – called nephroblastomatosis
Pediatric tumors
and tumor-like lesions

Clear cell sarcoma
Also known as bone-metastasizing renal tumor
 Comprises 4% of childhood renal tumors, peaks in
the 2nd year of life
 Gross




Large, sharply outlined and centered in the medullary or
central region of the kidney
Homogenous cut surface of light brownish gray color and
myxoid appearance
Consistency is hard and cystic formations are common
The tumor is well circumscribed and whitish, and it bulges on the
cut surface.
Clear cell sarcoma

Microscopic
 Diffuse
growth of relatively small cells with round
normochromatic nuclei, inconspicous nucleoli,
vacuolated cytoplasm, and indistinct cell margins
 Nuclear grooves are common, mitosis infrequent
Trabecular pattern of growth.
Clear cell sarcoma
Origin of neoplasm is uncertain
 Histogenetically related to Wilm’s tumor
 High tendency for relapse and propensity
for skeletal metastasis – skull
 Overall 5-year survival rate is 69%

Pediatric tumors
and tumor-like lesions

Rhabdoid tumor
 Most
cases occur in young infants
 Median age at diagnosis is 18 months
 Associated in about 15% of the cases with
primary embryonal tumors in the midline
posterior fossa particularly medulloblastoma
 Gross
 Solid,
soft, and relatively well circumscribed
Pediatric tumors
and tumor-like lesions

Rhabdoid tumor
 Microscopic
 Monomorphic
neoplasm involving the medullary
region
 Most characteristic feature is the presence of a
large cytoplasmic eosinophilic hyaline globule that
displaces the nucleus laterally
An eosinophilic amorphous (“hyaline”) material fills the
scanty cytoplasm and pushes the nucleus aside.
Pediatric tumors
and tumor-like lesions

Metanephric stromal tumor
 Presents
grossly as a fibrous lesion centered
in the renal medulla that contains smoothwalled cysts.
 Neoplastic cells are spindle shaped, with
onionskin cuffing around entrapped tubules
 Reactive to CD34
 Surgical excision is curative
Adult tumors and tumor-like
conditions

Renal cell Carcinoma




Average age of diagnosis is 55 – 60 years
Male:Female is 2:1; bilaterality is 1%
Cigarette smoking and HPN increases the risk
Conditions that may be complicated by RCC

von Hippel-Lindau disease

Acquired cystic disease
ADPKD and multicystic nephroma
Tuberous sclerosis
Neuroblastoma
Familial cutaneous leiomyomatosis
Malignant lymphoma





Renal cell carcinoma

Clinical features
 Presents
with hematuria (59%), flank pain (41%),
or abdominal mass (45%) – diagnostic triad (9%)
 Other manifestations




Weight loss – 28%
Anemia – 21%
Fever – 7%
Due to metastatic deposits – 10%
Renal cell carcinoma

Clinical features
 Systemic/Paraneoplastic manifestations
 Leukemoid reaction
 Systemic amyloidosis
 Polyneuropathy
 Gastrointestinal disturbances
 Hepatomegaly/hepatic dysfunction (Stauffer syndrome)
 Hypercalcemia
 HPN
 Polycythemia
 Gynecomastia
 Cushing’s syndrome
Renal cell carcinoma

Diagnosis
 IVP,

UTZ, CT-scan, MRI
Morphologic features
 Gross
 Well
delineated and centered on the cortex
 Cut surface – solid golden yellolw tumor sharply
separated from the surrounding tissues by fibrous
pseudocapsule
 Hemorrhage, necrosis, calcification, and cystic
change can occur
RCC developing in
ADPKD
Well circumscribed
with light yellow color
Variegated with a
combination of
cystic, solid, and
hemorrhagic areas
Well circumscribed and
homogenous
The tumor involves almost the
entire kidney and extends into the
renal vein
Renal cell carcinoma

Microscopic
 Tumor
cells are large, the appearance of the
cytoplasm ranging from optically clear, with
sharply outlined boundaries (“vegetable
cells”) to deeply granular with many
transitional forms
RCC, diffuse pattern of growth
with entrapment of glomeruli
HPO, optically clear cytoplasm and
sharply outlined cell membrane
Renal cell carcinoma

Cytology
 Examination
of voided urine or bladder
washing are inefficient - <25%
 Retrograde brushing cytology is better
 Percutaneous FNA is a safe and accurate
technique
Renal cell carcinoma

Spread and metastases
 1/3
of RCC are found to invade perinephric fat
and/or regional LN at the time of diagnosis
 Common finding is invasion of the main renal
vein
 Extend into the inferior vena cava, the right
atrium, and the renal sinus
 Distant metastasis to the lungs and skeleton
(pelvis and femur)
Renal cell carcinoma

Therapy

Primary treatment – surgical excision



Transabdominal or thoracoabdominal radical nephrectomy –
removal of the entire kidney, surrounding fat, Gerota’s
fascia, and adrenal gland
Some authors advocate node dissection in continuity with
nephrectomy or after the renal mass has been removed
(minimum distance of 4 – 6 cm above and below the renal
vessel
No benefits have yet been demonstrated for
administration of adjunctive radiation therapy or
chemotherapy
Renal cell carcinoma

Prognosis
 The
overall 5-year survival rate is
approximately 70%
 Stage
 Stage
I – confined to the kidney
 Stage II – extension to perirenal fat but within
Gerota’s fascia
 Stage III – renal vein or vena caval involvement
 Stage IV – extension to other organs other than
adrenal or distant metastases
Renal cell carcinoma

Prognosis
 Distant
metastases – the single most
important parameter
 Tumor size
 Tumor
size of 5.0 or 5.5 cm is more predictive of
the survival of Stage I patients after radical
nephrectomy
 Microscopic
 Low-grade
grade
= good
 High-grade = poor
Renal cell carcinoma

Prognosis
 Good
prognosis
 Clear
cell tumors
 Lymphocytic infiltration
Renal cell carcinoma

Prognosis
 Poor
prognosis
 Granular
cell tumors
 Renal vein invasion
 Increase cell proliferation
 p53 overexpression
 CD44S expression
 MUC1 expression
 Insulin-like growth factor I receptor
 Neural cell adhesion molecule
Adult tumors and tumor-like
conditions

Adenomas
 Tubulo-papillary
 Minute
adenomas
cortical foci of tubular or papillary
epithelium (measures 1-3mm in diameter)
 Present in approximately 20% or more of adult
kidneys
 Cytoplasm is acidophilic rather than clear and not
abundant
 Psammoma bodies may be present
Adult tumors and tumor-like
conditions

Adenomas
 Metanephric
 Occur
adenoma
in young, or middle-aged female patients
 Larger than tubulo-papillary adenoma
 Composed mostly of tiny tubules and papillae
accompanied by very scanty stroma
Metanephric adenoma showing papillary growth
pattern.
Adult tumors and tumor-like
conditions

Adenomas
 Metanephric
adenofibroma
 Previously
termed nephrogenic adenofibroma
 A biphasic tumor

An epithelial component similar to that of metanephric
adenoma admixed with a bland spindle cell stroma
Adult tumors and tumor-like
conditions

Oncocytoma
 Approximately
7% of all primary nonurothelial
epithelial renal neoplasms
 Gross
 Solid
and mahogany brown often have a central
stellate scar, and can reach huge sizes
 Can be multicentric and bilateral
 Invasion of renal capsule or renal vein can occur
The tumor is well circumscribed, mahogany brown and
has a central fibrous scar.
Oncocytoma

Microscopic
 Composed
of cells with abundant acidophilic
granular cytoplasm, growing in nesting or
tubular fashion
 Psammoma bodies can be present
Typical nesting pattern of renal oncocytoma
Adult tumors and tumor-like
conditions

Neuroendocrine tumors
 Small
cell neuroendocrine carcinoma
 Carcinoid tumor
Adult tumors and tumor-like
conditions

Angiomyolipoma
 Composed
of admixture of vessel, smooth
muscle, and fat
 Tumor found incidentally or result in
retroperitoneal hemorrhage
 1/3 of patients are associated with tuberous
sclerosis
 TSC2/PKD1, contigous gene syndrome,
increases the risk
Adult tumors and tumor-like
conditions

Angiomyolipoma
 Gross
 Depends
on the relative amounts of the various
components and may simulate RCC
 Capsular invasion is present in 25% of cases,
including perirenal soft tissue extension
 1/3 of cases are multiple; 15% are bilateral
Gross appearance of Angiomyolipoma.
Adult tumors and tumor-like
conditions

Angiomyolipoma
 Microscopic
 Shows
adipose tissue, tortous thick-walled blood
vessels lacking elastic tissue lamina, and bundles
of smooth muscle that seem to emanate from
vessel walls
Typical renal angiomyolipoma. The tumor is composed
of adipose tissue, smooth muscle and vessel.
Adult tumors and tumor-like
conditions

Juxtaglomerular cell tumor



Present clinically with HPN because of extensive renin
production
Grossly, unilateral and solitary, less than 3cm in
diameter and located in the cortex. Solid and well
circumscribed, with a grayish-white to light yellow cut
surface
Microscopically, reminiscent of hemangiopericytoma
and glomus tumor. Cells are uniform and round to
polyhedral with a granular acidophilic cytoplasm
The lesion has distinct vascular background
Other benign tumors and
tumor-like conditions
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Teratoma
Medullary fibroma
Leiomyoma
Lipoma
Myxoma
Hemangioma
Lymphangioma
Benign peripheral nerve tumor
Solitary fibrous tumor
Hydatid cyst