Wilm’s Tumor
Wilm’s Tumor
T. Ibnu Alferraly
Departement of Pathology Anatomic
Medical Faculty, North Sumatera University
led to a dramatic change in
the prognosis for most patients, and Wilms tumor has become a paradigm for multimodal
treatment of a pediatric malignant solid tumor. The author presents a case report of Wims tumor
in a 2-year-old boy with an intra-abdominal mass. Physical examination determined the boy had
abdominal mass, with symptoms of abdominal pain and vomiting in these last 3 months.
Laboratory finding of routine urinanalysis showed hematuria and proteinuria. Radiological
finding from CT-Scan showed inhomogeneous masses with areas of low density indicating
necrosis in the left kidney and the conclusion was left kidney tumor. The diagnosis was made by
histopathological technique which showed pattern of blastematous areas of primitive cells
surrounded by fibrous tissues with congestive blood vessels.
Keywords: wilms tumor, nephroblastoma, renal tumor, childhood tumor, histopathology
INTRODUCTION
Wilms tumor, or nephroblastoma, is the
most common primary tumor of the kidney in
children.
Most cases occur in children
between 2 and 5 years of age. This tumor
illustrates several important concepts of
childhood tumor: the relationship between
congenital malformation and increased risk of
tumors, also the histologic similarity between
tumor and developing organ.
Here we report a case of Wilms tumor
diagnosed by histopathological.. This Wilms
tumor presented with an abdominal mass
from a 2 year old boy. The histopathological
showed a malignant neoplasm of embryonal
nephrogenic elements composed of mixtures
of blastemal, stromal and epithelial tissues. In
our department Wilms tumor is a rare case,
here is the second case reported, at the first
time it diagnosed by cytology years ago.
CASE REPORT
A 2 year old boy was presented with an
intra-abdominal
mass.
Birth
and
developmental history were normal. Past
medical history was hypertension. Physical
examination determined the boy had
abdominal mass, with symptoms of abdominal
pain and vomiting in these last 3 months.
Laboratory finding of routine urinanalysis
84
showed
hematuria
and
proteinuria.
Radiological finding from CT-Scan showed
inhomogeneous masses with areas of low
density indicating necrosis in the left kidney
and the conclusion was left kidney tumor.
Then operation was done at March 26, 2005.
GROSS EXAMINATION
Grossly, the tumor mass was flattenround with multiple nodules, measuring 13 x
14 x 11 cm, was grey to black in color,
smooth surface and elastic in consistency.
The cut surface showed sharp demarcation
between tumor and the residual kidney,
correlated with pseudocapsule. There were
some areas of necrosis and hemorrhage.
Histopathological examination
The histological examination of H&E
stained specimen showed a growth of nodules
pattern of blastematous areas which were
extremely cellular, composing of small round
to oval primitive cells. Cells nuclei enlarged,
with coarse and clumping chromatine. Some
cells rounding vessels give rosette appearance.
Surrounding the blastemal areas were fibrous
tissues with congestive blood vessels. There
were also some abortive tubules. At the other
places showed necrotic areas and interstisial
Majalah Kedokteran Nusantara Volume
41 y No.
1 y Maret
2008
Universitas
Sumatera
Utara
T. Ibnu Alferraly
hemorrhage. The final histopatological
diagnosis was Wilms tumor in the left kidney.
DISCUSSION
Wilms tumor is a malignant neoplasm of
embryonal nephrogenic elements composed of
mixtures of blastemal, stromal, and epithelial
1,2
tissue. Wilms tumor is seen primarily in
infants, it is a frequent abdominal solid tumor,
with prevalence of 1 in 10,000. Fifty percent
of the cases occurring before the age of 3 years
and 90% before the age of 6 years. However,
Wilms tumor is only exceptional seen as a
congenital neoplasm, a point of great
importance in the differential diagnosis with
mesoblastic nephroma. The classic location for
3
Wilms tumor is the kidney.
In the large majority (90%) of cases of
Wilms tumor, the neoplasm is sporadic and
unilateral. In 5% of the cases, however, Wilms
tumor arises in the context of three different
congenital syndromes, all of which include an
increased risk for the development of this
cancer at an early age and often bilaterally:
• WAGR syndrome (for Wilms tumor,
aniridia, genitourinary anomalies, mental
retardation).
• Denys-Drash syndrome (DDS) (Wilms
tumor, intersexual disorders, glomerulopathy).
• Beckwith-Wiedemann syndrome (BWS)
(Wilms tumor, overgrowth ranging from
gigantism to hemihypertrophy, visceromegaly,
and macroglossia)
Some 6% of cases of Wilms tumor are
familial, have an early onset, and are bilateral
but are not associated with any other
syndrome.
Two decades ago, karyotypic analysis of
children with WAGR syndrome revealed a
deletion in the short arm of one copy of
chromosome 11 (11pl3). We now understand
that the WAGR deletion affects contiguous
genes, including PAX6, the aniridia gene, and
WT1, the Wilms tumor gene. The loss or
mutation of one WT1 allele leads to
genitourinary anomalies, whereas a defect in
the PAX6 gene is responsible for aniridia. One
third of children with WAGR syndrome
eventually develop Wilms tumor. The
presence of a germline mutation in one WT1
allele and loss of heterozygosity at this locus in
the tumors of WAGR syndrome imply that a
Wilm’s Tumor
second mutation in the normal WT1 allele is
responsible for the appearance of Wilms
tumor (similar to the pathogsnesis of
hereditary retinoblastoma). In contrast to the
deletions in WAGR syndrome, specific
mutations of the WT1 gene characterize
DDS. The fact that the phenotypic expression
of the abnormalities in DDS is far more severe
than that in WAGR syndrome suggests that
mutated WT1 is actually a dysfunctional gene
(dominant negative mutation).
WT1 is a tumor suppressor gene that
functions as a regulator of the transcription of
a number of other genes, including insulin-like
growth factor-2 (IGF-2) and platelet-derived
growth factor (PDGF). The WT1 gene
protein also forms a complex with the p53
protein. Whereas Wilms tumors arising in the
context of WAGR syndrome all display
defects of WT1, less than 10% of sporadic
tumors exhibit abnormalities of WT1. Thus, it
is believed that other genes play a more
critical role than does WT1 in the genesis of
sporadic Wilms tumors.
A second gene for susceptibility to Wilms
tumor (WT2) was discovered in sporadic
tumors that showed loss of heterozygosity
(LOH) on chromosome 11 (11p15), a site
distinct from, but close to, the WT1 gene.
WT2 is also linked to BWS. Interestingly, in
LOH of the WT2 locus in sporadic Wilms
tumors, the allele lost is invariably the
maternal one. Importantly, some patients with
BWS show a germline duplication of the
paternal WT2 allele, and others have inherited
both apparently normal copies of this gene
from the father and none from the mother
(paternal
uniparental
isodisomy). One
possibility is that WT2 is normally expressed
only by the paternal allele (genomic
imprinting), and, therefore, overexpression of
WT2 may be responsible for the overgrowth
characteristic of BWS. Since the IGF-2 gene
has also been mapped to chromosome 11p15
and is also paternally imprinted, it is possible
that an increased dosage of IGF-2 might
contribute both to BWS and to tumorigenesis.
Another possibility is that WT2 is expressed
only by the maternal allele acting as a tumor
suppressor. Thus, loss of the maternal allele
would contribute to tumorigenesis.
Majalah Kedokteran Nusantara Volume 41 y No. 1 y Maret 2008
Universitas Sumatera Utara85
Laporan Kasus
Nephrogenic rests (i.e., small foci of
persistent primitive blastemal cells) are found
in the kidneys of all children with syndromic
Wilms tumors and in one third of sporadic
cases. Since such rests in the nontumorous
kidney have been demonstrated to contain the
same somatic mutations in WT1 as are
present in the tumors, it is thought that these
rests represent clonal precursor lesions that
are at least one step along the pathway to
tumor formation.1,2,3,4
The classic clinical presentation of Wilms
tumor is in the form of an abdominal mass felt
by the mother when handling the child.
Hematuria and pain are rare. Hypertension,
present in a minority of the cases, has been
shown to be caused by renin secretion by the
tumor. Proteinuria may be caused by the
presence of tumor-associated glomerular
disease in the non-neoplastic kidney.
Sometimes the first symptoms are related to
traumatic rupture. 4,5,6
Grossly, most Wilms tumors are solitary,
well circumscribed, rounded, and of soft
consistency. Their size is extremely variable,
with a median of 550 g. The cut section is
predominantly solid and pale gray or tan and
often exhibits areas of cystic change, necrosis,
and hemorrhage. A lobular pattern resulting
from
Fibrous
septation
is
common.
Multicentric foci are appreciable in 7% of the
cases.2,3,4,5
Microscopically, three major components
are identified: undifferentiated blastema,
mesenchymal (stromal) tissue, and epithelial
tissue. Most Wilms tumors show a
representation of all three components, but
the proportions vary widely. Some tumors are
biphasic, and still others are monophasic
(monomorphous). The blastematous areas are
extremely cellular and composed of small
round-to-oval primitive cells; the cytoplasm is
usually very scanty, but sometimes it exhibits
an oncocytoid appearance. The pattern of
growth may be diffuse, nodular, cord-like
(serpentine), or basaloid (with peripheral
palisading). Wilms tumors in which the
blastematous component predominates can be
confused with any of the small round cell
tumors, including neuroblastoma. The
mesenchymal elements usually have a spindlecell fibroblast-like configuration but may also
exhibit differentiation toward various cell
types, particularly smooth muscle and skeletal
86
muscle.
Sometimes
this
mesenchymal
component predominates almost in the
exclusion of others. Wilms tumors with an
extensive skeletal muscle component are
invariably seen in young children and are
bilateral in over half of the cases.
Predominantly rhabdomyosarcomatous Wilms
tumors involving the renal pelvis acquire
morphologic features very similar to those of
botryoid rhabdomyosarcoma. In some instances,
these largely mesenchymal. Neoplasms are
seen in the opposite kidney of patients with
typical Wilms tumor.2,4,5,6,7,8
The epithelial component is characterized
by the formation of embryonic tubular (and
sometimes glomerular) structures that closely
recapitulate the appearance of normal developing
metanephric tubules (and glomeruli) at the
light microscopic, ultrastructural, and lectin
histochemistry levels. The differentiation can
be so pronounced that tumor analogs of nearly
all segments of the normal nephron can be
formed. These tubular structures can be small
and round, thus simulating the rosettes of
neuroblastoma. Features favoring tubules over
rosettes are the presence of a lumen, single cell
layer, distinct basal lamina, and surrounding
fibromyxoid stroma. The differential diagnosis
of predominantly epithelial Wilms tumors also
includes multicystic nephroma and renal cell
carcinoma. Exceptionally, marked hydropic
changes are seen in the tubular epithelium.4
In the type known as papillonodular,
grossly evident projections are seen extending
from the septa into the cyst lumina. The
resulting appearance on low power may be
4
fibroadenoma like.
Anaplastic features may be present focally
2,4,9
or extensively in Wilms tumors.
Additional morphologic features that can
be encountered in Wilms tumor include
ciliated, mucinous, squamous, or transitional
epithelium; endocrine cells of various types;
renin- producing cells; neuroepithelium,
neuroblasts. and mature ganglion cells;
neuroglia; adipose tissue; and cartilage, bone,
and hematopoietic cells. Sometimes the
variety of tissues present is such that the
distinction between Wilms tumor and
teratoma becomes blurred; the term teratoid
Wilms tumor is sometimes used for these
cases. On other occasions, foci of renal cell
carcinoma occur in otherwise typical Wilms
tumor.4
Majalah Kedokteran Nusantara Volume
41 y No.
1 y Maret
2008
Universitas
Sumatera
Utara
T. Ibnu Alferraly
DAFTAR PUSTAKA
rd
1. Jennette JC, Spargo BH. The kidney. 3
ed. Lippincott. Philadelphia. 1999. p 91315.
2. Grier HE, Atayde AP, Hoffer FA. Solid
tumors in childhood. In: Atlas of
rd
diagnostic oncology. 3
ed. Mosby.
London. 2003. p 560-66.
3. Kumar V, Cotran RS, Robbins SL.
th
Robbins basic pathology. 7 ed. Saunders.
Philadelphia. 2003. p 256-57.
4. Ordonez NG, Rosai J. Urinary tract. In:
th
Ackerman’s surgical pathology. Vol I. 8
ed. Mosby. Missouri. 1996. p 1135-40.
Wilm’s Tumor
5. Paulino AC. Wilms tumor. Available
from:
http//www.eMedicine_wilms
tumor.htm.
nd
6. Kissane JM. Pathology. 2
London. 1975. p 640-43.
ed. Mosby.
7. Solid malignancies of childhood. Available
from:
http//www.pathology.washington.edu.ph
p.
8. Wilms
tumor.
Available
http//www.webpathology.com.
from:
9. Wilms
tumor
available
from
http//www.cancer.gov/cancertopic/pdq/w
ilm.com.
Majalah Kedokteran Nusantara Volume 41 y No. 1 y Maret 2008
Universitas Sumatera Utara87
T. Ibnu Alferraly
Departement of Pathology Anatomic
Medical Faculty, North Sumatera University
led to a dramatic change in
the prognosis for most patients, and Wilms tumor has become a paradigm for multimodal
treatment of a pediatric malignant solid tumor. The author presents a case report of Wims tumor
in a 2-year-old boy with an intra-abdominal mass. Physical examination determined the boy had
abdominal mass, with symptoms of abdominal pain and vomiting in these last 3 months.
Laboratory finding of routine urinanalysis showed hematuria and proteinuria. Radiological
finding from CT-Scan showed inhomogeneous masses with areas of low density indicating
necrosis in the left kidney and the conclusion was left kidney tumor. The diagnosis was made by
histopathological technique which showed pattern of blastematous areas of primitive cells
surrounded by fibrous tissues with congestive blood vessels.
Keywords: wilms tumor, nephroblastoma, renal tumor, childhood tumor, histopathology
INTRODUCTION
Wilms tumor, or nephroblastoma, is the
most common primary tumor of the kidney in
children.
Most cases occur in children
between 2 and 5 years of age. This tumor
illustrates several important concepts of
childhood tumor: the relationship between
congenital malformation and increased risk of
tumors, also the histologic similarity between
tumor and developing organ.
Here we report a case of Wilms tumor
diagnosed by histopathological.. This Wilms
tumor presented with an abdominal mass
from a 2 year old boy. The histopathological
showed a malignant neoplasm of embryonal
nephrogenic elements composed of mixtures
of blastemal, stromal and epithelial tissues. In
our department Wilms tumor is a rare case,
here is the second case reported, at the first
time it diagnosed by cytology years ago.
CASE REPORT
A 2 year old boy was presented with an
intra-abdominal
mass.
Birth
and
developmental history were normal. Past
medical history was hypertension. Physical
examination determined the boy had
abdominal mass, with symptoms of abdominal
pain and vomiting in these last 3 months.
Laboratory finding of routine urinanalysis
84
showed
hematuria
and
proteinuria.
Radiological finding from CT-Scan showed
inhomogeneous masses with areas of low
density indicating necrosis in the left kidney
and the conclusion was left kidney tumor.
Then operation was done at March 26, 2005.
GROSS EXAMINATION
Grossly, the tumor mass was flattenround with multiple nodules, measuring 13 x
14 x 11 cm, was grey to black in color,
smooth surface and elastic in consistency.
The cut surface showed sharp demarcation
between tumor and the residual kidney,
correlated with pseudocapsule. There were
some areas of necrosis and hemorrhage.
Histopathological examination
The histological examination of H&E
stained specimen showed a growth of nodules
pattern of blastematous areas which were
extremely cellular, composing of small round
to oval primitive cells. Cells nuclei enlarged,
with coarse and clumping chromatine. Some
cells rounding vessels give rosette appearance.
Surrounding the blastemal areas were fibrous
tissues with congestive blood vessels. There
were also some abortive tubules. At the other
places showed necrotic areas and interstisial
Majalah Kedokteran Nusantara Volume
41 y No.
1 y Maret
2008
Universitas
Sumatera
Utara
T. Ibnu Alferraly
hemorrhage. The final histopatological
diagnosis was Wilms tumor in the left kidney.
DISCUSSION
Wilms tumor is a malignant neoplasm of
embryonal nephrogenic elements composed of
mixtures of blastemal, stromal, and epithelial
1,2
tissue. Wilms tumor is seen primarily in
infants, it is a frequent abdominal solid tumor,
with prevalence of 1 in 10,000. Fifty percent
of the cases occurring before the age of 3 years
and 90% before the age of 6 years. However,
Wilms tumor is only exceptional seen as a
congenital neoplasm, a point of great
importance in the differential diagnosis with
mesoblastic nephroma. The classic location for
3
Wilms tumor is the kidney.
In the large majority (90%) of cases of
Wilms tumor, the neoplasm is sporadic and
unilateral. In 5% of the cases, however, Wilms
tumor arises in the context of three different
congenital syndromes, all of which include an
increased risk for the development of this
cancer at an early age and often bilaterally:
• WAGR syndrome (for Wilms tumor,
aniridia, genitourinary anomalies, mental
retardation).
• Denys-Drash syndrome (DDS) (Wilms
tumor, intersexual disorders, glomerulopathy).
• Beckwith-Wiedemann syndrome (BWS)
(Wilms tumor, overgrowth ranging from
gigantism to hemihypertrophy, visceromegaly,
and macroglossia)
Some 6% of cases of Wilms tumor are
familial, have an early onset, and are bilateral
but are not associated with any other
syndrome.
Two decades ago, karyotypic analysis of
children with WAGR syndrome revealed a
deletion in the short arm of one copy of
chromosome 11 (11pl3). We now understand
that the WAGR deletion affects contiguous
genes, including PAX6, the aniridia gene, and
WT1, the Wilms tumor gene. The loss or
mutation of one WT1 allele leads to
genitourinary anomalies, whereas a defect in
the PAX6 gene is responsible for aniridia. One
third of children with WAGR syndrome
eventually develop Wilms tumor. The
presence of a germline mutation in one WT1
allele and loss of heterozygosity at this locus in
the tumors of WAGR syndrome imply that a
Wilm’s Tumor
second mutation in the normal WT1 allele is
responsible for the appearance of Wilms
tumor (similar to the pathogsnesis of
hereditary retinoblastoma). In contrast to the
deletions in WAGR syndrome, specific
mutations of the WT1 gene characterize
DDS. The fact that the phenotypic expression
of the abnormalities in DDS is far more severe
than that in WAGR syndrome suggests that
mutated WT1 is actually a dysfunctional gene
(dominant negative mutation).
WT1 is a tumor suppressor gene that
functions as a regulator of the transcription of
a number of other genes, including insulin-like
growth factor-2 (IGF-2) and platelet-derived
growth factor (PDGF). The WT1 gene
protein also forms a complex with the p53
protein. Whereas Wilms tumors arising in the
context of WAGR syndrome all display
defects of WT1, less than 10% of sporadic
tumors exhibit abnormalities of WT1. Thus, it
is believed that other genes play a more
critical role than does WT1 in the genesis of
sporadic Wilms tumors.
A second gene for susceptibility to Wilms
tumor (WT2) was discovered in sporadic
tumors that showed loss of heterozygosity
(LOH) on chromosome 11 (11p15), a site
distinct from, but close to, the WT1 gene.
WT2 is also linked to BWS. Interestingly, in
LOH of the WT2 locus in sporadic Wilms
tumors, the allele lost is invariably the
maternal one. Importantly, some patients with
BWS show a germline duplication of the
paternal WT2 allele, and others have inherited
both apparently normal copies of this gene
from the father and none from the mother
(paternal
uniparental
isodisomy). One
possibility is that WT2 is normally expressed
only by the paternal allele (genomic
imprinting), and, therefore, overexpression of
WT2 may be responsible for the overgrowth
characteristic of BWS. Since the IGF-2 gene
has also been mapped to chromosome 11p15
and is also paternally imprinted, it is possible
that an increased dosage of IGF-2 might
contribute both to BWS and to tumorigenesis.
Another possibility is that WT2 is expressed
only by the maternal allele acting as a tumor
suppressor. Thus, loss of the maternal allele
would contribute to tumorigenesis.
Majalah Kedokteran Nusantara Volume 41 y No. 1 y Maret 2008
Universitas Sumatera Utara85
Laporan Kasus
Nephrogenic rests (i.e., small foci of
persistent primitive blastemal cells) are found
in the kidneys of all children with syndromic
Wilms tumors and in one third of sporadic
cases. Since such rests in the nontumorous
kidney have been demonstrated to contain the
same somatic mutations in WT1 as are
present in the tumors, it is thought that these
rests represent clonal precursor lesions that
are at least one step along the pathway to
tumor formation.1,2,3,4
The classic clinical presentation of Wilms
tumor is in the form of an abdominal mass felt
by the mother when handling the child.
Hematuria and pain are rare. Hypertension,
present in a minority of the cases, has been
shown to be caused by renin secretion by the
tumor. Proteinuria may be caused by the
presence of tumor-associated glomerular
disease in the non-neoplastic kidney.
Sometimes the first symptoms are related to
traumatic rupture. 4,5,6
Grossly, most Wilms tumors are solitary,
well circumscribed, rounded, and of soft
consistency. Their size is extremely variable,
with a median of 550 g. The cut section is
predominantly solid and pale gray or tan and
often exhibits areas of cystic change, necrosis,
and hemorrhage. A lobular pattern resulting
from
Fibrous
septation
is
common.
Multicentric foci are appreciable in 7% of the
cases.2,3,4,5
Microscopically, three major components
are identified: undifferentiated blastema,
mesenchymal (stromal) tissue, and epithelial
tissue. Most Wilms tumors show a
representation of all three components, but
the proportions vary widely. Some tumors are
biphasic, and still others are monophasic
(monomorphous). The blastematous areas are
extremely cellular and composed of small
round-to-oval primitive cells; the cytoplasm is
usually very scanty, but sometimes it exhibits
an oncocytoid appearance. The pattern of
growth may be diffuse, nodular, cord-like
(serpentine), or basaloid (with peripheral
palisading). Wilms tumors in which the
blastematous component predominates can be
confused with any of the small round cell
tumors, including neuroblastoma. The
mesenchymal elements usually have a spindlecell fibroblast-like configuration but may also
exhibit differentiation toward various cell
types, particularly smooth muscle and skeletal
86
muscle.
Sometimes
this
mesenchymal
component predominates almost in the
exclusion of others. Wilms tumors with an
extensive skeletal muscle component are
invariably seen in young children and are
bilateral in over half of the cases.
Predominantly rhabdomyosarcomatous Wilms
tumors involving the renal pelvis acquire
morphologic features very similar to those of
botryoid rhabdomyosarcoma. In some instances,
these largely mesenchymal. Neoplasms are
seen in the opposite kidney of patients with
typical Wilms tumor.2,4,5,6,7,8
The epithelial component is characterized
by the formation of embryonic tubular (and
sometimes glomerular) structures that closely
recapitulate the appearance of normal developing
metanephric tubules (and glomeruli) at the
light microscopic, ultrastructural, and lectin
histochemistry levels. The differentiation can
be so pronounced that tumor analogs of nearly
all segments of the normal nephron can be
formed. These tubular structures can be small
and round, thus simulating the rosettes of
neuroblastoma. Features favoring tubules over
rosettes are the presence of a lumen, single cell
layer, distinct basal lamina, and surrounding
fibromyxoid stroma. The differential diagnosis
of predominantly epithelial Wilms tumors also
includes multicystic nephroma and renal cell
carcinoma. Exceptionally, marked hydropic
changes are seen in the tubular epithelium.4
In the type known as papillonodular,
grossly evident projections are seen extending
from the septa into the cyst lumina. The
resulting appearance on low power may be
4
fibroadenoma like.
Anaplastic features may be present focally
2,4,9
or extensively in Wilms tumors.
Additional morphologic features that can
be encountered in Wilms tumor include
ciliated, mucinous, squamous, or transitional
epithelium; endocrine cells of various types;
renin- producing cells; neuroepithelium,
neuroblasts. and mature ganglion cells;
neuroglia; adipose tissue; and cartilage, bone,
and hematopoietic cells. Sometimes the
variety of tissues present is such that the
distinction between Wilms tumor and
teratoma becomes blurred; the term teratoid
Wilms tumor is sometimes used for these
cases. On other occasions, foci of renal cell
carcinoma occur in otherwise typical Wilms
tumor.4
Majalah Kedokteran Nusantara Volume
41 y No.
1 y Maret
2008
Universitas
Sumatera
Utara
T. Ibnu Alferraly
DAFTAR PUSTAKA
rd
1. Jennette JC, Spargo BH. The kidney. 3
ed. Lippincott. Philadelphia. 1999. p 91315.
2. Grier HE, Atayde AP, Hoffer FA. Solid
tumors in childhood. In: Atlas of
rd
diagnostic oncology. 3
ed. Mosby.
London. 2003. p 560-66.
3. Kumar V, Cotran RS, Robbins SL.
th
Robbins basic pathology. 7 ed. Saunders.
Philadelphia. 2003. p 256-57.
4. Ordonez NG, Rosai J. Urinary tract. In:
th
Ackerman’s surgical pathology. Vol I. 8
ed. Mosby. Missouri. 1996. p 1135-40.
Wilm’s Tumor
5. Paulino AC. Wilms tumor. Available
from:
http//www.eMedicine_wilms
tumor.htm.
nd
6. Kissane JM. Pathology. 2
London. 1975. p 640-43.
ed. Mosby.
7. Solid malignancies of childhood. Available
from:
http//www.pathology.washington.edu.ph
p.
8. Wilms
tumor.
Available
http//www.webpathology.com.
from:
9. Wilms
tumor
available
from
http//www.cancer.gov/cancertopic/pdq/w
ilm.com.
Majalah Kedokteran Nusantara Volume 41 y No. 1 y Maret 2008
Universitas Sumatera Utara87