INTERNATIONAL HISTOLOGICAL

CLASSIFICATION OF TUMOURS
No.25

Histological Typing
of Kidney Tumours

WORLD HEALTH ORGANIZATION

 ISBN 9241760257
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 INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF
TUMOURS
No. 25

HISTOLOGICAL TYPING
OF KIDNEY TUMOURS
F. K. MOSTOFI
Head, WHO Collaborating Centre for the Histological Classification of Male
Urogenital Tract Tumours, Armed Forces Institute of Pathology,
Washington, DC, USA

in collaboration with

I. A. SESTERHENN L. H. SOBIN
Armed Forces Institute Pathologist,
of Pathology, World Health Organization,
Washington, DC, USA Geneva, Switzerland

and pathologists in seven countries

WORLD HEALTH ORGANIZATION

GENEVA
1981
 PARTICIPANTS
WHO Collaborating Centre for the Histological Classification of Male
Urogenital Tract Tumours/ Armed Forces Institute of Pathology, Wash-
ington, DC, USA

Head of Centre
Dr. F. K. Mostofi

Participants
Dr E. CHAVES, Department of Pathology, Cancer Hospital of Paraiba, Joao
Pessoa, Paraiba, Brazil
Dr L. GALINDO, Department of Pathology, Hospital Santa Cruz y San
Pablo, Fundaci6n Puigvert, Universidad Aut6noma, Barcelona, Spain
Dr C. GouYGOu, 2 Service central d'Anatomie pathologique, Centre hospi-
talo-universitaire Henri Mondor, Creteil, France
Dr N. A. KRAYEVSKY, Department of Pathology, Cancer Research Centre of
the USSR Academy of Medical Sciences, Moscow, USSR
Dr V. J. McGovERN, Fairfax Institute of Pathology, Royal Prince Alfred
Hospital, Camperdown, New South Wales, Australia
Dr M.S. RAGBEER, Department of Pathology, University ofthe West Indies,
Mona, Kingston, Jamaica, West Indies
Dr L. H. SoBIN, Cancer Unit, WHO, Geneva, Switzerland
Dr A. C. THACKRAY, Bland-Sutton Institute of Pathology, Middlesex Hos-
pital Medical School, London, England
1
This centre deals with tumours of the urinary bladder, testis, kidney, and prostate. The
participants listed here have dealt only with kidney tumours.
2
Deceased.
 ALREADY PUBLISHED IN THIS SERIES:

No. 1. Histological typing of lung tumours (1967)

No. 2. Histological typing of breast tumours (1968)
No. 3. Histological typing of soft tissue tumours (1969)
No. 4. Histological typing of oral and oropharyngeal tumours (1971)
No. 5. Histological typing of odontogenic tumours, jaw cysts, and allied
lesions (1971)
No. 6. Histological typing of bone tumours (1972)
No. 7. Histological typing of salivary gland tumours (1972)
No. 8. Nomenclature of cytology of the female genital tract (1973)
No. 9. Histological typing of ovarian tumours ( 1973)
No. 10. Histological typing of urinary bladder tumours (1973)
No. 11. Histological typing of thyroid tumours (1974)
No. 12. Histological typing of skin tumours (1974)
No. 13. Histological typing offemale genital tract tumours (1975)
No. 14. Histological and cytological typing of neoplastic diseases of hae-
matopoietic and lymphoid tissues (1976)
No. 15. Histological typing of intestinal tumours (1976)
No. 16. Histological typing of testis tumours (1977)
No. 17. Cytology of non-gynaecological sites (1977)
No. 18. Histological typing of gastric and oesophageal tumours (1977)
No. 19. Histological typing of upper respiratory tract tumours (1978)
No. 20. Histological typing of tumours of the liver, biliary tract and pancreas
(1978)
No. 21. Histological typing of tumours of the central nervous system ( 1979)
No. 22. Histological typing of prostate tumours (1980)
No. 23. Histological typing of endocrine tumours (1980)
No. 24. Histological typing of tumours of the eye and its adnexa (1980)
 CONTENTS

Page

General preface to the series 9

Preface to Histological typing of kidney tumours . 11

Introduction . 13

Histological classification of kidney tumours 15

Definitions and explanatory notes 17

Index. 25

Colour photomicrographs

The photomicrographs reproduced in this volume were taken by

Mr B. B. Allen, Jr, and Mr L. Duckett,
Armed Forces Institute of Pathology, Washington, DC, USA.

-7-
 GENERAL PREFACE TO THE SERIES

Among the prerequisites for comparative studies of cancer are international

agreement on histological criteria for the classification of cancer types and a
standardized nomenclature. At present, pathologists use different terms for the
same pathological entity, and furthermore the same term is sometimes applied
to lesions of different types. An internationally agreed classification of tumours,
acceptable alike to physicians, surgeons, radiologists, pathologists and statisti-
cians, would enable cancer workers in all parts of the world to compare their
findings and would facilitate collaboration among them.
1
In a report published in 1952, a subcommittee of the WHO Expert
Committee on Health Statistics discussed the general principles that should
govern the statistical classification of tumours and agreed that, to ensure the
necessary flexibility and ease in coding, three separate classifications were
needed according to (1) anatomical site, (2) histological type, and (3) degree of
malignancy. A classification according to anatomical site is available in the
International Classification of Diseases. 2
The question of establishing a universally accepted classification by histolog-
ical type has received much attention during the last 20 years and a particularly
valuable Atlas of Tumor Pathology-already numbering more than 40 vol-
umes-is being published in the USA by the Armed Forces Institute of
Pathology under the auspices of the National Research Council. An Illustrated
Tumour Nomenclature in English, French, German, Latin, Russian and
Spanish has also been published by the International Union Against Cancer
(UICC).
In 1956 the WHO Executive Board passed a resolution 3 requesting the
Director-General to explore the possibility that WHO might organize centres
in various parts of the world and arrange for the collection of human tissues
and their histological classification. The main purpose of such centres would be
to develop histological definitions of cancer types and to facilitate the wide
adoption of a uniform nomenclature. This resolution was endorsed by the Tenth
World Health Assembly in May 1957 4 and the following month a Study Group
on Histological Classification of Cancer Types met in Oslo to advise WHO on
its implementation. The Group recommended criteria for selecting tumour sites
1
, WHO Technical Report Series, No. 53, 1952, p. 45.
2
WoRLD HEALTH ORGANIZATION. Manual of the international statistical classification of
diseases, injuries, and causes of death, 1975 revision. Geneva, 1977.
3
WHO Official Records, No. 6R, 1956, p. 14 (resolution EB 17.R40).
4
WHO Official Records, No. 79, 1957, p. 467 (resolution WHAIO.lS).

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lO INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF TUMOURS

for study and suggested a procedure for the drafting of histological classifica-
tions and testing their validity. Briefly, the procedure is as follows:
For each tumour site, a tentative histopathological typing and classification
is drawn up by a group of experts, consisting of up to ten pathologists working
in the field in question. A centre and a number of collaborating laboratories are
then designated by WHO to evaluate the proposed classification. These labo-
ratories exchange histological preparations, accompanied by clinical informa-
tion. The histological typing is then made in accordance with the proposed
classification. Subsequently, one or more technical meetings are called by
WHO to facilitate an exchange of opinions and the classification is amended
to take account of criticisms.
In addition to preparing the publication and the photomicrographs for it, the
centre produces up to 100 sets of microscope slides showing the major histolog-
ical types for distribution to national societies ofpathology.
Since 1958, WHO has established 23 centres covering tumours of the lung;
breast; soft tissues; oropharynx; bone; ovaries; salivary glands; thyroid; skin;
male urogenital tract; jaws; female genital tract; stomach and oesophagus;
intestines; central nervous system; liver, biliary tract and pancreas; upper
respiratory tract; eye; and endocrine glands; as well as oral precancerous
conditions; the leukaemias and lymphomas; comparative oncology; and exfol-
iative cytology. This work has involved more than 300 pathologists from over
50 countries. Most of these centres have completed their work, and their
classifications have already been published (see page 6).
The World Health Organization is indebted to the many pathologists who
have participated in this large undertaking. The pioneer work of many other
international and national organizations in the field of histological classification
of tumours has greatly facilitated the task undertaken by WHO. Particular
gratitude is expressed to the National Cancer Institute, USA, which, through
the National Research Council and the USA National Committee for the
International Council of Societies of Pathology, is providing financial support
to accelerate this work. Finally, WH 0 wishes to record its appreciation of the
valuable help it has received from the International Council of Societies of
Pathology (ICSP) in proposing participants and in undertaking to distribute
copies of the classifications to national societies ofpathology all over the world.
 PREFACE TO HISTOLOGICAL TYPING OF
KIDNEY TUMOURS

The WHO Collaborating Centre for the Histological Classification of Male

Urogenital Tract Tumours was established at the Armed Forces Institute of
Pathology, Washington, DC, USA.

The Centre prepared and distributed microscope specimens from selected

cases of kidney tumours to the participants for histological typing according to
a tentative classification. This was subsequently reviewed and modified in the
light of the study.

It will, of course, be appreciated that the classification reflects the present

state of knowledge, and modifications are almost certain to be needed as
experience accumulates. Although the present classification has been adopted
by the members of the group, it necessarily represents a view from which some
pathologists may wish to dissent. It is nevertheless hoped that, in the interests
of international cooperation, all pathologists will try to use the classification as
put forward. Criticism and suggestions for its improvement will be welcomed;
these should be sent to the World Health Organization, Geneva.

The publications in the series International Histological Classification of

Tumours are not intended to serve as textbooks but rather to promote the
adoption of a uniform terminology of tumours that will facilitate and improve
communication among cancer workers. For this reason the literature references
have intentionally been kept to a minimum and readers should refer to standard
works on the subject for extensive bibliographies.

-11-
 INTRODUCTION

This classification is based primarily on the microscope characteristics of

tumours and therefore is concerned with morphologically identifiable cell
types and histological patterns as seen with conventional light microscopy.
The term tumour is used synonymously with neoplasm. The phrase tumour-
like is applied to lesions which clinically or morphologically resemble
neoplasms, but do not behave biologically in a neoplastic manner. They are
included in this classification because they give rise to problems in differ-
ential diagnosis and because of the unclear borderline between neoplasms
and certain non-neoplastic lesions. Synonyms are listed only if they have
been widely used, or if they are considered to be helpful for the understand-
ing of the lesion. In such cases, the preferred term is given first, followed by
the synonym in brackets.
Although the emphasis of this classification is on histological typing, in
the examination of kidney tumours consideration should be given to the
degree of cellular anaplasia, extent of local spread, vascular and lymphatic
invasion and the occurrence of metastasis.
The scheme of histological grading suggested here is as follows: Grade I
applies to the tumours that have the least degree of cellular anaplasia
compatible with a diagnosis of malignancy; Grade II I applies to tumours
with the most severe degrees of cellular anaplasia; and Grade II lies in
between. This scheme is applicable to the carcinomas of the renal paren-
chyma and pelvis.
In addition to histological assessment, the clinical and histopathological
staging of the extent of the tumour should be taken into account for the
purposes of treatment and prognosis. Such a system of staging has been
developed by the International Union Against Cancer. 1 The main histopath-
ological categories for renal cell carcinoma regarding local spread are as
follows:
pTl A small tumour without enlargement of the kidney. There is limited
calyceal distortion or deformity and the tumour is surrounded by renal
parenchyma.
pT2 A large tumour with deformity and/or enlargement of the kidney or
calyceal or pelvic involvement. The continuity of the cortex is pre-
served.
pT3 Evidence of spread into perinephric fat, peripelvic fat or hilar renal
vessels.
1
HARMER, M. H. (ED.) TN M classification of malignant tumours, 3rd ed. Geneva, Interna-
tional Union Against Cancer, 1978.
-13-
14 INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF TUMOURS

pT4 Evidence of extension into neighbouring organs or abdominal wall.

The histological classification which appears on pages 15 and 16 contains
the corresponding morphology code numbers of the International Classifi-
cation of Diseases for Oncology (ICD-0) 1 for tumours, and of the Systema-
tized Nomenclature of Medicine (SNOMED) 2 for tumour-like lesions.

1
WoRLD HEALTH ORGANIZATION. International classification of diseases for oncology (ICD-
0). Geneva, 1976.
2
COLLEGE OF AMERICAN PATHOLOGISTS. Systematized nomenclature of medicine
(SNOMED). Chicago, IL, 1976.
 HISTOLOGICAL CLASSIFICATION OF KIDNEY
TUMOURS

I. EPITHELIAL TUMOURS OF RENAL PARENCHYMA

A. ADENOMA 8140/0*
B. CARCINOMA
I. Renal cell carcinoma 8312/3
2. Others

II. EPITHELIAL TUMOURS OF RENAL PEL VIS

A. TRANSITIONAL CELL PAPILLOMA 8120/0
B. TRANSITIONAL CELL CARCINOMA 8120/3
c. SQUAMOUS CELL CARCINOMA 8070/3
D. ADENOCARCINOMA OF RENAL PELVIS 8140/3
E. UNDIFFERENTIATED CARCINOMA OF RENAL PELVIS 8020/3

III. NEPHROBLASTIC TUMOURS

A. NEPHROBLASTOMA (WILMS' TUMOUR] 8960/3
B. MESOBLASTIC NEPHROMA 8960/1
c. MULTILOCULAR CYSTIC NEPHROMA a

IV. NON-EPITHELIAL TUMOURS

A. BENIGN
I. Angiomyolipoma 8860/0
2. Fibroma 8810/0
3. Haemangioma 9120/0
4. Others
B. MALIGNANT

V. MISCELLANEOUS TUMOURS
A. JUXTAGLOMERULAR CELL TUMOUR 8361/1
B. OTHERS

• These numbers refer to the morphology coding of the ICD-0 and SNOMED.
"No code available.

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16 INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF TUMOURS

VI. SECONDARY TUMOURS ____ j6b

VII. UNCLASSIFIED TUMOURS 8000/-c

VIII. TUMOUR-LIKE LESIONS

A. PERSISTENT RENAL BLASTEMA 21400

a
B. MASSIVE RENAL BLASTEMA
c. RENAL DYSGENESIS 20000
D. VASCULAR MALFORMATIONS 24600
E. CYSTS 33400
F. RENAL TUBULAR HYPERPLASIA 72000
G. XANTHOGRANULOMATOUS PYELONEPHRITIS 44070
H. MALAKOPLAKIA 43180
I. OTHERS

"No code available.

b Code specific type.
' /0 for benign; /3 for malignant tumours.
 DEFINITIONS AND EXPLANATORY NOTES

I. EPITHELIAL TUMOURS OF RENAL PARENCHYMA

A. ADENOMA (Fig. 1-7): A benign epithelial tumour of the renal paren-

chyma.
A renal adenoma is composed of uniform cells with regular nuclei seldom
exhibiting mitotic activity. The cytoplasm is scant and may be clear or
granular, or a mixture. The tumour is circumscribed but has no capsule.
Adenomas may be compact, or to a varying extent cystic, and the tumour
cells may either line tubular structures or be arranged in papillary formations.
These descriptive terms may be applied to appropriate tumours but as the
arrangement and proportions of the cells may vary in different areas of any
one tumour, and as there seems to be no practical value in further subdivi-
sions, the tumours are best classified simply as "adenoma".
Rarely, some or all of the cells have finely granular strikingly eosinophilic
cytoplasm, rich in mitochondria, the so-called oncocytic appearance. Tu-
mours entirely composed of such cells may reach a large size, with a
characteristic brownish cut surface.
Although the distinction between adenomas and small grade I carcinomas
may not be possible on a histological basis, single layers of cells with little
cytoplasm and small regular nuclei and the presence of prominent fibrovas-
cular stalks in papillary tumours (Fig. 1) favour the diagnosis of a benign
tumour.
Adenomas rarely cause symptoms and are usually found incidentally
during surgical procedures or radiographic examinations, or at autopsy.
B. CARCINOMA
l. Renal cell carcinoma (Fig. 8-29): A malignant epithelial tumour of the
renal parenchyma.
These tumours often show a glandular pattern with cuboidal and columnar
cells arranged in acinar, tubular, cystic, and papillary formations of varied
size and shape. Some tumours, however, contain large areas where the cells
are in cords or pavemented masses, and a few are entirely solid.
The tumour cells may have a fmely granular cytoplasm, but most often
the cells are large and contain abundant lipid and glycogen in their cyto-
plasm, which appears vacuolated or even quite clear in paraffin sections.
These clear cells are the commonest cell type and may be the only component.
Cell membranes are distinct. Nuclei are usually small, dense and regular
with little mitotic activity. These cytoplasmic and nuclear characteristics
often result in a deceptively bland appearance. A few tumours are entirely
made up of granular cells. Mixtures of these two main cell types are often
seen. Rarely, cells of oncocytic type may be found in malignant tumours. In
-17-
18 INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF TUMOURS
anaplastic tumours, there is pleomorphism, with or without giant cells, and
increased mitotic activity. One variety has spindle-shaped cells and this
spindle cell carcinoma may give rise to confusion with leiomyosarcoma or
invading pelvic carcinomas.
The stroma of renal cell carcinomas varies in its density and extent, but is
usually scant and very vascular with large thin-walled blood spaces which
give a characteristic angiographic appearance. The papillary-cystic and
spindle cell varieties are very much less vascular.
Collections of foamy histiocytes, haemorrhages, necrosis, and calcification
are frequent in these tumours. Cartilaginous and osseous metaplasia have
been described. Around the expanding tumour, there is often dense capsule-
like fibrosis. Blood vessel and lymphatic invasion, renal capsular penetration
and involvement of renal pelvis and hilar structures are common.
These structural variables account for the typically variegated macroscop-
ical appearance.
Cysts may form within tumours and carcinomas may arise in the lining of
a pre-existing cyst. The occurrence of multiple renal tumours, i.e., carcinomas
and adenomas, and cysts is a feature of von Hippel-Lindau disease.
Renal cell carcinoma has been known as renal adenocarcinoma, hyper-
nephroma, and Grawitz tumour.
2. Others
Most renal cell carcinomas arise in the cortex, probably from convoluted
tubules. Rarely, carcinomas originate in the medulla and some of these may
mimic the epithelium of the collecting tubules, i.e., ducts of Bellini, with
appearances ranging from columnar to stratified. Tubular, papillary, trabe-
cular and solid patterns occur, frequently mixed (Fig. 30-33).

II. EPITHELIAL TUMOURS OF RENAL PEL VIS

The classification, definitions and terminology of tumours of the renal

pelvis correspond to the scheme devised for tumours of the urinary bladder.'
A. TRANSITIONAL CELL PAPILLOMA: A papillary tumour with a delicate
fibrovascular stroma covered by regular transitional epithelium indistin-
guishable from that of the normal renal pelvis and not more than six
layers thick.
The individual cells are slender and lie parallel to each other, at right
angles to the basement membrane. Mitotic figures are either extremely rare
or entirely absent. If present, they are located in the basal region. The nuclei
are of uniform size and show finely distributed chromatin. Anaplasia is
absent.
Transitional cell papilloma as defined is very rare, and most papillary
tumours of the renal pelvis are carcinomas.
1
MOSTOFI, F. K., SOBIN, L. H. & TORLONI, H. Histological typing of urinary bladder
tumours. Geneva, World Health Organization, 1973 (International Histological Classification of
Tumours, No. 10).
 HISTOLOGICAL TYPING OF KIDNEY TUMOURS 19

B. TRANSITIONAL CELL CARCINOMA (Fig. 34-36): A tumour of transitional

epithelium showing anaplasia or invasion.
The criteria for anaplasia are: increased cellularity, nuclear crowding,
disturbances of cellular polarity, failure of differentiation from the base to
the surface, irregularity in size and shape of cells, variations of shape and
chromatin pattern of the nuclei, displaced or abnormal mitotic figures, and
giant cells. It must be emphasized that some of these features may be present
in certain inflammatory, reactive or regenerative conditions, without signi-
fying malignancy.
A papillary lesion showing any degree of anaplasia as defined above
should be diagnosed as carcinoma. This diagnosis can and should be made
on the basis of such anaplastic changes, even in the absence of any evidence
of invasion.
The degree of cellular anaplasia forms the basis of histological grading of
these tumours (see Introduction).
The growth patterns of transitional cell carcinomas of the renal pelvis are
similar to those of the bladder, namely, papillary; papillary and infiltrating;
infiltrating; and nonpapillary-noninfiltrating (carcinoma in situ).
As in the bladder, transitional cell carcinoma may contain foci of squa-
mous and/ or glandular elements.
C. SQUAMOUS CELL CARCINOMA (Fig. 37): A malignant epithelial tumour
with cells forming keratin or having intercellular bridges. The tumour
must be of one cell type.
0. ADENOCARCINOMA OF RENAL PELVIS (Fig. 38): A malignant epithelial
tumour with cells forming glands, with varying amounts of mucus
production.
This rare tumour must be distinguished from pyelitis glandularis and
pyelitis cystica, which are more common conditions.
E. UNDIFFERENTIATED CARCINOMA OF RENAL PELVIS: A malignant tumour
of epithelial structure that is too poorly differentiated to be placed in any
of the other groups of pelvic carcinoma.
The term "undifferentiated" is used in a histological sense and is not
employed here as a synonym for cellular anaplasia.
When an undifferentiated pelvic tumour invades the kidney substance,
there may be difficulty in distinguishing it from a primary tumour of the
parenchyma or secondary tumour from elsewhere.

III. NEPHROBLASTIC TUMOURS

The entities described in this section and some of those considered to be

tumour-like lesions, namely, persistent renal blastema, massive renal blas-
tema and renal dysgenesis (VIlLA, Band C below) occur mainly in infants
and children and rarely in adults. Occasionally, and particularly in infants
and children, a renal tumour may contain elements of more than one of the
above entities, indicating that a distinct interrelationship exists.
20 INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF TUMOURS
A. NEPHROBLASTOMA (WILMS' TUMOUR] (Fig. 39-55): A malignant tumour
of primitive nephroblastic tissue which forms structures resembling those
of embryonic kidney. It occurs primarily in children.

This process may result in the formation of recognizable structures or may

halt at less mature stages. A typical nephroblastoma is one in which there is
a mixture of primitive nephroblastic tissue, epithelial cells forming tubules,
glomerulus-like structures, and mesenchymal, often oedematous, tissue,
sometimes with smooth and skeletal muscle, cartilage and bone. While most
nephroblastomas show this mixed pattern, the tumour may consist predom-
inantly or entirely of blastemal, epithelial or mesenchymal elements.
The blastema! pattern shows a predominance of nests of small darkly
stained primitive undifferentiated cells without tubular structures. The epi-
thelial form has tubules l~ned by primitive epithelium. The presence of
tubules distinguishes this from neuroblastoma and immaturity of these cells,
from renal cell carcinoma and pelvic carcinoma. The mesenchymal or stromal
variety is composed typically of stromal elements mixed with some primitive
nephroblastic tissue, i.e., blastema.
Areas of leiomyosarcoma or rhabdomyosarcoma may be present in the
mixed form, as may papillary, mucous or squamous epithelial structures.
Very rarely, foci resembling neuroblastoma (with rosettes) and ganglion cells
occur in a nephroblastoma.
Nephroblastomas are distinguished from persistent and massive renal
blastemas by the presence of stromal elements in the neoplasms and the
typical subcapsular location of the blastemas.

B. MESOBLASTIC NEPHROMA (Fig. 56-59): A tumour composed of spindle

cells resembling smooth muscle arranged in interlacing bundles without
sharp demarcation from the surrounding renal parenchyma, commonly
intermingled with nephrons. These tumours typically occur in newborns
and young infants.

The lesion can involve the kidney in a segmental manner extending from
the renal pelvis to the capsule. It may contain scattered islands of cartilage
as well as cysts. Mitoses, even if frequent, do not necessarily indicate
malignancy. Although in most cases this lesion is benign and often regarded
as hamartomatous in nature, recurrence and local extension have been
observed. In rare cases foci of nephroblastoma or sarcoma occur, and these
should be recorded.
The terms leiomyomatous hamartoma, fetal hamartoma, and congenital
mesoblastic nephroma have also been used.

C. MULTILOCULAR CYSTIC NEPHROMA (Fig. 60-65): A solitary, multilocular

cystic lesion, usually unilateral, containing mesenchymal stroma.
Microscopically, the cysts vary in size and are lined by flattened or hobnail
epithelium. They are set in a loose mesenchymal stroma which in adults is
usually more cellular than in infants and resembles ovarian stroma. This
lesion occurs predominantly in adult females and male infants and is usually
 HISTOLOGICAL TYPING OF KIDNEY TUMOURS 21
benign. Foci of nephroblastoma may be present and very rarely the stroma
is sarcomatous. These should be recorded.
This lesion has also been referred to as multilocular cyst.

IV. NON-EPITHELIAL TUMOURS

A. BENIGN
l. Angiomyolipoma (Fig. 66-69): A benign tumour consisting of a mixture
of fat cells, smooth muscle and tortuous vessels which may have very
cellular or hyalinized thick walls. There may be cellular pleomorphism
with giant cell formation.
This lesion is sometimes a component of the tuberous sclerosis complex,
in which case small and multiple tumours are usually present.
In rare instances local extension and lymph node involvement have been
noted but it is not known whether this represents multicentric development
of the lesion or metastasis. The pleomorphic appearances of the cells may
simulate sarcoma. The absence of lipoblasts and the paucity of mitoses help
to distinguish this lesion from liposarcomas and leiomyosarcomas, respec-
tively.
2. Fibroma (Fig. 70)
These are most frequently found in the medulla. It has been suggested
that some or all medullary fibromas are derived from medullary interstitial
cells and may have an endocrine-like antihypertensive action. The term
renomedullary interstitial cell tumour has been proposed.
3. Haemangioma (Fig. 71)
These occur most commonly in the wall of the renal pelvis but also in the
pyramids and may be difficult to find in the resected kidney because of
collapse of the vessels.
4. Others
These include lipomas, leiomyomas, and neurilemmomas.
B. MALIGNANT (Fig. 72-74)
A variety of malignant non-epithelial tumours may rarely occur in the
kidney. These must be distinguished from spindle cell forms of carcinoma
and from retroperitoneal sarcomas invading the kidney.

V. MISCELLANEOUS TUMOURS

A. JUXTAGLOMERULAR CELL TUMOUR (Fig. 75-77): A tumour of the juxta-

glomerular apparatus.
These are rare renin-secreting tumours, composed of small cells with PAS-
positive cytoplasmic granules, which are arranged in sheets and cords or in
a perivascular manner. Confirmation of the diagnosis depends upon the
demonstration of renin secretion, or on the identification of typical diamond-
shaped inclusions by electron microscopy.
22 INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF TUMOURS
B. OTHERS
Renal involvement may be a feature of adrenal neuroblastoma and
ganglioneuroblastoma. In rare instances, the kidney has been reported to be
the primary site (Fig. 78). Neuroblastoma-like areas with rosettes, and
ganglion cells may occur in nephroblastomas.
Carcinoid tumours (Fig. 79) and teratomas rarely occur in the kidney.
Carcinosarcomas have been described in the kidney but it is probable that
the majority of these are nephroblastomas or carcinomas forming spindle
cells. Tubules engulfed by invading sarcoma may also lead to a mistaken
diagnosis of carcinosarcoma.

VI. SECONDARY TUMOURS

·· Tumours in this category may be metastases, direct extensions, or renal

involvement by systemic neoplastic processes such as lymphoma (Fig. 80)
and leukaemia. Renal failure may be the first clinical manifestation of a
malignant lymphoma. In rare cases the kidney may be the initial or only site
of lymphoma.

VII. UNCLASSIFIED TUMOURS

These are benign or malignant tumours that cannot be placed in any of

the categories described above.

VIII. TUMOUR-LIKE LESIONS

A number of non-neoplastic lesions can resemble renal tumours clinically

and histologically. Abnormalities of development of the kidney may result
in a mixture of primitive renal elements which may be mistaken for nephro-
blastic tumours.
A. PERSISTENT RENAL BLASTEMA (Fig. 81-82): Subcapsular, usually bilateral,
small, often microscopic foci of embryonal nephrogenic tissue without a
primitive mesenchymal component.
Varying degrees of tubular differentiation may occur. The lesions appear
to regress or differentiate with age. They have been found in the non-
neoplastic portion of kidneys containing nephroblastoma, in association with
trisomy 18, and in the kidneys of otherwise normal individuals.
This is also known as nodular renal blastema, persistent nephrogenic
blastema, nodular metanephric blastema and metanephric hamartoma.
B. MASSIVE RENAL BLASTEMA (Fig. 83-84): Embryonal nephrogenic tissue
extensively replacing renal cortical parenchyma.
It appears to be an exaggerated form of persistent renal blastema, being
bilateral, multifocal, and/or diffuse, and may occupy the greater part of the
renal cortex.
It may coexist with nephroblastoma; this should be recorded because of
 HISTOLOGICAL TYPING OF KIDNEY TUMOURS 23
the possibility of bilateral and familial tumours in this setting, and an
association with congenital anomalies.
This lesion has also been referred to as nephroblastomatosis, nephroblas-
tematosis, and hyperplastic renal blastema.
C. RENAL DYSGENESIS (Fig. 85-86): A malformed kidney consisting of cysts
and tubules surrounded by mesenchymal stroma, and admixed with
varying numbers of nephrons.
Cartilage is not infrequent. The lesion may involve the entire kidney or
segments of the kidney, or occur as microscopic foci. In adults the stroma is
more mature. This condition is also known as renal dysplasia.
D. VASCULAR MALFORMATIONS (Fig. 87)
Certain vascular malformations and anastomoses which are not true
angiomas may simulate tumours.
E. CYSTS
Cysts can pose as neoplasms, clinically. Carcinoma may be found m
association with cysts or arising in a cyst wall.
F. RENAL TUBULAR HYPERPLASIA
Focal tubular hyperplasia, e.g., adjacent to foci of pyelonephritis, may be
indistinguishable from a small adenoma.
G. XANTHOGRANULOMATOUS PYELONEPHRITIS (Fig. 88): An inflammatory
condition characterized by the accumulation of large histiocytes with
clear or granular cytoplasm. It may resemble the clear cell renal carci-
noma.
H. MALAKOPLAKIA (Fig. 89)
This chronic inflammatory lesion may resemble renal cell carcinoma with
granular cells but there is inflammation and the histiocytes contain Michae-
lis-Gutmann bodies. A variant of this lesion, located primarily in the cortex
and containing poorly defined Michaelis-Gutmann bodies, is referred to as
megalocytic interstitial nephritis.
I. OTHERS
Squamous metaplasia, particularly in hydronephrosis and in pyelonephri-
tis, may lead to entrapment of squamous cells within the renal parenchyma,
which may mimic squamous cell carcinoma. Large collections of keratin
may result in the formation of a cholesteatoma (Fig. 90).
Fibroepithelial polyp as described in the bladder occurs rarely in the renal
pelvis. Some polypoid structures have a complex epithelial and stromal
arrangement suggesting a hamartoma, so-called pelvic hamartoma (Fig. 91 ).
Adrenal rests are usually subcapsular and may rarely attain a large size.
Adrenal-renal fusion (Fig. 92) may simulate a tumour.
 INDEX

Page Figures

Adenocarcinoma, renal pelvis 19 38

Adenoma. 17 1-7
Adrenal rest . 23
Adrenal-renal fusion 23 92
Angiomyolipoma 21 66-69
Arteriovenous malformation 23 87

Blastema, hyperplastic renal, see Blastema, massive renal 22

Blastema, massive renal 22 83-84
Blastema, nodular metanephric, see Blastema, persistent renal . 22
Blastema, nodular renal, see Blastema, persistent renal 22
Blastema, persistent nephrogenic, see Blastema, persistent renal 22
Blastema, persistent renal 22 81-82

Carcinoid tumour 22 79
Carcinoma, Bellini duct 18 30--33
Carcinoma, renal cell . 17 8-29
Carcinoma, squamous cell 19 37
Carcinoma, transitional cell 19 34-36
Carcinoma, undifferentiated, renal pelvis 19
Carcinoma in situ, renal pelvis 19 34
Carcinosarcoma 22
Cholesteatoma 23 90
Cysts 23

Dysgenesis, renal 23 85-86

Dysplasia, renal, see Dysgenesis, renal 23

Fibroma 21 70

Grawitz tumour, see Carcinoma, renal cell 18

Haemangioma 21 71
Hamartoma, fetal, see Nephroma, mesoblastic 20
Harmartoma, leiomyomatous, see Nephroma, mesoblastic 20
Hamartoma, metanephric, see BlastC<ma, persistent renal 22
Hamartoma, pelvic . 23 91
Histiocytoma, malignant fibrous 21 72
Hypernephroma, see Carcinoma, renal cell 17
Hyperplasia, renal tubular 23

Juxtaglomerular cell tumour 21 75-77

Leiomyoma 21
Leiomyosarcoma 21 74

-25-
26 INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF TUMOURS

Page Figures

Leukaemia 22
Lipoma 21
Liposarcoma 21 73
Lymphoma, malignant 22 80

Malakoplakia 23 89
Metaplasia, squamous 23

Nephritis, megalocytic interstitial 23

N ephroblastoma 20 39-55
Nephroblastematosis, see Blastema, massive renal 22
Nephroblastomatosis, see Blastema, massive renal 22
Nephroma, congenital mesoblastic, see Nephroma, mesoblastic . 20
Nephroma, mesoblastic . 20 56-59
Nephroma, multilocular cystic 20 60-65
Neurilemmoma 21
Neuroblastoma 21 78

Papilloma, transitional cell . 18

Polyp, fibroepithelial 23
Pyelitis, papillary 19
Pyelitis cystica 19
Pyelitis glandularis . 19
Pyelonephritis, xanthogranulomatous .. 23 88

Teratoma. 22
Tumour, renomedullary interstitial cell 21

Vascular malformations 23 87
von Hippel-Lindau disease 18

Wilms' tumour 20 39-55

Unless otherwise stated, all the preparations shown in the photomicrographs

reproduced on the following pages were stained with haematoxylin-eosin.
Fig . 1. Adenoma
Papillae with prominent fibrovasc ular sta lk s. x 100.

Fig . 2 . Adenoma
Same tumour as Fig . 1. Uniform cells with reg ular nuc lei and small amounts of granular cy toplasm. x 160.
Fig. 3 . Adenoma
Papillary and acinar struc tures. Small uniform tumour cells merge with renal parenc hyma. x 1 25.

Fig. 4 . Adenoma
Solid , tubular and papill ary struc tures . x 1 50 .
Fig . 5. Adenoma
Tubul ar pattern . Small uniform ce lls. Oedematous strom a. X 160.

Fig . 6 . Adenoma
Oncocytic variety. Nests and cords of eosinophi lic cells. Oedema taus hypocellular stro ma is typica l of th is
form . x 60.
Fi g. 7. Ad enoma
Oncocytic va riety. Same tu mou r as Fig. 6 . Abundant eos inophilic granular cytop lasm . Small regu lar
nuclei. X 160.

Fig . 8 . Renal cell ca rc inoma

Clea r cell s in large acinar st ruct ures wit h proteinaceous sec reti ons. x 160.
Fig . 9 . Renal ce ll carc inoma
Clea r ce ll s in acinar. tubular and solid arrangements. x 100.

Fig _ 10. Renal cell ca rc inom a

Large clear c ell s in solid and tubular patt ern s. x 60.
Fig. 11. Renal cell carcinoma
Clea r ce lls in tubul ar arrangement. x 100.

Fig . 12. Renal cell carcinoma

Cords of c lear ce ll s separated by thin-walled vasc ular c hannels. X 150.
Fig . 13. Renal cell carcinoma
Thic k c ord s of c lear cells with dilated vascu lar c hannels. x 60.

Fig . 14. Renal cell carcinoma

From a larg e cystic clear ce ll tu mour. x 60 .
Fig . 15. Renal ce ll carcin oma
Co rd s of c lea r cell s with unusuall y abund ant stroma. x 150.

Fi g. 1 6 . Renal cell carc inoma

Papill ary pattern with small ce lls having scant cytoplasm. x 160.
Fig. 17 . Ren al cell carcinoma
Small g ran ul ar ce ll s fo rmin g papi ll ary and tubul ar structures . Collections of lipid-laden histiocytes.
X 160.

Fig. 18. Renal cell ca rcinoma

Granular ce ll s forming papill ary and tubul ar stru ctu res. x 160.
Fig. 19. Renal cell carcinoma
Large granular ce lls forming solid and acinar structures. X 160.

Fig. 20. Renal cell carcinoma

Large granular ce ll s forming tubular and papillary structures. X 160 .
Fig . 21 . Renal cell carcinoma
Large eosinophilic cell s rese mbling oncocytes. x 1 40 .

Fig . 22. Renal cell carcinoma

Cells with vacuo lated cytoplasm . x 110 .
Fig. 23. Renal ce ll carci noma
Mi xture of clea r and granular ce lls in tubular arrangement. X 160.

Fig . 24. Renal ce ll carcinoma

Mixture of clea r and granular ce ll s. x 160 .
Fi g. 25. Renal cell ca rc in oma
Tubu lar and solid patterns. Granular ce lls. x 160 .

Fi g. 26. Renal cell ca rc in oma

Pl eomorphic ce ll s. x 160.
Fig . 27 . Renal cell carcinoma
Solid and spindle cell areas. x 160 .

Fig . 28. Renal cell carcinoma

Spindle cell va riety. x 1 60 .
Fig. 29 . Renal cell carcinoma
Microcysti c stru ctures containing clumps of tumour ce lls. X 100.

Fig . 30. Carcinoma

Tumo ur of medulla resembling ducts of Bellini with papillary proj ectio ns o n renal pelvi s . x 100 .
Fig. 31 . Carcinoma
Same tumour as Fi g. 30. Typica l growth pattern of ··sellini duct carc inomas." x 100.

Fig . 32 . Carc inoma

Papillary portion of tum ou r in Fig . 30. x 100.
Fig. 33 . Carcinoma
Tumour of medu ll a showi ng another growth pattern see n in " Bellini duct ca rcinomas ·. x 100.

Fig . 34. Carc inoma in situ , ren al pelvi s

Anaplasti c cell s have replaced the norma l epithelium . x 160 .
 -
~

-.
' - '
. \· .
~~ . ' ~ . :-

.
...........
..

Fig . 35. Transitional cell carcinoma, renal pelvis

Large papillary tumour. x 40.

Fig . 36. Transitional cell carcinoma, renal pelvis

Papillary and infiltrating tumour , Grade II. x 60 .
Fig . 37 . Squamous cell carcinoma, renal pelvis
Deeply infiltrating tumour, Grade II. x 100.

Fig. 38. Adenocarcinoma, renal pelvis

Superficially infiltrating tumour . x 40 .
Fig. 39. Neph roblastoma
Blastemal, epithel ial and mesenchymal co mponents. x 60.

Fig . 40. Nephroblastoma

Immature glomeruli and tubul es in a predomin antly blastema! fi eld. x 100.
Fig. 41 . Nephroblastoma
Tub ules appea r to arise in islands o f blastem a. Some are lined by mucin-producing cell s. X 100.

Fig. 4 2. Nephro blastom a

Islands of glial ti ssue in a predominan tl y blastema! fi eld . x 100.
Fig . 43. Nephroblastoma
Striated muscle fibres adjacent to primitive epithelial elements. x 160.

Fig. 44. Nephroblastoma

Wall of a cystic tumour partly lined by mucus-secreting columnar epithelium. x 160.
Fig . 45 . Nephroblastoma
Tumour consisting entirely of blastema! elements. X 1 20.

Fig. 46 . Nephroblastoma
Unusual appearance of blastema! tissue: cells with abundant cytoplasm. x 1 50.
Fig . 4 7. Nephroblastoma
Predominantl y st romal area. x 1 30 .

Fig . 48 . Nephroblastoma
Same tumour as Fig. 4 7 composed of epitheli al structures . x 100.
Fig . 49 . Nephroblastoma
Epithelial and blastema! componen ts. x 100.

Fig. 50. Nephroblastoma

Numerous cysts in a predominantly epi thelial field . x 100.
Fig . 51 . Nephroblastoma
Cystic spaces in a mesenchymal tumour. x 160 .

Fig . 52 . Nephroblastoma
Mesenchymal tumour with rare epithelial struc tu res. x 160.
Fig . 53. Nephroblastoma
Blastema! and mesenchymal components. The mesenchymal tissue is more mature than that of
Fig . 52 . X 100.

Fig . 54. Nephroblastoma.

Cyst resembling those in multilocular cystic nephroma. x 160.
Fig. 5 5. Nephroblastoma
Blastema! and epithelial tumour ti ss ue with smoo th muscl e and apparently entrapped renal tub ules
resemblin g mesoblastic nephroma. x 100 .

Fig . 5 6 . Mesobl asti c nephroma

Interlacing bundles of smooth mu scle with entrapped renal tiss ue. x 60.
Fi g . 57. Mesoblastic nephroma
Same tumour as Fig. 56 . X 160.

Fig . 58. Mesoblasti c nephroma

Poorl y diffe rentiated st roma adjacent to norm al renal ti ssue. X 160.
Fig. 59. Mesoblastic nephroma
Mitotic activi ty in poorly differentiated stroma. x 400 .

Fig . 60. Multilocular cystic nephroma

Multiple cysts with varying amounts of intervening stroma surrounded by a thick fibrous capsule. Renal
tissue is compressed. x 9.
Fig. 61 . Multilocular cystic nephroma
Characteristic hotrnail epithelium . x 115.

Fig . 62. Multilocular cystic nephroma

Immature cellular stroma typical of lesions found in adult females . x 150.
Fig . 63. Multilocular cystic nephroma
M ature fibrous st ro ma usually seen in lesions of infants and ch ildren. x 40.

Fig . 64 . Multilocular cystic nephroma

Immature sa rcomatous stroma fro m a predomin antly cysti c tumo ur. X 160.
Fig . 65. Multilocu lar cystic nephroma
Bl astematous ti ssue in an oth erwise typical multilocular cystic nephroma . X 160.

Fig . 66. Angiomyolipom a

Mature fat cell s, thick-walled vesse ls and spindl e-shaped muscle cell s from a co rtical tumour. x 100.
Fig . 67 . Angi omyolipo ma
Thick-walled tortuous vesse ls, partially hyalinized . embedded in highly cellular smooth muscle and
tat. x 100 .

Fig. 68. Angiomyolipoma

Small vessels with thic k mu sc ular walls . x 130.
Fig . 69. Angiomyolipoma
Smooth mu scle with nuclear pl eo morphism . Simul ates sa rcoma . x 1 60 .

Fig . 70. Fibroma

Edge of a partiall y hya linized medullary tumou r with int erl ac ing bu ndl es of fibrous ti ss ue. Seve ral
entrapped tubules. x 100.
Fig. 71. Cavern ous haemangioma
From a peripe lvic tumour whi ch e xtended along the ureter. x 15 .

Fig. 72. Malignant fibrous histiocytoma

X 100.
Fig. 73. Liposa rcoma
X 100 .

Fig. 74. Leiomyosarco ma

X 100.
Fig . 75 . Ju xtag lomerular cell tumour
Poorl y demarcated groups of plump cell s. x 150 .

Fi g . 76 . Ju xtaglomerul ar ce ll tum our

Same tumour as Fig. 75. Abundant cytoplasm wit h ill-defined coa rse granules. x 400.
Fig . 77 . Ju xtaglomerul ar cell tumour
Clusters of cells in a well-vascu larized st roma. x 160.

Fig. 78. Neuroblastoma

From a primary tumour of the kidney. x 250 .
Fig. 79 . Carcinoid tumour
Prim ary in the kidney . x 150 .

Fig . 80. Malignant lymphoma

X 60.
Fig . 81 . Persistent renal bl astema
Subcapsul ar primitive renal tissue from a 2-yea r-old. X 10.

Fig. 82 . Persistent renal blastema

Nodule of primitive blastema in renal cort ex. X 100.
Fig. 83 . Massive renal blastema
Nodules of blastema and metanephric tubules. x 10.

Fig . 84 . Massive renal blastema

High magnifica tion of lesion in Fig. 83. x 160.
Fig. 85 . Renal dysgenesis
Tubules embedded in mesenchymal st roma; cysts and nephrons. x 40 .

Fig . 86. Renal dysgenesis

Dilated tubules surrounded by cellular stroma . From an adult. x 100.
Fig . 87 . Arteriovenous malformation
X 100 .

Fig . 88 . Xanthogranulomatous pyelonephritis .

Lipid-laden macrophages simul ate carcin oma ce ll s. X 1 50 .
Fig . 89. Malakoplakia
Ce lls with large amoun ts of granular cytoplasm . x 250.

Fig . 90 . Cholesteatoma
Tum ou r-like collection of sq uamous ti ssue and keratin extends deeply into parenc hyma. X 60.
Fig . 91. Pelvic ham artoma
Po lypoid stru ctur es composed of ce llular strom a, th ic k-wall ed vessels and covered b y transi tio nal epith e-
lium . X 40.

Fig . 92 . Adrenal-renal fusion

Subco rti cal adrenal ti ssue with entra pped tubules. X 40.
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