TUMOURS OF THE KIDNEY AND

URINARY TRACT

DR. NAW MAY EMERALD

WHO CLASSIFICATION OF RENAL TUMOUR
I. Primary tumour II.Secondary tumour
Benign
Cortical adenoma From Lung and breast
Angiomyolipoma
Mesoblastic nephroma
leiomyoma
Malignant
Renal cell carcinoma
Wilm’s tumour
Renal pelvis transitional call
carcinoma
Lymphoma
leiomyosarcoma
 RENAL CELL CARCINOMA
(HYPERNEPHROMA, GRAWITZ TUMOUR)

Origin- renal tubular epithelium

Most- sporadic,
Some (4%) - hereditary: autosomal dominant familial cancer
occurs in young individual
Peak incidence - b/t 6th – 7th decade of life, rare under 40
M:F = 2:1
Predisposing / risk factors

Most significant risk factor

 Tobacco-, Cigarette smoker,s pipe and cigar smokers
Additional risk factors
 Obesity (female) , hypertension,unopposed oestrogen therapy and
exposure to asbestos, petrolium products and heavy matters
 Increased risk in patients with end stage renal disease – chronic
kidney disease and acquired cystic disease and tuberous sclerosis
 Acquired dialysed cystic kidney
 Genetics- VHL genes –involve in both sporadic & familial clear cell
carcinoma
 Von Hippel Lindau Syndrome- chromosome translocation, loss of
expression of the VHL gene (70% risk)
 Chromosome 3p deletion

 Radiation – acquired through treatment of cancer( Cervix & testis)

 Exposure to asbestos, petroleum, heavy metals
TYPES
Clear Cell Carcinomas -most common type, 70% to 80%

Papillary Renal Cell Carcinomas -10% to 15%

Chromophobe Renal Carcinomas - least common, 5 %

MORPHOLOGY
Gross
Solitary (infrequently multiple)
Unilateral (infrequently multiple)
Site: any portion, more common affects
the poles - usually upper pole
Size- approximately 3-15 cm
Renal outline- distorted
roughly spherical & lobular in shape
Expansile growth pattern- has pseudo
capsule(+) formed by compressed
surrounding renal parenchyma
Bisected surface- variegated appearance
Brightly yellow colour (lipochrome pigment)
Gray white tumour necrosis
Red to black areas of haemorrhage
Foci of calcification and cystic degeneration
Yellow flaky friable papillae
Local extension
Striking characteristic of RCC – tendency to invade the renal vein,
grows as solid column , extends up to VC to Rt Ht as snake like
fashion
Hilar region- renal pelvis, calyces, ureter
Renal capsule- perinephric fat, adrenal gld
Satellite nodules in other parts of kidney
Renal cell carcinoma:
typical cross-section of
yellowish, spherical
neoplasm in one pole of
the kidney.
Note the tumor in the
dilated, thrombosed
renal vein.
I. Clear cell type
(70-80%)
95% are sporadic,
GROSS- Usu; occurs as solitary
unilateral lesion
Arise from proximal tubular epithelium
Gross- bright yellow grey white spherical
masses of variable size that distort the
renal outline
HISTOLOGY
• Most common, made up of cells with
clear or granular cytoplasm
• Non- papillary, solid sheets, trabecular
pattern
• +ve for glycogen and lipid with special
stain
• may be familial or association with VHL
disease.
II. Papillary carcinoma (10-
15%)
Both familial & sporadic forms
• 10-15% of all renal cancers
• Arises from distal convoluted tubules
GROSS- Can be multifocal and bilateral
• Haemorrhagic & cystic tumours if it is
large
HISTOLOGY
• Shows papillary growth pattern
• Complex neoplastic papillae with
fibrovascular core
• Lined by cuboidal to low columnar
cells
• Interstitial foam cells in the papillary
core
• Psammoma bodies (+)
 Papillary Renal Cell Carcinoma

The tumor cells have abundant eosinophilic cytoplasm and mildly atypical
nuclei. Interstitial foam cells in the papillary core.
III. Chromophobe
RCC (5%)
• Pale eosinophilic cells
• Distinct cytoplasmic membrane
with perinuclear halo
• Arrange in solid sheets
• Orientated around blood vessels
• Thought to grow from
intercalated cells of collecting
ducts
• Has excellent prognosis than
clear and papillary type
chromophobe renal cell
carcinoma: a well-
circumscribed solitary mass
in the kidney . The cut
surface may be yellow,
beige, or brown. A central
scar is seen in this
specimen.
DIAGNOSIS OF RCC

Clinical features

investigations
Clinical features

Diversities of sign and symptoms

A. Triad of classical diagnostic features
1. Painless haematuria
 90% haematuria –frank or may be microscopic
 Intermittant and painless , May remain silent until it attains a
large size
2. Costovertebral pain- 10%
3. Palpable mass
ALL THREE ARE SEEN IN 10% OF CASES
*Has tendency to metastasize widely before giving rise
to any local s/s
B. General constitutional symptoms
 Persistant pyrexia
 Anaemia,anorexia, weakness, malaise, wt loss ( during
asymptomatic growth)
C. Secondary menifestations/ metastatic s/s
 Bone pain, pathological #-33%
 Haemoptysis-50%
 Jaundice The most common
 Neurological s/s sites of metastasis
 Skin nodules – lungs (50%),
 Hypoadrenalism bones(33%) L/N,
liver, adrenal ,
brain ,
D. Paraneoplastic syndrome - due to abnormal hormone /like
substance production
Polycythemia (Secondary )- erythropoietin
Hypercalcemia- ectopic PTH like
Hypertension - renin
Feminization & musculinization – ectopic androgen
Cushing’s syndrome-ectopic ACTH
Gynaecomastia-ectopic GTH
Galactorrhoea- ectopic prolactin
Leukemoid reaction, eosinophilia
Secondary amyloidosis
 PROGNOSIS

Average 5 – year survival rate is about 70% and

as high as 95% in the absence of distant metastasis
Reduced to 60% if renal vain invasion or extension into
perinephric fat
WILM’S TUMOUR (NEPHROBLASTOMA)

Early childhood malignant tumour, derived from renal

blastema cells
Age- peak 2-4 yrs old
Large expansile, spherical mass
Usually unilateral, bilateral in 5-10% of cases
Genetics- deleted chromosome 11
 MORPHOLOGY
Gross
Cut sectionVariegated appearance:
myxoid area, soft fleshy area, solid
grey hyaline cartilagenous t/s
Histology
Nests and sheets of primitive
blastema cells
Abortive tubules and glomeruli
Spindle cell stroma
Area of necrosis
Cholesterol crystals, foam cells

Wilms' Tumor : Three components

The triphasic nature of Wilms Tumor - The epithelial elements attempting to form rosettes.
, nodules of blastema and myxoid stroma.
Wilms' Tumor : Epithelium – sheets of densely packed small
rosettes(+) blue cells(Blastema

unfavorable histology contain anaplasia

Clinical features

Large abdominal mass, unilateral ; May extend across the mid

line and down to pelvis
Haematuria
Fever, pain in abdomen
Intestinal obstruction
Hypertension
Pulmonary metastasis
Prognosis
Depends on degree of anaplasia
>90% long time survival with chemoRx, radio Rx and Sx
PELVICALYCEAL UROTHELIAL CARCINOMA

Papillary TCC (Transitional cell carcinoma)

Associated with analgesic abuse (phenacetin)
C.F
 Haematuria
 Flank pain
 Urinary obstruction
URINARY BLADDER TUMOUR
 TUMOURS OF THE URINARY BLADDER

1. Urothelial tumours (transitional tumours)

2. Exophytic papilloma
3. Inverted papilloma
4. Papillary urothelial neoplasms of low malignant potential
5. Low-grade & high grade papillary urothelial cancer
6. CIS ( flat noninvasive urothelial carcinoma)
7. Mixed carcinoma
8. Adenocarcinoma
9. Small cell carcinoma
10.Sarcoma
 WHO CLASSIFICATION**
Primary tumours 2. Mesenchymal
1. Epithelial (95%)
Leiomyoma/
Benign leiomyosarcoma
 Transitional papilloma
 Squamous papilloma

Malignant
 Transitional cell carcinoma-
90%(Urothelial carcinoma)
 Squamous cell ca.--7%
 Adenocarcinoma
 Small cell carcinoma
 Undifferentiated
Predisposing factors of bladder tumours
Cigerette smoking – absorption of aromatic amine from cigarette
smoke and their excretion in urine
Occupational Exposure to chemical carcinogen (Aryl amines)
- Aniline dye (beta napthylamine)
-Occupational hazard- textile dye, rubber, cable, petroleum,
leather, printing press paint, sewage workers
-cancers appear 15-40 years after the first exposure
Shistoma haematobium infection (squamous cell carcinoma)
- An established risk
- Ova are deposited in the bladder wall and incite a brisk chronic
inflammatory response that induces progressive
mucosqamous metaplasia and dysplasia and neoplasia
Genetics – Several acquired genetic alterations have
been observed.; activation of growth factor signeling
pathway
genetic deficiency of enzymes that can metabolise
chemicals, risk factors of bladder tumours
Others
Analgesic (eg. Phenacetin ) abuse
Heavy long term exposure to cyclophosphamide
treatment- causes haemorrhagic cystitis and increased
risk of bladder cancer
Irradiation
UROTHELIAL TUMOURS
 Represent 90% of all bladder tumours
 Varies from small benignl esions to fatal malignant tumours
 Many are multifocal at presentation
 Can occur any sites where there is urothelium – from renal
pelvis to distalurethra

(2) Distinct PRECURSOR LESIONS to invasive urothelial carcinoma

1. Non invasive papillary tumours- most common, originates from

papillary urothelial hyperplasia

2. Flat non invasive papillary carcinoma- CIS

Transitional cell carcinoma/urothelial
carcinoma of bladder
Most common type of bladder tumour
M:F = 3:1
Age incidence – between 50-80 yrs
Arising from bladder urothelium, wide field multicentric (involving
renal pelvis, calyces, ureter)
Recurrence is common
Local extension than distant metastasis
MORPHOLOGY
Purely papillary pattern to nodular or flat
(4) Morphologic patterns
 MORPHOLOGY
Gross - Insitu / Invasive -
Single/multicentric
Site – most arise from lateral or
posterior wall of the bladder base

Histology –
Urothelial carcinoma - Neoplastic
transitional epithelial cells
arranged in papillary structures,
invasive nets
Papillary Urothelial Carcinoma – Gross morphology
TCC - bladder

Papillary Urothelial Carcinoma, Low-grade

HISTOLOGIC GRADING –

Degree of differentiation of neoplastic cells

Stratification & polarization of neoplastic cells
Nuclear atypia, hyperchromasia and mitotic activity

Tumour Staging - Depth of invasion

( lamina propia, muscle layer, serosa)

PROGNOSIS – Extent of invasion and spread at the time of

diagnosis is the most important factor
SQUAMOUS CELL CARCINOMA OF U BLADDER
Predisposing factors
 Chronic irritation (bladder stone)
 Chronic inflammation ( schistosomiasis)
 Diverticular formation
Morphology
 Gross – Flat / nodular
 Histology – Neoplastic squamous cells in sheets
Poor histological grade and tumour stage

ADENOCARCINOMA
Predisposing factor – urachal remnant, cystitis
Histology – Neoplastic glands ( variable differentiation)
DIAGNOSIS
Clinical Features
 Painless, frank haematuria
 Frequency, urgency, dysuria (S/S of UTI)
 Features of obstructive urine flow (hydronephrosis,
pyonephrosis)
 Features of invasion & fistula formation (vagina & rectum)
Investigations
 Urine cytology
 Cystoscopic exam
 Biopsy and histology
 Radiology ( IVP, USG, CT & MRI)
 Blood urea and electrolytes