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RCC

Renal Cell Carcinoma

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Usman Yusuf
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10 views

RCC

Renal Cell Carcinoma

Uploaded by

Usman Yusuf
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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RENAL CELL

CARCINOMA
Dr Abdullahi Abdulwahab-Ahmed
Department of Surgery
Usmanu Danfodiyo University Sokoto
LEARNING OBJECTIVES

At the end of this lecture, students should be able to understand-


 the epidemiologic features of RCC
 the Pathology and pathophysiology of RCC
 The clinical approach to an RCC patient
 the current investigative treatment protocol and the future trend in
the management RCC
EPIDEMIOLOGY

 Grawitz’s tumour or hypernephroma, is an adenocarcinoma of the


kidney.
 In its common occurrence, it arises from the epithelium of the
proximal convoluted tubule of the nephron.
 Sporadic form by far the commonest.
 It account for 85% of all renal malignancies
 Male preponderance 3:2, 2:1.
 Peak age of incidence in the 7th decade.
 There is increase incidence of the disease as a result of wide use of
abdominal ultrasounds.
AETIOLOGICAL FACTORS

 Genetics:
von-Hippel-Lindau (VHL): renal and pancreatic cysts, phaeochromocytoma,
cerebellar haemangioblastoma and RCC (50%).
Loss of copies of tumour suppressor gene 3p25-26.
Accumulation of hypoxia inducible factor (HIF⍺) leads to angiogenesis- tumour
formation.
Birt-Hogg-Dube (BHD): AD, disorder of fibrofolliculomas on the skin, pulmonary cyst
with spontaneous pneumothorax and renal tumours (chromophobe RCC &
Oncocytoma) derived from distal nephron tubules.
17p11.2 12q the genetic abnormality resulting in mal function of folliculin a tumour
supressor gene
Trisomy 7 & 17: activation of c-met proto-oncogene leads to various kind of tumours including
papillary RCC.
AETIOLOGICAL FACTORS

Environmental/lifestyle:
 Smoking
 Obesity
 Hypertension
 Low socioeconomic class
 Urban dwelling
 Phenacetin
 Exposure to asbestos
 Thorium dioxide
AETIOLOGICAL FACTORS

 Nutrition:
 Vitamins A, C, E, fruits and vegetables are protective.

 Anatomic:
 Polycystic kidney
 Horseshoe kidney
PATHOLOGY

 RCC is an adenocarcinoma arising from the proximal convoluted


tubule epithelium
 Multifocal in about 20% of cases
 Predominantly solid and tan colour on cut surface
 Cystic in 10-25% cases
 10-20% cases contain calcifications
 Its rarely infiltrative, possesses false capsule of compressed normal
tissue.
PATHOLOGY

 Histological types:
 Conventional/ clear cell- 70-90% of all RCC is an highly vascular tumour,
cytoplasm is reach in mitochondria, eosinophilic granules and cholesterol &
glycogen.
 Papillary RCC- 10-15% of RCC there are papillary, tubular and solid variant. 40%
are multifocal.
 Chromophobe RCC- 4-5% od RCC arises from the cortical portion of the
collecting ducts. On microscopy possesses perinuclear halo of microvesicles
 Others:
 Collecting duct of Bellini-rare seen in the young and of poor prognosis
 Medullary cell type-arises from calyceal epithelium seen in young sickle cell disease,
poor prognosis
 Sarcomatoid type- infiltrative, poorly differentiated variant of any type RCC. Poor
prognosis
PATHOLOGY

 SPREAD:
 Direct to adrenal gland-7.5% in tumour >5cm
 Through renal capsule into renal vein seen in 5% cases at presentation; ivc
and ra.
 By lymphatics to hilar and para-aortic lymph nodes
 By haematogenous spread to lungs-75%, bone-20%, liver-18% and brain-
8%
PATHOLOGY

 Staging:
 Robinson’s Modification of Kadesky-
1. Confined to kidney, true capsule not breached
2. Extends to perinephric fat but within Gerota
3. Involves renal vein, ivc or lymph nodes
a. Venous invasion

b. Venous and perinephric fat invasion

c. Lymph node invasion

4. Local direct spread or distant spread


a. Involvement of adjacent organs

b. Distant spread
PATHOLOGY

STAGING
Management

 Diagnosis

 Imaging:

 Ultrasound: Initial evaluation.

 CT scan: Gold standard for diagnosis and staging.

 MRI: Useful in specific cases (e.g., assessing renal vein involvement).

 Biopsy: Typically avoided unless diagnosis is uncertain


Management

 Localized disease:

 Surgery: Radical nephrectomy or partial nephrectomy.

 Ablative therapies: For non-surgical candidates.

 Advanced/metastatic disease:

 Targeted therapies (e.g., tyrosine kinase inhibitors like sunitinib).

 Immunotherapy (e.g., checkpoint inhibitors such as nivolumab).

 Cytoreductive nephrectomy in select cases.


Prognosis

 Prognosis depends on stage at diagnosis.

 5-year survival for localized RCC is over 70%, but drops significantly in
metastatic disease.

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