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RENAL CELL CARCINOMA

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RENAL CELL CARCINOMA THANK YOU * RCC. Typical cross section of yellowish, spherical neoplasm in one pole of the kidney. Note tumor in the dilated thrombosed ... – PowerPoint PPT presentation

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Title: RENAL CELL CARCINOMA


1
RENAL CELL CARCINOMA
2
RENAL CELL CARCINOMA
  • Also known as
  • Adenocarcinoma,
  • Hypernephroma
  • Hypernephroid tumor
  • Grawitz tumor

3
INTRODUCTION
  • commonest malignant tumor of the kidney in adults
  • Sixth leading cause of Ca death and is more
    common in people of Northern European ancestry
    (Scandinavians North Americans than in those of
    Asian or African descent)
  • Twice as common in men as in women
  • Occurs most commonly between ages 40-70, but the
    disease has been reported in younger people who
    belong to family clusters

4
AETIOLOGY
  • The exact cause is unknown.
  • Risk factors include
  • Cigarette smoking doubles the risk of RCC and
    contributes to as many as one third of all cases.
    The risk appears to increase with the amount of
    cigarette smoking in a dose-dependent fashion.
  • Obesity esp in women increasing body weight has
    a linear relationship with increasing risk.

5
  • RISK FACTORS cont.
  • Hypertension
  • Treatment for hypertension
  • Unopposed estrogen therapy
  • Occupational exposure to petroleum products,
    heavy metals, solvents, coke-oven emissions, or
    asbesto
  • Renal transplantation With its associated
    immunosuppression, renal transplantation confers
    an 80-fold increase in the risk of renal cell
    cancer

6
RISK FACTORS cont.
  • Abuse of phenacetin-containing analgesics
  • Acquired cystic kidney disease associated with
    chronic renal insufficiency
  • Renal dialysis
  • Tuberous sclerosis
  • Genetics At least 4 hereditary syndromes
    associated with renal cell carcinoma are
    recognized
  • von Hippel-Lindau (VHL) syndrome
  • hereditary papillary renal carcinoma (HPRC)
  • familial renal oncocytoma (FRO) associated with
    Birt-Hogg-Dube syndrome (BHDS)
  • Hereditary renal carcinoma (HRC)

7
PATHOLOGY
  • RCC arises from the PCT but occasionally may
    arise from the ducts of Bellini.
  • Renal cancer occurs in both a sporadic
    (nonhereditary) and a hereditary form, and both
    forms are associated with structural alterations
    of the short arm of chromosome 3 (3p).
  • Initially it is encapsulated and solid and is
    golden yellow because of the cholesterol in the
    cells. Later there may be areas of brown or red
    from bleeding into the tumor.
  • As it enlarges it becomes lobulated and displaces
    or invades the calyces, renal pelvis and blood
    vessels.

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PATHOLOGY cont
  • The tumor may spread as follows
  • Directly thru the renal capsule to the
    perinephric fat invading the renal veins and the
    liver. It may grow from the left renal vein to
    occlude the spermatic vein giving rise to a left
    varicocele. It may also occlude the inferior vena
    cava causing bilateral edema of the lower limbs
  • Haematogenously to the liver, lungs, brain and
    bone especially the long bones
  • Via the lymphatics to the para-aortic and hilar
    LN and occasionally to the left supraclavicular
    LN via the thoracic duct.
  • Lung (75)
  • Soft tissues (36)
  • Bone (20)
  • Liver (18)
  • Cutaneous sites (8)
  • Central nervous system (8)

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13
CLINICAL FEATURES
  • Asymptomatic (25-30) of pts are asymptomatic,
    and their RCC are found on incidental Radiologic
    studies
  • Metastatic disease(30)
  • . Most common presentations
  • Hematuria (40)
  • Flank pain (40)
  • Palpable mass in the flank or abdomen (25)

14
  • Other signs and symptoms
  • Weight loss (33)
  • Fever (20)
  • Polyneuromyopathy,
  • Amyloidosis
  • Anemia,
  • Dermatomyositis,
  • Increased erythrocyte sedimentation rate
  • Hypertension (20)
  • Night sweats
  • Malaise
  • Varicocele, usually left sided, due to
    obstruction of the testicular vein (2 of males)

15
  • Paraneoplastic syndromes. The classic triad of
    flank pain, hematuria, and flank mass is uncommon
    (10) and is indicative of advanced disease
  • Hypercalcaemia (5)
  • erythrocytosis,
  • Stauffer syndrome RCC with hepatosplenomegaly,
    elevated alkaline phosphatase and serum
    haptoglobin, and prolonged prothrombin (bleeding)
    time

16
INVESTIGATIONS
  • Lab Studies
  • Laboratory studies in the evaluation of renal
    cell carcinoma should include a workup for
    paraneoplastic syndromes. Initial studies are as
    follows
  • Urine analysis
  • CBC count with differential
  • Electrolytes
  • Renal profile
  • Liver function test
  • Calcium
  • Erythrocyte sedimentation rate
  • Prothrombin time
  • Activated partial thromboplastin time
  • Other tests indicated by presenting symptoms

17
INVESTIGATIONS cont
  • Imaging Studies
  • A large proportion of patients diagnosed with
    renal cancer have small tumors discovered
    incidentally on imaging studies.
  • A number of diagnostic modalities are used to
    evaluate and stage renal masses, including the
    following
  • Excretory urography
  • CT scan
  • Ultrasonography
  • Arteriography
  • Venography
  • MRI

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  • INVESTIGATIONS cont
  • Determining whether a space-occupying renal mass
    is benign or malignant can be difficult.
    Radiologic studies should be tailored to enable
    further characterization of renal masses, so that
    nonmalignant tumors can be differentiated from
    malignant ones.
  • Excretory urography is not used frequently in the
    initial evaluation of renal masses because of its
    low sensitivity and specificity. A small- to
    medium-sized tumor may be missed by excretory
    urography.
  • Contrast-enhanced CT scanning has become the
    imaging procedure of choice for diagnosis and
    staging of renal cell cancer and has virtually
    replaced excretory urography and renal
    ultrasound. In most cases, CT imaging can
    differentiate cystic masses from solid masses and
    supplies information about lymph node, renal
    vein, and inferior vena cava involvement.

23
INVESTIGATIONS cont
  • Ultrasound examination provides excellent staging
    and diagnostic information. Ultrasound provides
    accurate anatomic detail of extrarenal extension
    of tumor, adrenal or lymph node involvement, and
    infiltration of adjacent viscera. Ultrasonography
    can be useful in evaluating questionable cystic
    renal lesions if CT imaging is inconclusive.
    Large papillary renal tumors are frequently
    undetectable by renal ultrasound.
  • Renal arteriography is not used in the evaluation
    of a suspected renal mass as frequently now as it
    was in the past. When inferior vena cava
    involvement is suspected, either inferior
    venacavography or MRI is used. MRI is currently
    the preferred imaging technique. Knowledge of
    inferior vena cava involvement is important in
    planning the vascular aspect of the operative
    procedure.
  • A bone scan is recommended for bony symptoms with
    elevated alkaline phosphatase level.

24
STAGING
  • The Robson modification of the Flocks and Kadesky
    system is uncomplicated and is used commonly in
    clinical practice. This system is employed to
    correlate stage at presentation with prognosis.
    The Robson staging system is as follows
  • Stage I - Tumor confined within capsule of kidney
  • Stage II - Tumor invading perinephric fat but
    still contained within the Gerota fascia
  • Stage III - Tumor invading the renal vein or
    inferior vena cava (A), or regional lymph-node
    involvement (B), or both (C)
  • Stage IV - Tumor invading adjacent viscera
    (excluding ipsilateral adrenal) or distant
    metastases

25
TNM STAGING
  • The tumor, nodes, and metastases (TNM). The major
    advantage of the TNM system is that it clearly
    differentiates individuals with tumor thrombi
    from those with local nodal disease. In the
    Robson system, stage III inferior vena caval
    involvement (IIIA) is the same stage as local
    lymph node metastases (IIIB). Although patients
    with Robson stage IIIB renal carcinoma have
    greatly decreased survival rates, the prognosis
    for patients with stage Robson IIIA renal
    carcinoma is not markedly different from that for
    patients with Robson stage I or II renal
    carcinoma. The TNM classification system is as
    follows

26
  • Primary tumor (T)
  • TX - Primary tumor cannot be assessed
  • T0 - No evidence of primary tumor
  • T1 - Tumor 7 cm or smaller in greatest dimension,
    limited to the kidney
  • T2 - Tumor larger than 7 cm in greatest
    dimension, limited to the kidney
  • T3 - Tumor extends into major veins or invades
    adrenal gland or perinephric tissues but not
    beyond the Gerota fascia
  • T3a - Tumor invades adrenal gland or perinephric
    tissues but not beyond the Gerota fascia
  • T3b - Tumor grossly extends into the renal
    vein(s) or vena cava below the diaphragm
  • T3c - Tumor grossly extends into the renal
    vein(s) or vena cava above the diaphragm
  • T4 - Tumor invading beyond the Gerota fascia
  • Regional lymph nodes (N) - Laterality does not
    affect the N classification
  • NX - Regional lymph nodes cannot be assessed
  • N0 - No regional lymph node metastasis
  • N1 - Metastasis in a single regional lymph node
  • N2 - Metastasis in more than 1 regional lymph
    node
  • Distant metastasis (M)
  • MX - Distant metastasis cannot be assessed
  • M0 - No distant metastasis
  • M1 - Distant metastasis

27
TREATMENT
  • The treatment options for RCC
  • Surgery
  • Radiation therapy
  • Chemotherapy
  • Hormonal therapy
  • Immunotherapy
  • Combination of the above

28
SURGERY
  • Surgical resection remains the only known
    effective treatment for localized renal cell
    carcinoma, and it also is used for palliation in
    metastatic disease.
  • Radical nephrectomy, is the standard procedure
    for treatment of localized renal carcinoma,
    involves
  • complete removal of the Gerota fascia and its
    contents, including a resection of kidney,
  • perirenal fat, and
  • ipsilateral adrenal gland, with or without
    ipsilateral lymph node dissection

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SURGERY
  • The renal vessels are ligated before handling the
    tumor to prevent tumor cell embolization. Radical
    nephrectomy provides a better surgical margin
    than simple removal of the kidney, since
    perinephric fat may be involved in some patients.
    20-30 of patients with clinically localized dx
    develop metastatic dx after nephrectomy . Some
    surgeons believe that the adrenal gland should
    not be removed because of the low probability of
    ipsilateral adrenal metastasis and the morbidity
    associated with adrenalectomy. In the absence of
    distant metastatic dx with locally extensive and
    invasive tumors, adjacent structures such as
    bowel, spleen, or psoas muscle may be excised en
    bloc during radical nephrectomy

31
RADIOTHERAPY
  • Renal cell carcinoma is a relatively radio
    resistant tumor although post operative
    radiotherapy to the renal bed to destroy any
    residual microscopic or gross tumor is advocated
    by some there is currently no evidence to support
    its routine use however it may be beneficial in
    the palliative treatment of skeletal metastasis.

32
IMMUNOTHERAPY
  • Renal cell carcinoma is an immunogenic tumor,
    and spontaneous regressions have been documented.
    Many immune modulators, such as interferon, IL-2
    (aldesleukin Proleukin), bacillus
    Calmette-Guérin (BCG) vaccination,
    lymphokine-activated killer (LAK) cells plus
    IL-2, tumor-infiltrating lymphocytes, and
    nonmyeloablative allogeneic peripheral blood
    stem-cell transplantation, have been tried.

33
CHEMOTHERAPY
  • Renal cell carcinoma is refractory to most
    chemotherapeutic agents because of multidrug
    resistance mediated by p-glycoprotein. Normal
    renal proximal tubules and renal cell carcinoma
    both express high levels of p-glycoprotein.
    Calcium channel blockers or other drugs that
    interfere with the function of p-glycoprotein can
    diminish resistance to vinblastine and
    anthracycline in human renal cell carcinoma cell
    lines

34
  • THANK
  • YOU
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