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Renal cell carcinoma: clinical feature

Renal cell carcinoma (RCC) often presents with vague symptoms in its early stages, and patients may remain asymptomatic. As the disease progresses, common clinical features may include: Hematuria: Blood in the urine is a common sign, often presenting as either visible blood or microscopic hematuria. Flank Pain: Discomfort or pain in the side or lower back, potentially associated with tumor expansion or pressure on surrounding structures. Palpable Abdominal Mass: A palpable lump or mass in the abdomen may be felt during a physical examination. Weight Loss and Fatigue: Advanced stages may lead to unintended weight loss and fatigue. Paraneoplastic Syndromes: Some RCCs produce hormones or cytokines, leading to paraneoplastic syndromes, such as elevated erythropoietin levels causing polycythemia. Pathology: Histological Subtypes: Clear cell, papillary, chromophobe, and other rare subtypes exist. Clear cell is the most common and typically associated with worse prognosis. Genetic and Molecular Alterations: Mutations in tumor suppressor genes (e.g., VHL, PBRM1, BAP1), chromosomal deletions, and alterations in cellular pathways contribute to RCC development. Tumor Grading: Fuhrman grade and ISUP grading system assess tumor differentiation, with higher grades indicating a poorer prognosis. Tumor Necrosis: Histologic coagulative tumor necrosis is an independent predictor of outcome. Imaging: CT Scan: High-resolution computed tomography (CT) imaging is the primary modality for RCC diagnosis and staging, providing detailed visualization of the tumor, surrounding structures, and potential metastases. MRI: Magnetic resonance imaging (MRI) offers additional soft tissue contrast and is particularly useful for characterizing renal masses. Ultrasound: Ultrasound may be used for initial assessment and is effective in detecting solid masses but may have limitations in characterizing complex lesions. Nuclear Medicine: Positron emission tomography (PET) scans can be used for staging and detecting distant metastases. Prognosis: TNM Staging: The tumor, node, metastasis (TNM) staging system stratifies patients based on the extent of disease. Anatomic Factors: Invasion into the renal vein or inferior vena cava, perinephric fat extension, and involvement of the urinary collecting system impact prognosis. Histopathological Factors: Clear cell histology, higher tumor grade, and tumor necrosis are associated with a worse prognosis. Molecular Markers: Various molecular markers, genetic alterations, and gene expression profiles can provide additional prognostic information. Survival Rates: Prognosis varies widely, with early-stage disease having better survival rates compared to advanced stages. Advances in targeted therapies and immunotherapy have improved outcomes for some patients with advanced RCC.

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RENAL CELL CARCINOMA: Clinical feature, Pathology,
prognosis
DR. SUMIT KUMAR
Assistant Professor
NEIGRIHMS, Shillong
Treatment decisions are tailored to individual cases, taking into account factors such as the patient's overall health
and the specific characteristics of the cancer.
Kidney neoplasms can be primary or secondary. Secondary tumors are often clinically insignificant and discovered
postmortem.
Renal Cell Carcinomas (RCCs): 80-85% of primary renal neoplasms; originate in the renal cortex.
Transitional Cell Carcinomas: Approximately 8%; affect the renal pelvis.
Other Parenchymal Epithelial Tumors: Rare; includes oncocytomas, collecting duct tumors, and renal sarcomas.
Nephroblastoma (Wilms Tumor): Common in children (5-6% of primary renal tumors).
The incidence of RCC varies geographically, with higher rates in developed countries.
Risk factor include smoking, obesity, hypertension, family history of kidney cancer, and certain genetic conditions
like VHL disease.
Surgical removal of the affected kidney (nephrectomy) is often the primary treatment for localized disease.
Advanced cases may require additional approaches, including targeted therapies, immunotherapy, or radiation.
• Global Variation: Varies widely globally, with the highest rates in the Czech Republic and North
America.
• INDIA: 21TH rank
• Male Dominance: twofold more common in males than females.
• Age Distribution: Predominantly occurs in the 6th to 8th decade, with a median age at diagnosis
around 64 years.
• Survival Rates: Comparable 5-year survival for African American and White American patients
(over 75%).
• Extent of Disease (SEER Data, 2009-2015):
• Localized Disease: 65 percent.
• Regional Disease: 17 percent.
• Metastatic Disease: 16 percent.
• Unstaged: 3 percent.
• Mortality and Survival Rates:
• Improved Survival: Five-year survival rate doubled from 34 % in 1954 to 75 % from 2009 to
2015.
• Mortality vs. Incidence: Incidence has risen more than threefold higher than the mortality rate.
• Early Detection Impact: Improved survival attributed to earlier detection of smaller tumors (<4
cm) and curative surgical treatment.
RISK
FACTOR:
RCC
Smoking
Hyperten
sion
Obesity
Acquired
Cystic
Disease
and CKD
Occupati
onal
Exposure
Analgesic
s
Genetic
Factors
Cytotoxic
Chemoth
erapy
Chronic
Hepatitis
C
Infection
Sickle Cell
Disease
Kidney
Stones
Modifiers
Independent Link: Hypertension
independently predisposes to RCC.
Biological Unknowns: How hypertension
connects to RCC remains unclear
Risk Increase: Cigarette smoking
linked to higher RCC risk.
Severity Impact: More smoking,
more advanced disease at diagnosis.
Diabetes Impact: Modest RCC risk increase in some studies.
Alcohol Effect: Alcohol intake associated with lower RCC risk.
Additional Factors: Diet, reproductive factors, and prior
radiation therapy may modify RCC risk.
Childhood Survivors: Increased RCC risk, especially with prior
kidney-directed radiation or cisplatin exposure
Association: History of kidney stones
tied to higher RCC and transitional cell
carcinoma risk.
Study Limitations: Some study
limitations, including recall bias.
Specific Risk: Sickle cell trait
and disease increase risk for
renal medullary carcinoma
Virus Impact: Chronic infection
significantly increases RCC risK
Childhood Association: Childhood
chemotherapy linked to translocation
RCC later on
Second RCC Risk: Higher risk in those treated
for one renal cancer, especially at a younger
age.
Hereditary Syndromes: Several syndromes
associated with RCC; genetic factors play a role
Chronic Use Risk: Prolonged analgesic
use, especially aspirin, linked to RCC.
Usage Impact: Risk varies with type;
NSAIDs associated with higher risk.
Carcinogen Link: Exposure to
cadmium, asbestos, and petroleum
byproducts increases RCC risk.
Genetic Connection: May be linked to
pathogenic variants, like VHL.
Dialysis Risk: Up to 30x higher RCC risk
in dialysis patients.
Incidence Correlation: Higher risk with
lower eGFR in non-dialysis patients.
Weight Impact: Excess body weight
increases RCC risk.
Better Prognosis: Higher weight
associated with lower stage and grade;
longer survival in metastatic cases.
• Many patients remain asymptomatic until
advanced stages.
• Approximately 25% present with distant
metastases or advanced locoregional disease.
• In a series of 701 patients: Incidentally diagnosed
patients had significantly better disease-specific
survival at five years (76% vs. 44% in symptomatic
cases).
• Multivariate analysis attributes the difference to
lower stage and histologic grade at diagnosis.
• In one review of 309 consecutive patients with
RCC, the most common presenting symptoms
were hematuria, abdominal mass, pain, and
weight loss
1.Classic Triad (Present in ≤9%):
• Flank Pain
• Hematuria
• Palpable Abdominal Renal Mass
2.Hematuria:
• Indicates Tumor Invasion of Collecting System
• Severe Cases Cause Clots and Colicky Discomfort
• Clot Presence Significant for Unexplained Hematuria
3.Abdominal/Flank Mass:
• Common with Lower Pole Tumors
• Characteristics: Firm, Homogeneous, Nontender
• Movement with Respiration
4.Scrotal Varicoceles (11% in Males):
• Typically Left-Sided
• Fail to Empty Recumbent: Suspicion of Gonadal Vein Obstruction
5.Inferior Vena Cava Involvement:
• Manifestations: Lower Extremity Edema, Ascites, Hepatic Dysfunction, Pulmonary Emboli
• Possible Budd-Chiari Syndrome
6.Metastatic Disease Symptoms:
• Sites: Lungs, Lymph Nodes, Bone, Liver, Brain
• Diagnosis: Often Through Biopsy of Accessible Metastasis Alongside Abdominal CT-Confirmed Renal Mass.

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Renal cell carcinoma: clinical feature

  • 1. RENAL CELL CARCINOMA: Clinical feature, Pathology, prognosis DR. SUMIT KUMAR Assistant Professor NEIGRIHMS, Shillong
  • 2. Treatment decisions are tailored to individual cases, taking into account factors such as the patient's overall health and the specific characteristics of the cancer. Kidney neoplasms can be primary or secondary. Secondary tumors are often clinically insignificant and discovered postmortem. Renal Cell Carcinomas (RCCs): 80-85% of primary renal neoplasms; originate in the renal cortex. Transitional Cell Carcinomas: Approximately 8%; affect the renal pelvis. Other Parenchymal Epithelial Tumors: Rare; includes oncocytomas, collecting duct tumors, and renal sarcomas. Nephroblastoma (Wilms Tumor): Common in children (5-6% of primary renal tumors). The incidence of RCC varies geographically, with higher rates in developed countries. Risk factor include smoking, obesity, hypertension, family history of kidney cancer, and certain genetic conditions like VHL disease. Surgical removal of the affected kidney (nephrectomy) is often the primary treatment for localized disease. Advanced cases may require additional approaches, including targeted therapies, immunotherapy, or radiation.
  • 3. • Global Variation: Varies widely globally, with the highest rates in the Czech Republic and North America. • INDIA: 21TH rank • Male Dominance: twofold more common in males than females. • Age Distribution: Predominantly occurs in the 6th to 8th decade, with a median age at diagnosis around 64 years. • Survival Rates: Comparable 5-year survival for African American and White American patients (over 75%). • Extent of Disease (SEER Data, 2009-2015): • Localized Disease: 65 percent. • Regional Disease: 17 percent. • Metastatic Disease: 16 percent. • Unstaged: 3 percent. • Mortality and Survival Rates: • Improved Survival: Five-year survival rate doubled from 34 % in 1954 to 75 % from 2009 to 2015. • Mortality vs. Incidence: Incidence has risen more than threefold higher than the mortality rate. • Early Detection Impact: Improved survival attributed to earlier detection of smaller tumors (<4 cm) and curative surgical treatment.
  • 4. RISK FACTOR: RCC Smoking Hyperten sion Obesity Acquired Cystic Disease and CKD Occupati onal Exposure Analgesic s Genetic Factors Cytotoxic Chemoth erapy Chronic Hepatitis C Infection Sickle Cell Disease Kidney Stones Modifiers Independent Link: Hypertension independently predisposes to RCC. Biological Unknowns: How hypertension connects to RCC remains unclear Risk Increase: Cigarette smoking linked to higher RCC risk. Severity Impact: More smoking, more advanced disease at diagnosis. Diabetes Impact: Modest RCC risk increase in some studies. Alcohol Effect: Alcohol intake associated with lower RCC risk. Additional Factors: Diet, reproductive factors, and prior radiation therapy may modify RCC risk. Childhood Survivors: Increased RCC risk, especially with prior kidney-directed radiation or cisplatin exposure Association: History of kidney stones tied to higher RCC and transitional cell carcinoma risk. Study Limitations: Some study limitations, including recall bias. Specific Risk: Sickle cell trait and disease increase risk for renal medullary carcinoma Virus Impact: Chronic infection significantly increases RCC risK Childhood Association: Childhood chemotherapy linked to translocation RCC later on Second RCC Risk: Higher risk in those treated for one renal cancer, especially at a younger age. Hereditary Syndromes: Several syndromes associated with RCC; genetic factors play a role Chronic Use Risk: Prolonged analgesic use, especially aspirin, linked to RCC. Usage Impact: Risk varies with type; NSAIDs associated with higher risk. Carcinogen Link: Exposure to cadmium, asbestos, and petroleum byproducts increases RCC risk. Genetic Connection: May be linked to pathogenic variants, like VHL. Dialysis Risk: Up to 30x higher RCC risk in dialysis patients. Incidence Correlation: Higher risk with lower eGFR in non-dialysis patients. Weight Impact: Excess body weight increases RCC risk. Better Prognosis: Higher weight associated with lower stage and grade; longer survival in metastatic cases.
  • 5. • Many patients remain asymptomatic until advanced stages. • Approximately 25% present with distant metastases or advanced locoregional disease. • In a series of 701 patients: Incidentally diagnosed patients had significantly better disease-specific survival at five years (76% vs. 44% in symptomatic cases). • Multivariate analysis attributes the difference to lower stage and histologic grade at diagnosis. • In one review of 309 consecutive patients with RCC, the most common presenting symptoms were hematuria, abdominal mass, pain, and weight loss
  • 6. 1.Classic Triad (Present in ≤9%): • Flank Pain • Hematuria • Palpable Abdominal Renal Mass 2.Hematuria: • Indicates Tumor Invasion of Collecting System • Severe Cases Cause Clots and Colicky Discomfort • Clot Presence Significant for Unexplained Hematuria 3.Abdominal/Flank Mass: • Common with Lower Pole Tumors • Characteristics: Firm, Homogeneous, Nontender • Movement with Respiration 4.Scrotal Varicoceles (11% in Males): • Typically Left-Sided • Fail to Empty Recumbent: Suspicion of Gonadal Vein Obstruction 5.Inferior Vena Cava Involvement: • Manifestations: Lower Extremity Edema, Ascites, Hepatic Dysfunction, Pulmonary Emboli • Possible Budd-Chiari Syndrome 6.Metastatic Disease Symptoms: • Sites: Lungs, Lymph Nodes, Bone, Liver, Brain • Diagnosis: Often Through Biopsy of Accessible Metastasis Alongside Abdominal CT-Confirmed Renal Mass.
  • 7. 1. Anemia: • Precedes RCC Diagnosis in 29-88% of Advanced Cases • Disproportionately Severe, Normocytic or Microcytic • Often Associated with Anemia of Chronic Disease 2. Hepatic Dysfunction (Stauffer Syndrome): • Uncommon, 21% Paraneoplastic Alkaline Phosphatase Elevation • Associated with Fever, Weight Loss, Fatigue • May Result from Tumor Cytokine Production (GM-CSF, IL-6) • Nephrectomy May Improve Hepatic Dysfunction 3. Fever: • Up to 20% of Patients • Intermittent, Accompanied by Night Sweats, Anorexia, Weight Loss, Fatigue • Unclear Origin 4. Hypercalcemia: • Occurs in 15% of Advanced RCC • Mechanisms: Lytic Bone Metastases, PTHrP Overproduction, IL-6 Action • NSAID (Indomethacin) Administration may be Effective 5.Cachexia: • Significant Weight Loss and Muscle Atrophy 6.Erythrocytosis: • 1-5% of Advanced RCC • Due to Constitutive Erythropoietin Production • Impaired Regulation of Hypoxia-Inducible Proteins 7.Secondary (AA) Amyloidosis: • Up to 5% of Patients • Reflects Chronic Inflammatory Response • Amyloid Fibrils Composed of Serum Amyloid A Protein Fragments 8.Thrombocytosis: • Rare, Poor Prognosis • Associated with Tumor IL-6 Production 9.Polymyalgia Rheumatica-like Syndrome: • Resembles Polymyalgia Rheumatica • Unresponsive to Prednisone, Often Corrected by Nephrectomy
  • 8. Imaging Modalities: • Abdominal CT or Ultrasonography: Initial tests for suspected RCC or incidental findings. • CT Advantages: High sensitivity; useful for detailed assessment. • Ultrasonography: Less sensitive but aids in distinguishing simple cysts from tumors. • MRI: Utilized when CT or ultrasonography is inconclusive or iodinated contrast is contraindicated. • MRI Advantages: Assess tumor growth into the collecting system or vessels; helpful in neoplasm diagnosis. Criteria for Simple Cyst Differentiation (Ultrasonography): • Cyst is round, sharply demarcated with smooth walls. • No echoes within the cyst (anechoic). • Strong posterior wall echo, indicating good transmission through a cyst. • If criteria met, no further evaluation needed due to low malignancy likelihood. CT Findings (Simple Cyst vs. Tumor): • Simple Cyst: Smooth appearance, no enhancement with intravascular contrast, water- density. • Tumor: Thickened irregular walls or septa, enhancement after contrast injection. MRI with Dynamic Gadolinium Contrast: • Useful in distinguishing papillary or clear cell RCC from other solid renal neoplasms. • Does not replace the need for tissue diagnosis. • Sensitivity for papillary RCC: 86%, Specificity: 92%. Angiography: • Indications: Rarely necessary; useful for preoperative vasculature mapping. • Alternatives: CT or MR angiography preferred for nephron-sparing surgery planning.
  • 10. •Specific CT Findings: •Enhancement Pattern: Less intense enhancement compared to clear cell. •Cystic Changes: May have central necrosis or cystic components. •Specific CT Findings: •Intermediate Enhancement: Between clear cell and papillary types. •Distinctive Histology: Pale, eosinophilic cytoplasm with perinuclear halos. •Specific CT Findings: •Hypervascular Mass: Enhances intensely in the arterial phase. •Clear Cytoplasm: Due to lipid and glycogen content. •exophytic appearance •Characteristics: Solid, enhancing lesion in the kidney. •Specific Findings: •Hypervascularity: Rapid enhancement during the arterial phase. •Washout: Contrast washes out during the venous and delayed phases. Enhancing Renal Mass: Clear Cell RCC: Papillary RCC: Chromophobe RCC:
  • 11. •CT Findings: •Fat Content: Presence of macroscopic fat (negative Hounsfield Units) is characteristic. •Enhancement: May enhance with contrast. •CT Features: •Enhancement Pattern: Often shows homogeneous enhancement. •Central Scar: May have a central stellate scar. •Simple Renal Cysts: •CT Appearance: Smooth, thin-walled, anechoic (no internal echoes). •Enhancement: No enhancement with contrast. •Complex Renal Cysts: •CT Appearance: Irregular, thickened walls, internal septations, or solid components. •Enhancement: May show variable enhancement patterns. •Specific CT Findings: •Aggressive Features: Invasion of adjacent structures, heterogeneous enhancement. •High-Grade Appearance: Mimics features of a sarcoma. Sarcomatoid RCC: Cystic Renal Lesions (Cyst Differentiation): Renal Angiomyolipoma (AML): Oncocytoma:
  • 12. • Classification by Cell Type and Growth Pattern: • RCCs were initially classified based on cell type and growth pattern. • The classification has evolved to consider morphology, growth pattern, cell of origin, histochemical, and molecular characteristics. • Subtypes of RCC: • Clear Cell (75 to 85 percent): Most common subtype. • Papillary (10 to 15 percent): Characterized by papillary structures. • Chromophobe (5 to 10 percent): Distinctive large, polygonal cells. • Oncocytic (3 to 7 percent): Cells with eosinophilic, granular cytoplasm. • Collecting Duct (Very Rare): Uncommon subtype. • Molecularly Defined RCCs (Rare): Subtypes identified based on molecular characteristics. • Unclassified (Up to 5 percent): Tumors that do not fit into specific subtypes. • Prognosis and Unclassified RCCs: • Up to 5 percent of RCCs are considered unclassified. • Reports suggest worse prognosis compared to clear cell cancers, but findings are inconsistent and may depend on clinicopathologic features. • Sarcomatoid Features: • RCC with sarcomatoid features is not considered a distinct subtype. • Sarcomatoid dedifferentiation can occur in any histologic subtype of RCC. • Small Tumors and Malignancy: • Tumors smaller than 3 cm were previously thought to be benign adenomas. • Current understanding recognizes that even small tumors can represent carcinomas, and size alone may not be sufficient for the malignant-benign distinction.
  • 13. 1.Clear Cell Carcinomas (CCC): • Origin: Arise from the proximal tubule. • Macroscopic Appearance: Can be solid or, less commonly, cystic. • Association: Specifically associated with von Hippel- Lindau (VHL) disease. • Prognosis: Poor prognosis associated with higher nuclear grade or the presence of a sarcomatoid pattern, especially in early-stage disease. • Variants: Multilocular cystic clear cell RCC has a more favorable prognosis compared to other clear cell carcinomas. 2.Genomic Alterations: Chromosome-Level Alterations: • Loss of 3p (91 to 94 percent): Contains genes associated with RCC, including VHL, BAP-1, PBRM1, among others. • Gain of 5q (67 to 69 percent). • Monosomy or partial loss of 14q (42 to 45 percent). • 7q gain (20 percent). • 8p deletion (32 percent).
  • 14. • Common dedifferentiation in RCC, not a distinct subtype. • Histology: Presence of sarcoma-like cells, resembling fibrosarcoma or fibrous histiocytoma. • Grading: Categorized as grade IV; sarcomatoid component can range from 1 to 100 percent. • Prognosis: Higher sarcomatoid proportion may indicate worse prognosis, but no validated cutoff. • Aggressive Features: Often accompanied by necrosis (90%), microvascular invasion (30%), and rhabdoid features (25%). • Molecular Insights: Molecular profiles similar to epithelioid component; specific alterations like NF2, BAP1, CDKN2A, and EZH2 enrichment. • Treatment and Prognosis: Rapid disease progression, less responsive to antiangiogenic therapies; potential robust response to immune checkpoint inhibitors. • Immunotherapy Targets: CD274 (PD-L1 gene) amplifications, higher PD-L1 protein expression, increased CD8+ T cell infiltration, and upregulation of interferon-gamma response genes. • Clinical Implications: Molecular alterations offer potential h featuring large numbers of discohesive rhabdoid tumor cells (arrows)
  • 15. • Represents approximately 15% of kidney cancers, originating from the proximal tubule. • Classification: • Historical Types (Type I and Type II): Once classified based on cytopathologic findings, but this classification is no longer used due to poor reliability. • Current Classifications: MET status (MET-driven versus not) and morphology (biphasic, Warthin-like, solid, papillary renal neoplasm with reverse polarity). • Genomic Features: • Type 1 Papillary RCC: • Typically presents with stage I or II disease, with a relatively favorable prognosis. • Associated with hereditary papillary RCC with activating germline MET pathogenic variants. • Somatic MET pathogenic variants identified in 10 to 20% of nonhereditary cases. • Altered MET status or increased chromosome 7 copy number identified in 81% of cases. • Biomarker-driven classification proposed in advanced papillary RCC based on MET pathogenic variants. • Type 2 Papillary RCC: • Often associated with aggressive disease, advanced stage, and poor prognosis. • Many tumors previously categorized as type 2 have been reclassified into other molecularly defined RCC subtypes. • Less likely to have alterations in the MET pathway compared to type 1. Notice the frequent psammomatous calcifications (arrows) and macrophages filled with hemosiderin pigment;
  • 16. Histology: • Composed of darker cells than clear cell carcinoma. • Originates from the intercalated cells of the collecting system. • Lacks abundant lipid and glycogen. Genetic Characteristics: • Hypodiploid number of chromosomes. • Does not delete the 3p chromosomal genetic locus. • Comparative genomic hybridization studies show a variety of abnormalities, including loss of chromosomes 1, 2, 6, 10, 13, 17, or 21. • Upregulation of the KIT oncogene on the cell membranes. Prognosis: • Disease Progression: May have a lower risk compared to clear cell carcinomas, potentially influenced by lower stage at presentation. • Recurrence and Mortality Rates: Vary; one series with 392 patients showed a 9% recurrence rate and 6% cancer-related mortality at a median follow-up of 44 months. • Survival Rates: In one series of 124 patients, the five-year disease-specific survival was initially better than clear cell carcinoma (78% vs. 60%), but this difference disappeared when corrected for stage. TCGA Project Findings: • Analysis of 66 chromophobe RCCs. • Mitochondrial DNA and gene expression analysis highlight mitochondrial function as an important component of disease biology. • Genomic rearrangements show recurrent structural breakpoints within the TERT promoter region, correlating with highly elevated TERT expression. showing the characteristic perinuclear clearing and distinctive (plant-like) cellular borders
  • 17. Characteristics: Uncommon tumors with 3 to 7 percent incidence among renal tumors. Composed of well-differentiated oncocytes with intensely eosinophilic granular cytoplasm due to numerous mitochondria. Typically unilateral and single; multiple and bilateral cases associated with tuberous sclerosis complex (TSC) and Birt-Hogg-Dubé syndrome. Histological Challenges: Distinguishing from RCC can be difficult histologically. Some solid tumors initially thought to be RCCs may actually be oncocytomas. Genetic Characteristics: Chromosomal analyses show heterogeneity, including loss of Y and 1, rearrangements involving CCND1 at 11q13, involvement of 12q12-13, and loss of 14q. Cyclin D1 (CCND1) overexpression and rearrangement can help distinguish oncocytoma from chromophobe RCC. Behavior and Prognosis: Behave in a generally benign fashion despite a growth rate similar to RCC. Well encapsulated, rarely invasive, and rarely associated with metastases. Coexistence with RCC: Coexisting RCC identified in 10 to 32 percent, especially in cases of diffuse oncocytic nodules (renal oncocytosis). Close monitoring advised, and treatment considered for rapidly growing tumors. Risk of Metachronous Tumors: Low risk after resection; retrospective series (median follow-up seven years) showed 4 percent subsequent renal tumors, including oncocytomas and RCCs.
  • 18. Primary tumor (T) T category T criteria TX Primary tumor cannot be assessed T0 No evidence of primary tumor T1 Tumor <_ 7 cm in greatest dimension, limited to the kidney T1a Tumor <_4 cm in greastest dimension, limited to the kidney T1b Tumor >4 cm but < 7 cm in greatest dimension, limited to the kidney T2 Tumor >7 cm in greatest dimension, limited to the kidney T2a Tumor >7 cm but < 10 cm in greatest dimension, limited to kidney T2b Tumor>10 cm , limited to kidney T3 Tumor extends into major veins or perinephric tissues, but not into the ipsilateral adrenal gland and not beyond Gerota’s fascia T3a Tumor extends into the renal vein or its segmental branches, or invades the pelvicalyceal system, or invades perinal and/ or renal sinus fat but not beyond Gerota’s fascia T3b Tumor extends into the vena cava beloiw the diaphragm T3c Tumor extends into the vena cava above the diaphragm or invades the wall of the vena cava T4 Tumor invades beyond Gerota’s fascia ( including contiguous extension into the ipsilateral adrenal gland) Regional lymph nodes (N) N category N criteria NX Regionlal lymph node cannot be assessed N0 No regional lymph node metastases N1 Metastasis in regional lymph node(s) Distant metastasis (M0 Mctegory Mcriteria M0 No distant metastasis M1 Distant metastasis
  • 19. Initial evaluation Evidence of distant metastases on imaging Yes No Metastatic disease confirmed by biopsy? Yes No 1 to 3 metastases with resectable primary? <4cm? Nephrectomy and metastasectomy Candidate for upfront cytoreductive nepectomy? Small renal mass: Partial nephrectomy preferred Is the patient a candidate for definitive surgery? Observation : systemic therapy only for recurrence Cytoreductive nephrectomy followed by systemic therapy Systemic therapy :possible cytoreductive neppherectomy if major response Choice of procedure Radical nephrectomy preffered Centrally located Suspected lymph node involvement Renal vein or IVC involvement Direct extension into the ipsilateral adrenal gland Systemic therapy, palliative care Partial nephrectomy preffered: Solitary kidney Multiple, small, and/or bilateral tumors With or at risk for chronic renal disease Yes No No Yes Yes No Yes No
  • 20. STAGE DISCRIPTION 5- YR SURVIVAL RATE I Localized tumor, no invasion beyond the kidney >90% II Localized tumor, some invasion into nearby areas 75-95% III Tumor extends beyond the kidney and nearby areas 59-70% Stage IV: •Survival Improvement: Overall survival for stage IV RCC has improved in the era of immunotherapy and targeted therapy. •In subsequent studies of patients receiving either targeted therapies (such as pazopanib or sunitinib) or checkpoint inhibitor immunotherapy (with nivolumab plus ipilimumab), median overall survival was over two years (approximately 28 months)and almost five years (56 months), respectively
  • 21. 1.Urinary Collecting System Invasion: • Stage III Impact: Significantly worse disease-specific and overall survival. • Data: Multivariate analysis in Stage III cases showed 34% vs. 59% and 30% vs. 52% five-year rates. 2.Venous Involvement (T3a, T3b, T3c): • Impact: Recognized as a prognostic factor in the TNM system. • Data: Invasion of renal vein, inferior vena cava below diaphragm (T3b), and wall invasion or extension above diaphragm (T3c) adversely affects prognosis. 3.Perinephric Fat Extension (T3a): • Conflicting Data: Inconsistent impact on prognosis. • Studies: Varied results; two studies found no difference compared to T1 and T2 tumors, while others identified it as a prognostic factor.
  • 22. 1.Tumor Type: • Impact: Controversial, with clear cell histology possibly associated with poorer cancer-specific survival. • Aggressive Variants: Collecting duct, renal medullary carcinomas, and histologies with sarcomatoid or rhabdoid features indicate a more aggressive nature. 2.Tumor Grade: • Correlation: Higher histologic grade independently correlates with lower survival. • Systems: Fuhrman grade and ISUP grading system are commonly used. • Survival Rates: Grades 1 associated with higher (89%) and grades 3 to 4 with lower (46%) five-year survival rates. 3.Tumor Necrosis: • Predictor: Histologic coagulative tumor necrosis independently predicts outcomes, especially in clear cell and chromophobe RCC. • Integrated Staging: Part of staging systems like SSIGN score
  • 23. • Karnofsky performance status score <80 • Time from original diagnosis to initiation of targeted therapy <1 year • Hemoglobin less than the lower limit of normal • Serum calcium greater than the upper limit of normal • Neutrophil count greater than the upper limit of normal • Platelet count greater than the upper limit of normal Favorable risk: None of the above risk factors present. Intermediate risk: 1 or 2 of the above risk factors present. Poor risk: 3 or more risk factors present.
  • 25. Renal cell carcinomas (RCCs) are the most common primary tumor arising in the kidney, accounting for approximately 80 to 85 percent of such tumors Risk factors associated with a significantly increased incidence of RCC include smoking, obesity, hypertension, and others Abnormalities of the von Hippel- Lindau (VHL) tumor suppressor gene are implicated in most cases of clear cell RCC (both sporadic and familial). Abdominal computed tomography (CT) or ultrasound can confirm the presence of a mass, distinguish RCC from a benign cyst, and assess the extent of disease. RCC is more frequently being diagnosed incidentally as a consequence of increased use of imaging procedures for other reasons For patients presenting with localized renal cell carcinoma (RCC), the tumor, node, metastasis (TNM) staging system provides the primary prognostic information
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