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Renal cell carcinoma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D., Serge Korjian M.D., Shanshan Cen, M.D. [2]

Synonyms and keywords: RCC; Renal cell CA; Kidney cancer; Kidney carcinoma; Kidney CA; Grawitz tumor; Hypernephroma

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Faizan Sheraz, M.D. [2]

Overview

Historical Perspective

Renal cell carcinoma was first described in 1826. Following contradictory hypotheses regarding the origin of renal tumors, it was not until 1960 that Oberling and colleagues showed that renal carcinomas originate from renal cells.

Classification

Classification of renal cell carcinomas according to histopathological subtypes is based on the 1997 classification by Heidelberg and colleagues. Classification may also be according to the stage of renal cell carcinoma, which often is based on Robson classification system or the tumor-lymph node-metastasis (TNM) system.

Pathophysiology

The pathophysiology of renal cell carcinomas plays an important role in differentiating different types of renal cell carcinomas and in choosing appropriate targeted medical therapies. Sporadic forms of clear cell renal carcinomas, the most common form of renal cell carcinomas, have similar pathophysiological mechanisms to those of von Hippel Lindau (VHL) disease. On the other hand, MET proto-oncogene seems to play a role in the disease pathogenesis of papillary forms of renal cell carcinoma. Uniquely also, oncocytomas are benign tumors that arise from type A intercalated cells, whereas chromophobe renal cell carcinoma arises from type B intercalated cells.

Causes

The causes of renal cell carcinoma include von hippel-lindau (VHL), hereditary paragangliomas, leiomyomatosis, birt-hogg-dube syndrome, and several other genetic factors.

Differentiating Renal cell carcinoma from other Diseases

The differential diagnosis of renal cell carcinomas includes metastastic disease, cysts, abscesses, lymphomas, and other benign and malignant tumors, and associated syndromes.

Epidemiology and Demographics

In 2011, the age-adjusted prevalence of kidney cancer was 85.9 per 100,000 in the United States, the incidence was 15.28 per 100,000 persons. The male to female ratio is approximately 2 to 1. The median age of presentation is typically 60 years old.

Risk Factors

Common risk factors of renal cell carcinoma include cigarette smoking, obesity, hypertension, end-stage renal failure, acquired cystic renal disease, acetaminophen and analgesic drug use, asbestos or trichloroethylene exposure, tuberous sclerosis, von-Hippel Lindau, hereditary paraganglioma, leiomyomatosis, and birt-hogg-dube syndrome.

Screening

There are currently no guidelines for screening for renal cell carcinoma.

Natural History, Complications and Prognosis

Common complications of renal cell carcinoma include hypertension, hypercalcemia, budd-chiari syndrome, hepatic vein thrombosis, polycythemia, renal failure, metastasis. Prognosis is generally poor, and the 5-year mortality of renal cell carcinoma is approximately 73.2%.

Diagnosis

Diagnostic study of choice

A needle biopsy should always be performed when the finding of a renal mass is detected on imaging.

History and Symptoms

Common symptoms of renal cell carcinoma include hematuria, flank pain, palpable abdominal mass,weight loss and anorexia.

Physical Examination

Common physical examination findings of renal cell carcinoma include low body mass index, high blood pressure, palpation of abdominal mass, auscultation of abdominal bruit, varicocele, muscle atrophy, skin pallor, facial flushing, and supraclavicular lymphadenopathy.

Laboratory Findings

Laboratory findings of renal cell carcinoma include anemia, polycythemia, hypercalcemia, elevated ESR, elevated liver function tests, elevated alkaline phosphatase, elevated lactate dehydrogenase, elevated serum creatinine, hematuria, and cancer cells on urine cytology.

Electrocardiogram

There are no ECG findings associated with renal cell carcinoma.

X-ray

There are no x-ray findings associated with renal cell carcinoma. However, an x-ray may be helpful in the diagnosis of pulmonary metastasis of renal cell carcinoma.

Ultrasound

Ultrasound may be helpful in the diagnosis of renal cell carcinoma. Ultrasound may be helpful when CT scan results are equivocal.

CT scan

Renal CT scan may be helpful in the diagnosis of renal cell carcinoma. CT may be used to detect neoplastic masses that may define renal cell carcinoma or metastasis of primary cancer.

MRI

Renal MRI may be helpful in the diagnosis of renal cell carcinoma. Due to the use of IV gadolinium in MRI, the risk of nephrogenic systemic fibrosis (NSF) must always be considered.

Other Imaging Findings

PET CT and angiography may be helpful in the diagnosis or following-up patients with renal cell carcinoma. Bone scan is recommended in patients with elevated alkaline phosphatase to rule out bone metastasis.

Other Diagnostic Studies

There are no other diagnostic studies associated with renal cell carcinoma.

Treatment

Medical treatment

The medical therapies of renal cell carcinoma include chemotherapy, hormone treatment, immunotherapy, and targeted therapy.

Surgery

Surgery is the mainstay of treatment for renal cell carcinoma. Partial nephrectomy and ablation are recommended for patients who develop small renal masses. For patients with locally advanced renal tumors, radical nephrectomy is recommended. Moreover, radical nephrectomy or organ sparing treatment, along with the use of interferon alfa, is also used as part of a more aggressive management plan in cases with metastatic renal tumors.

Primary prevention

Primary prevention strategies include early screening, changing lifestyle, decreasing exposure to occupational risk factors, and controlling of hypertension.

Secondary prevention

There are no established measures for the secondary prevention of renal cell carcinoma.


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Historical Perspective

Historical Perspective

Overview

Renal cell carcinoma was first discovered by Koenig in 1826. In 1960, Oberling and colleagues proved that renal carcinomas originate from renal tubular cells.

Historical Perspective

  • Renal cell carcinoma was first described by Koenig in 1826, when he published his pathological classification of renal tumors. At the time, he classified renal tumors according to their macroscopic forms: scirrhous, steatomatous, fungoid, and medullary.[1]
  • In 1883, Grawitz, a German pathologist, noted that alveolar (clear cell) renal tumors differed from their papillary counterparts. He stated that clear cell renal tumors, characterized by their lipomatous components, are neoplastic tumors called hypernephromas that originate from transformed adrenal cortical tissue into renal cortical tissue.[2]
  • On the other hand, Sudeck and Robin disagreeably hypothesized that both alveolar and papillary tumors originate from the same renal tubular origin.[3]
  • It was not until 1960 when Oberling and colleagues proved finally that renal carcinomas originate from renal tubular cells in their publication “Ultrastructure of the clear cells in renal carcinomas and its importance for the demonstration of their renal origin”.[4]

References

  1. ↑ Buskirk SJ, Smalley SR, Zincke H (2000). Kidney and ureteral cancer. In: Gunderson LL, Tepper JE (eds) Clinical radiation oncology, 1st edn. pp. 863–878. Unknown parameter |City= ignored (help); Unknown parameter |published= ignored (help)
  2. ↑ Grawitz VP (1883). “Die sogenannten lipome de niere”. Pathol Anat. 93: 39.
  3. ↑ Buskirk SJ, Smalley SR, Zincke H (2000). Kidney and ureteral cancer. In: Gunderson LL, Tepper JE (eds) Clinical radiation oncology, 1st edn. pp. 863–878. Unknown parameter |City= ignored (help); Unknown parameter |published= ignored (help)
  4. ↑ OBERLING C, RIVIERE M, HAGUENAU F (1960). “Ultrastructure of the clear cells in renal carcinomas and its importance for the demonstration of their renal origin”. Nature. 186: 402–3. PMID 14428164.
Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Renal cell carcinoma may be classified according to histologic appearance of the tumor into 6 subtypes: conventional (clear cell), papillary, chromophobe, oncocytoma, collecting duct, and unclassified.

Classification

The following table classifies renal cell carcinoma according to histologic appearance and differentiates sporadic from hereditary forms of renal cell carcinoma. Clear type (also called Conventional type) renal cell carcinoma is considered the most common type of renal carcinoma. The most common classification of renal cell carcinoma is based on the histopathological appearance of the tumor. There are currently six subtypes of renal cell carcinoma, most common of which are the conventional (also called clear cell) renal carcinoma, accounting for approximately 75% of all cases.[1] Renal cell carcinoma may also be clinically classified based on the staging of the tumor, as shown below.

Histologic Appearance

The following table summarizes the incidence of various histological types of renal tumors:

Heidelberg Classification Renal Cell Carcinoma According to Histological Appearance (1997)[1][2]
Histologic Appearance Incidence (%)
Conventional (Clear Cell) 75
Papillary 12
Chromophobe 4
Oncocytoma 4
Collecting Duct < 1
Unclassified 3 – 5
Adapted from Cohen HT, McGovern FJ. Renal-cell carcinoma.N Engl J Med. 2005; 353:2477-90

More than 70% of renal cell carcinomas are clear cell carcinomas. Papillary carcinomas are the second most common renal cell carcinomas. The least common types of renal cell carcinomas are collecting-duct renal cell carcinomas, accounting for less than 1% of all cases.[1]

References

  1. ↑ 1.0 1.1 1.2 Cohen HT, McGovern FJ (2005). “Renal-cell carcinoma”. N Engl J Med. 353 (23): 2477–90. doi:10.1056/NEJMra043172. PMID 16339096.
  2. ↑ Kovacs G, Akhtar M, Beckwith BJ, Bugert P, Cooper CS, Delahunt B; et al. (1997). “The Heidelberg classification of renal cell tumours”. J Pathol. 183 (2): 131–3. doi:10.1002/(SICI)1096-9896(199710)183:2<131::AID-PATH931>3.0.CO;2-G. PMID 9390023.


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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

The pathophysiology of renal cell carcinomas plays an important role in differentiating between the types of renal cell carcinomas and in choosing appropriate targeted medical therapies. Sporadic forms of clear cell renal carcinomas, the most common form of renal cell carcinomas, have similar pathophysiological mechanisms to those of von Hippel-Lindau (VHL) disease. On the other hand, MET proto-oncogene seems to play a role in the disease pathogenesis of papillary forms of renal cell carcinoma. Uniquely also, oncocytomas are benign tumors that arise from type A intercalated cells, whereas chromophobe renal cell carcinoma arises from type B intercalated cells.

Pathophysiology

Sporadic Forms of Clear Cell Renal Carcinoma

  • Although Von Hippel-Lindau (VHL), an autosomal dominant disorder, is characterized by the mutation of the VHL gene – a tumor suppressor gene – and the consequential development of renal clear cell carcinomas following the silencing of the remaining normal VHL gene, the gene itself has been identified to be similarly responsible of the development of sporadic forms of renal clear cell carcinomas.[1]

Familial Forms of Clear Cell Renal Carcinoma

  • The translocation and loss of chromosome 3p at the site 3p14 is hypothesized to be responsible for the development of renal clear cell carcinomas in other familial forms not related to VHL gene.[14]

Papillary Renal Cell Carcinoma

Papillary renal cell carcinoma has 2 histologic types:

Types of Papillary Renal Cell Carcinoma[1]
Type Cell Size Cytoplasm Nucleus Nucleolus
Type I Small Pale Small and oval Indistinct
Type II Large Abundant eosinophilic Large and spherical Distinct
Adapted from Cohen HT, McGovern FJ. Renal-cell carcinoma. N Engl J Med. 2005 Dec 8;353(23):2477-90

Oncocytoma and Chromophobe Renal Cell Carcinoma

Collecting Duct Renal Cell Carcinoma

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Cohen HT, McGovern FJ (2005). “Renal-cell carcinoma”. N Engl J Med. 353 (23): 2477–90. doi:10.1056/NEJMra043172. PMID 16339096.
  2. ↑ 2.0 2.1 Iliopoulos O, Kibel A, Gray S, Kaelin WG (1995). “Tumour suppression by the human von Hippel-Lindau gene product”. Nat Med. 1 (8): 822–6. PMID 7585187.
  3. ↑ 3.0 3.1 Chen F, Kishida T, Duh FM, Renbaum P, Orcutt ML, Schmidt L; et al. (1995). “Suppression of growth of renal carcinoma cells by the von Hippel-Lindau tumor suppressor gene”. Cancer Res. 55 (21): 4804–7. PMID 7585510.
  4. ↑ Iliopoulos O, Levy AP, Jiang C, Kaelin WG, Goldberg MA (1996). “Negative regulation of hypoxia-inducible genes by the von Hippel-Lindau protein”. Proc Natl Acad Sci U S A. 93 (20): 10595–9. PMC 38198. PMID 8855223.
  5. ↑ Cockman ME, Masson N, Mole DR, Jaakkola P, Chang GW, Clifford SC; et al. (2000). “Hypoxia inducible factor-alpha binding and ubiquitylation by the von Hippel-Lindau tumor suppressor protein”. J Biol Chem. 275 (33): 25733–41. doi:10.1074/jbc.M002740200. PMID 10823831.
  6. ↑ Ohh M, Park CW, Ivan M, Hoffman MA, Kim TY, Huang LE; et al. (2000). “Ubiquitination of hypoxia-inducible factor requires direct binding to the beta-domain of the von Hippel-Lindau protein”. Nat Cell Biol. 2 (7): 423–7. doi:10.1038/35017054. PMID 10878807.
  7. ↑ Tanimoto K, Makino Y, Pereira T, Poellinger L (2000). “Mechanism of regulation of the hypoxia-inducible factor-1 alpha by the von Hippel-Lindau tumor suppressor protein”. EMBO J. 19 (16): 4298–309. doi:10.1093/emboj/19.16.4298. PMC 302039. PMID 10944113.
  8. ↑ Ohh M, Yauch RL, Lonergan KM, Whaley JM, Stemmer-Rachamimov AO, Louis DN; et al. (1998). “The von Hippel-Lindau tumor suppressor protein is required for proper assembly of an extracellular fibronectin matrix”. Mol Cell. 1 (7): 959–68. PMID 9651579.
  9. ↑ Feldman DE, Spiess C, Howard DE, Frydman J (2003). “Tumorigenic mutations in VHL disrupt folding in vivo by interfering with chaperonin binding”. Mol Cell. 12 (5): 1213–24. PMID 14636579.
  10. ↑ Hergovich A, Lisztwan J, Barry R, Ballschmieter P, Krek W (2003). “Regulation of microtubule stability by the von Hippel-Lindau tumour suppressor protein pVHL”. Nat Cell Biol. 5 (1): 64–70. doi:10.1038/ncb899. PMID 12510195.
  11. ↑ Zhou MI, Wang H, Ross JJ, Kuzmin I, Xu C, Cohen HT (2002). “The von Hippel-Lindau tumor suppressor stabilizes novel plant homeodomain protein Jade-1”. J Biol Chem. 277 (42): 39887–98. doi:10.1074/jbc.M205040200. PMID 12169691.
  12. ↑ Zhou MI, Wang H, Foy RL, Ross JJ, Cohen HT (2004). “Tumor suppressor von Hippel-Lindau (VHL) stabilization of Jade-1 protein occurs through plant homeodomains and is VHL mutation dependent”. Cancer Res. 64 (4): 1278–86. PMID 14973063.
  13. ↑ Zhou MI, Foy RL, Chitalia VC, Zhao J, Panchenko MV, Wang H; et al. (2005). “Jade-1, a candidate renal tumor suppressor that promotes apoptosis”. Proc Natl Acad Sci U S A. 102 (31): 11035–40. doi:10.1073/pnas.0500757102. PMC 1182408. PMID 16046545.
  14. ↑ Cohen AJ, Li FP, Berg S, Marchetto DJ, Tsai S, Jacobs SC; et al. (1979). “Hereditary renal-cell carcinoma associated with a chromosomal translocation”. N Engl J Med. 301 (11): 592–5. doi:10.1056/NEJM197909133011107. PMID 470981.
  15. ↑ Delahunt B, Eble JN (1997). “Papillary renal cell carcinoma: a clinicopathologic and immunohistochemical study of 105 tumors”. Mod Pathol. 10 (6): 537–44. PMID 9195569.
  16. ↑ Gunawan B, von Heydebreck A, Fritsch T, Huber W, Ringert RH, Jakse G; et al. (2003). “Cytogenetic and morphologic typing of 58 papillary renal cell carcinomas: evidence for a cytogenetic evolution of type 2 from type 1 tumors”. Cancer Res. 63 (19): 6200–5. PMID 14559804.
  17. ↑ Lubensky IA, Schmidt L, Zhuang Z, Weirich G, Pack S, Zambrano N; et al. (1999). “Hereditary and sporadic papillary renal carcinomas with c-met mutations share a distinct morphological phenotype”. Am J Pathol. 155 (2): 517–26. doi:10.1016/S0002-9440(10)65147-4. PMC 1866853. PMID 10433944.
  18. ↑ Schmidt L, Duh FM, Chen F, Kishida T, Glenn G, Choyke P; et al. (1997). “Germline and somatic mutations in the tyrosine kinase domain of the MET proto-oncogene in papillary renal carcinomas”. Nat Genet. 16 (1): 68–73. doi:10.1038/ng0597-68. PMID 9140397.
  19. ↑ Zbar B, Glenn G, Lubensky I, Choyke P, Walther MM, Magnusson G; et al. (1995). “Hereditary papillary renal cell carcinoma: clinical studies in 10 families”. J Urol. 153 (3 Pt 2): 907–12. PMID 7853572.
  20. ↑ Zhuang Z, Park WS, Pack S, Schmidt L, Vortmeyer AO, Pak E; et al. (1998). “Trisomy 7-harbouring non-random duplication of the mutant MET allele in hereditary papillary renal carcinomas”. Nat Genet. 20 (1): 66–9. doi:10.1038/1727. PMID 9731534.
  21. ↑ Fischer J, Palmedo G, von Knobloch R, Bugert P, Prayer-Galetti T, Pagano F; et al. (1998). “Duplication and overexpression of the mutant allele of the MET proto-oncogene in multiple hereditary papillary renal cell tumours”. Oncogene. 17 (6): 733–9. doi:10.1038/sj.onc.1201983. PMID 9715275.
  22. ↑ Nickerson ML, Warren MB, Toro JR, Matrosova V, Glenn G, Turner ML; et al. (2002). “Mutations in a novel gene lead to kidney tumors, lung wall defects, and benign tumors of the hair follicle in patients with the Birt-Hogg-Dubé syndrome”. Cancer Cell. 2 (2): 157–64. PMID 12204536.
  23. ↑ Khoo SK, Kahnoski K, Sugimura J, Petillo D, Chen J, Shockley K; et al. (2003). “Inactivation of BHD in sporadic renal tumors”. Cancer Res. 63 (15): 4583–7. PMID 12907635.
  24. ↑ da Silva NF, Gentle D, Hesson LB, Morton DG, Latif F, Maher ER (2003). “Analysis of the Birt-Hogg-Dubé (BHD) tumour suppressor gene in sporadic renal cell carcinoma and colorectal cancer”. J Med Genet. 40 (11): 820–4. PMC 1735328. PMID 14627671.

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Causes

Causes

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References

Differentiating Renal cell carcinoma from other Diseases

Differentiating Renal cell carcinoma from other Diseases


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Renal cell carcinoma must be differentiated from other diseases presenting as hematuria, weight loss and a renal mass. The differentials include Wilm’s tumor, rhabdoid kidney disease, polycystic kidney disease, pheochromocytoma, dysplastic kidney, hydronephrosis, nephroma, angiomyolipoma and rhabdomyosarcoma.


Differentiating renal cell carcinoma from other diseases

Renal cell carcinoma should be differentiated from other diseases presenting as a hematuria, weight loss and a renal mass. The differentials include the following:

Disease Symptoms Signs Diagnosis Comments
Abdominal Pain Hematuria Headache Abdominal mass Abdominal tenderness Ultrasonography CT scan Histology
Renal cell carcinoma + + +/- + –
  • Ultrasound (US) may be helpful when CT scan results are equivocal. It is noteworthy to mention that not all renal cell carcinomas are detectable on ultrasound.
 Both CT and MRI may be used to detect neoplastic masses that may define renal cell carcinoma or metastasis of the primary cancer. CT scan and use of intravenous (IV) contrast is generally used for work-up and follow-up of patients with renal cell carcinoma. The histological pattern of renal cell carcinoma depends whether it is papillary, chromophobe or collecting duct renal cell carcinoma.
Wilms tumor + + – + +
  • Wilms tumor has a triphasic appearance.
  • It is comprised of 3 types of cells:
  • All the 3 types are not required for the diagnosis of Wilms tumor.
  • Primitive tubules and glomeruli are often seen comprised of neoplastic cells.
  • Beckwith and Palmer reported in NWTS the different histopathologic types of Wilms tumor to categorize them based on prognosis.[4]
Rhabdoid kidney disease + + – + –
  • CT scan may be diagnostic of malignant rhabdoid tumor. Findings on CT scan suggestive of malignant rhabdoid tumor include a large, heterogenous, centrally located mass, which is lobulated with individual lobules separated by intervening areas of decreased attenuation, relating to either previous hemorrhage or necrosis. Enhancement is similarly heterogeneous. Calcification is relatively common, observed in 20-50% of cases and is typically linear and tends to outline tumor lobules.
  • Malignant rhabdoid tumor is characterized by the round blue tumor cells of high cellularity composed of atypical cells with eccentric nuclei, small nucleoli, and abundant amounts of eosinophilic cytoplasm with frequent mitotic figures.
Polycystic kidney disease + + + (from hypertension) + –

Ultrasound may be helpful in the diagnosis of polycystic kidney disease. Findings on an ultrasound diagnostic of polycystic kidney disease include:[5][6]

  • At least three unilateral or bilateral cysts in patients 15 – 39 years old
  • Atleast two cysts in each kidney in patients 40 – 59 years old
  • Atleast four cysts in each kidney in patients 60 years of age or older

Renal CT scan may be helpful in the diagnosis of polycystic kidney disease. Findings on CT scan diagnostic of ADPKD include:

  • Numerous renal cysts of varying size and shape with little intervening parenchyma with water attenuation and very thin wall.
  • Reduction in sinus fat due to expansion of the cortex
  • Occasional complex cysts with hyperdense appearance, with possible septations or calcifications
  • Multiple homogeneous and hypoattenuating cystic lesions in the liver in patients with liver involvement
  • On microscopic histopathological analysis, interstitial fibrosis, tubular atrophy, thickening and lamellation of tubular basement membranes, microcysts and negative immunofluorescence for complement and immunoglobulin are characteristic findings of ADPKD.[7][8][9][10]
Pheochromocytoma – – + (as a part of the hypertension paroxysm) – –
  • CT is the preferred imaging modality for the diagnosis of pheochromocytoma.
 The following findings may be observed on CT scan:[11]
  • On microscopic pathology, Pheochromocytoma typically demonstrates a nesting (Zellballen) pattern on microscopy. This pattern is composed of well-defined clusters of tumor cells containing eosinophilic cytoplasm separated by fibrovascular stroma.
Burkitt lymphoma +/- (in non-endemic or sporadic form of the disease) – – – –
  • On microscopic histopathological analysis, characteristic findings of Burkitt’s lymphoma include:[16]
  • Medium-sized (~1.5-2x the size of a RBC) with uniform size (“monotonous”) — key feature (i.e. tumor nuclei size similar to that of histiocytes or endothelial cells)
  • Round nucleus
  • Small nucleoli
  • Relatively abundant cytoplasm (basophilic)
  • Brisk mitotic rate and apoptotic activity
  • Cellular outline usually appears squared off
  • “Starry-sky pattern”:
  • The stars in the pattern are tingible-body macrophages (macrophages containing apoptotic tumor cells.
  • The tumour cells are the sky
Intussusception + – – +/- +
  • Ultrasound is the gold standard imaging modality used to diagnose intussusception[17]
    • Target or doughnut sign[18]
      • Edematous intussuscipien forms an external ring around the centrally located intussusceptum
      • Target sign is usually seen in right lower quadrant
    • Layers of intussusception forms pseudo-kidney appearance on the transverse view
  • CT scan may be helpful in the diagnosis of intussusception. CT scan maybe used when other image modalities like x-ray and ultrasound have not given positive results but suspicion of intussusception is high.
  • Intussusception occurs if there is an imbalance between the longitudinal and radial smooth muscle forces of intestine that maintain its normal structure. This imbalance leads to a segment of intestine to invaginate into another segment and cause entero-enteral intussusception. Etiology of intussusception is either idiopathic or pathologic (lead point). 
Hydronephrosis + +/- – – + (CVA tenderness in case of pyelonephritis)
  • In the case of renal colic (one sided loin pain usually accompanied by a trace of blood in the urine) the initial investigation is usually an intravenous urogram. This has the advantage of showing whether there is any obstruction of flow of urine causing hydronephrosis as well as demonstrating the function of the other kidney. Many stones are not visible on plain x ray or IVU but 99% of stones are visible on CT and therefore CT is becoming a common choice of initial investigation.
  • The kidney undergoes extensive dilation with atrophy and thinning of the renal cortex.
Dysplastic kidney N/A N/A N/A N/A N/A

MCDK is usually diagnosed by ultrasound examination before birth.

  • Mass of non-communicating cysts of variable size.
  • Unlike severe hydronephrosis, in which the largest cystic structure (the renal pelvis) lies in a central location and is surrounded by dilated calices, in multicystic dysplastic kidney the cyst distribution shows no recognizable pattern.
  • Dysplastic, echogenic parenchyma may be visible between the cysts, but no normal renal parenchyma is seen.
  • MCKD can be discovered accidentally on CT scan.
  • CT scan shows myltiple cysts with absence of renal parenchyma.
  • MCKD is the result of abnormal differentiation of the renal parenchyma.
Pediatric Neuroblastoma + – – +/- +/-
  • CT scan is the investigation of choice for the diagnosis of neuroblastoma.[20]
  • On CT scan, neuroblastoma is characterized by:[21]
  • On microscopic histopathological analysis the presence of round blue cells separated by thin fibrous septa are characteristic findings of neuroblastoma.
  • Other findings of neuroblastoma on light microscopy may include:[22]
  • Homer-Wright rosettes (rosettes with a small meshwork of fibers at the center)
  • Neuropil-like stroma (paucicellular stroma with a cotton candy-like appearance)
Pediatric Rhabdomyosarcoma + +/- +/- – +/- On CT scan, rhabdomyosarocma is characterized by:
  • Soft tissue density
  • Some enhancement with contrast
  • Adjacent bony destruction (over 20% of cases)
Mesoblastic nephroma + + – + –
  • Ultrasound may be helpful in the diagnosis of mesoblastic nephroma.
  • Mesoblastic nephroma may presents as a well-defined mass with low-level homogeneous echoes.[23]
  • The presence of concentric echogenic and hypoechoic rings can be a helpful diagnostic feature of mesoblastic nephroma.
  • CT scan may be helpful in the diagnosis of mesoblastic nephroma.
  • Findings on CT scan suggestive of mesoblastic nephroma include:
  • Solid hypoattenuating renal lesion
  • Variable contrast enhancement
  • No calcification

Classic mesoblastic nephroma

Cellular mesoblastic nephroma

  • Plump cells with vesicular nuclei
  • Well-defined border
  • Mitotically active

Mixed mesoblastic nephroma

  • Both classic pattern and cellular pattern areas are present
 Most common renal tumor that occurs in 1st month of life

References

  1. ↑ Hartman DS, Sanders RC (April 1982). “Wilms’ tumor versus neuroblastoma: usefulness of ultrasound in differentiation”. J Ultrasound Med. 1 (3): 117–22. PMID 6152936.
  2. ↑ De Campo JF (1986). “Ultrasound of Wilms’ tumor”. Pediatr Radiol. 16 (1): 21–4. PMID 3003660.
  3. ↑ Cahan LD (1985). “Failure of encephalo-duro-arterio-synangiosis procedure in moyamoya disease”. Pediatr Neurosci. 12 (1): 58–62. PMID 4080660.
  4. ↑ Jolly RD, Stellwagen E, Babul J, Vodkaĭlo LV, Titov VL, Moldomusaev DM, Maianskiĭ AN (November 1975). “Mannosidosis of Angus Cattle: a prototype control program for some genetic diseases”. Adv Vet Sci Comp Med. 19 (23): 1–21. PMID 1978.
  5. ↑ Chapman AB, Devuyst O, Eckardt KU, Gansevoort RT, Harris T, Horie S, Kasiske BL, Odland D, Pei Y, Perrone RD, Pirson Y, Schrier RW, Torra R, Torres VE, Watnick T, Wheeler DC (July 2015). “Autosomal-dominant polycystic kidney disease (ADPKD): executive summary from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference”. Kidney Int. 88 (1): 17–27. doi:10.1038/ki.2015.59. PMC 4913350. PMID 25786098.
  6. ↑ Pei Y, Obaji J, Dupuis A, Paterson AD, Magistroni R, Dicks E, Parfrey P, Cramer B, Coto E, Torra R, San Millan JL, Gibson R, Breuning M, Peters D, Ravine D (January 2009). “Unified criteria for ultrasonographic diagnosis of ADPKD”. J. Am. Soc. Nephrol. 20 (1): 205–12. doi:10.1681/ASN.2008050507. PMC 2615723. PMID 18945943.
  7. ↑ Stavrou C, Koptides M, Tombazos C, Psara E, Patsias C, Zouvani I, Kyriacou K, Hildebrandt F, Christofides T, Pierides A, Deltas CC (October 2002). “Autosomal-dominant medullary cystic kidney disease type 1: clinical and molecular findings in six large Cypriot families”. Kidney Int. 62 (4): 1385–94. doi:10.1111/j.1523-1755.2002.kid581.x. PMID 12234310.
  8. ↑ Bleyer AJ, Kmoch S, Antignac C, Robins V, Kidd K, Kelsoe JR, Hladik G, Klemmer P, Knohl SJ, Scheinman SJ, Vo N, Santi A, Harris A, Canaday O, Weller N, Hulick PJ, Vogel K, Rahbari-Oskoui FF, Tuazon J, Deltas C, Somers D, Megarbane A, Kimmel PL, Sperati CJ, Orr-Urtreger A, Ben-Shachar S, Waugh DA, McGinn S, Bleyer AJ, Hodanová K, Vylet’al P, Živná M, Hart TC, Hart PS (March 2014). “Variable clinical presentation of an MUC1 mutation causing medullary cystic kidney disease type 1”. Clin J Am Soc Nephrol. 9 (3): 527–35. doi:10.2215/CJN.06380613. PMC 3944763. PMID 24509297.
  9. ↑ Faguer S, Decramer S, Chassaing N, Bellanné-Chantelot C, Calvas P, Beaufils S, Bessenay L, Lengelé JP, Dahan K, Ronco P, Devuyst O, Chauveau D (October 2011). “Diagnosis, management, and prognosis of HNF1B nephropathy in adulthood”. Kidney Int. 80 (7): 768–76. doi:10.1038/ki.2011.225. PMID 21775974.
  10. ↑ Heidet L, Decramer S, Pawtowski A, Morinière V, Bandin F, Knebelmann B, Lebre AS, Faguer S, Guigonis V, Antignac C, Salomon R (June 2010). “Spectrum of HNF1B mutations in a large cohort of patients who harbor renal diseases”. Clin J Am Soc Nephrol. 5 (6): 1079–90. doi:10.2215/CJN.06810909. PMC 2879303. PMID 20378641.
  11. ↑ Bravo EL (1991). “Pheochromocytoma: new concepts and future trends”. Kidney Int. 40 (3): 544–56. PMID 1787652.
  12. ↑ Whalen RK, Althausen AF, Daniels GH (1992). “Extra-adrenal pheochromocytoma”. J Urol. 147 (1): 1–10. PMID 1729490.
  13. ↑ Baid SK, Lai EW, Wesley RA, Ling A, Timmers HJ, Adams KT; et al. (2009). “Brief communication: radiographic contrast infusion and catecholamine release in patients with pheochromocytoma”. Ann Intern Med. 150 (1): 27–32. PMC 3490128. PMID 19124817.
  14. ↑ Bravo EL (1991). “Pheochromocytoma: new concepts and future trends”. Kidney Int. 40 (3): 544–56. PMID 1787652.
  15. ↑ Burkitt lymphoma. MedlinePlus. https://www.nlm.nih.gov/medlineplus/ency/article/001308.htm Accessed on September 30, 2015
  16. ↑ Bellan C, Lazzi S, De Falco G, Nyongo A, Giordano A, Leoncini L (2003). “Burkitt’s lymphoma: new insights into molecular pathogenesis”. J. Clin. Pathol. 56 (3): 188–92. PMC 1769902. PMID 12610094. Unknown parameter |month= ignored (help)
  17. ↑ Ko HS, Schenk JP, Tröger J, Rohrschneider WK (2007). “Current radiological management of intussusception in children”. Eur Radiol. 17 (9): 2411–21. doi:10.1007/s00330-007-0589-y. PMID 17308922.
  18. ↑ Boyle MJ, Arkell LJ, Williams JT (1993). “Ultrasonic diagnosis of adult intussusception”. Am. J. Gastroenterol. 88 (4): 617–8. PMID 8470658.
  19. ↑ Neuroblastoma. Radiopaedia (2015) http://radiopaedia.org/articles/neuroblastoma Accessed on October, 8 2015
  20. ↑ Colon NC, Chung DH (2011). “Neuroblastoma”. Adv Pediatr. 58 (1): 297–311. doi:10.1016/j.yapd.2011.03.011. PMC 3668791. PMID 21736987.
  21. ↑ Neuroblastoma. Radiopaedia (2015) http://radiopaedia.org/articles/neuroblastoma Accessed on October, 8 2015
  22. ↑ Neuroblastoma. Libre Pathology(2015) http://librepathology.org/wiki/index.php/Adrenal_gland#Neuroblastoma Accessed on October, 5 2015
  23. ↑ Mesoblastic nephroma.Dr Ayush Goel and Dr Yuranga Weerakkody et al. Radiopaedia.org 2015. http://radiopaedia.org/articles/mesoblastic-nephroma
Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul; Serge Korjian; Rim Halaby, M.D. [2]

Overview

In 2011, the age-adjusted prevalence of kidney cancer was 85.9 per 100,000 in the United States, the incidence was 15.28 per 100,000 persons. The male to female ratio is approximately 2 to 1. The median age of presentation is typically 60 years old.

Epidemiology

Prevalence

  • Renal cell carcinoma accounts for approximately 2-3% of all malignant tumors in the adult population.[1] Most cases of renal cell carcinoma are sporadic; whereas only approximately 2-3% of all cases are familial, most of which have an autosomal-dominant pattern of inheritance.[1]
  • In the United States, the age-adjusted prevalence of kidney cancer is 85.9 per 100,000 in 2011.[2]
  • In 2012, there were an estimated 375,925 people living with kidney and renal pelvis cancer in the United States.[3]

Incidence

  • The delay-adjusted incidence of kidney cancer in 2011 was estimated to be 15.88 per 100,000 persons in the United States.[2]
  • In 2011, the age-adjusted incidence of kidney cancer was 15.28 per 100,000 persons in the United States.[2]
  • Estimated new cases and deaths from renal cell (kidney and renal pelvis) cancer in the United States in 2015 are 61,560 and 14,080 respectively. [4]

Age

  • The median age of presentation is typically 60 years.[1]
  • While the overall age-adjusted incidence of kidney cancer in the United States between 2007 and 2011 is 15.5 per 100,000, the age-adjusted incidence of kidney cancer by age category is:[2]
    • Under 65 years: 8.3 per 100,000
    • 65 and over: 65 per 100,000

Gender

  • Renal cell carcinomas is considered the 7th most common cancer in men and the 9th most common cancer in women.
  • The male to female ratio is approximately 2 to 1.[1] The ratio increases dramatically increases in sporadic cases of papillary renal cell carcinomas, reaching a 5 to 1 ratio.[5]
  • In the United States, the age-adjusted prevalence of kidney cancer by gender in 2011 is:[2]
    • In males: 113.2 per 100,000
    • In females: 63.3 per 100,000
  • In the United States, the delay-adjusted incidence of kidney cancer by gender in 2011 is:[2]
    • In males: 21.84 per 100,000 persons
    • In females: 10.81 per 100,000 persons
  • In the United States, the age-adjusted incidence of kidney cancer by gender in 2011 is:[2]
    • In males: 21.02 per 100,000 persons
    • In females: 10.4 per 100,000 persons
  • Shown below is an image depicting the delay-adjusted incidence and observed incidence of kidney cancer by gender and race in the United States between 1975 and 2011. These graphs are adapted from SEER: The Surveillance, Epidemiology, and End Results Program of the National Cancer Institute.[2]

Delay-adjusted incidence and observed incidence of kidney cancer by gender and race in the United States between 1975 and 2011

Race

  • Shown below is a table depicting the age-adjusted prevalence of kidney cancer by race in 2011 in the United States.[2]
All Races White Black Asian/Pacific Islander Hispanic
Age-adjusted prevalence 85.9 per 100,000 90.8 per 100,000 91.3 per 100,000 46.7 per 100,000 86.7 per 100,000
  • Shown below is an image depicting the incidence of kidney cancer by race in the United States between 1975 and 2011.[2]

Incidence of kidney cancer by race in the United States between 1975 and 2011

API: Asian/Pacific Islander; AI/AN: American Indian/ Alaska Native

References

  1. ↑ 1.0 1.1 1.2 1.3 Rini BI, Campbell SC, Escudier B (2009). “Renal cell carcinoma”. Lancet. 373 (9669): 1119–32. doi:10.1016/S0140-6736(09)60229-4. PMID 19269025.
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 Howlader N, Noone AM, Krapcho M, Garshell J, Miller D, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z,Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2011, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2011/, based on November 2013 SEER data submission, posted to the SEER web site, April 2014.
  3. ↑ National Cancer Institute.Surveillance, Epidemiology, and End Results Program 2015.http://seer.cancer.gov
  4. ↑ National Cancer Institute. Physician Data Query Database 2015. http://www.cancer.gov/publications/pdq
  5. ↑ Cohen HT, McGovern FJ (2005). “Renal-cell carcinoma”. N Engl J Med. 353 (23): 2477–90. doi:10.1056/NEJMra043172. PMID 16339096.
Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

Common risk factors for the development of renal cell carcinoma include cigarette smoking, obesity, hypertension, end-stage renal failure, acquired cystic renal disease, acetaminophen and analgesic drug use, asbestos or trichloroethylene exposure, tuberous sclerosis, Von-Hippel Lindau disease, hereditary paraganglioma, leiomyomatosis, and birt-hogg-dube syndrome.

Risk factors

Common risk factors in the development of renal cell carcinoma include:[1][2][3][4][5][6][7][8]

References

  1. ↑ Hunt JD, van der Hel OL, McMillan GP, Boffetta P, Brennan P (2005). “Renal cell carcinoma in relation to cigarette smoking: meta-analysis of 24 studies”. Int J Cancer. 114 (1): 101–8. doi:10.1002/ijc.20618. PMID 15523697.
  2. ↑ Yuan JM, Castelao JE, Gago-Dominguez M, Yu MC, Ross RK (1998). “Tobacco use in relation to renal cell carcinoma”. Cancer Epidemiol Biomarkers Prev. 7 (5): 429–33. PMID 9610793.
  3. ↑ Bjørge T, Tretli S, Engeland A (2004). “Relation of height and body mass index to renal cell carcinoma in two million Norwegian men and women”. Am J Epidemiol. 160 (12): 1168–76. doi:10.1093/aje/. PMID 15583369.
  4. ↑ van Dijk BA, Schouten LJ, Kiemeney LA, Goldbohm RA, van den Brandt PA (2004). “Relation of height, body mass, energy intake, and physical activity to risk of renal cell carcinoma: results from the Netherlands Cohort Study”. Am J Epidemiol. 160 (12): 1159–67. doi:10.1093/aje/. PMID 15583368.
  5. ↑ Ishikawa I, Saito Y, Asaka M, Tomosugi N, Yuri T, Watanabe M; et al. (2003). “Twenty-year follow-up of acquired renal cystic disease”. Clin Nephrol. 59 (3): 153–9. PMID 12653256.
  6. ↑ Rakowski SK, Winterkorn EB, Paul E, Steele DJ, Halpern EF, Thiele EA (2006). “Renal manifestations of tuberous sclerosis complex: Incidence, prognosis, and predictive factors”. Kidney Int. 70 (10): 1777–82. doi:10.1038/sj.ki.5001853. PMID 17003820.
  7. ↑ McCredie M, Pommer W, McLaughlin JK, Stewart JH, Lindblad P, Mandel JS; et al. (1995). “International renal-cell cancer study. II. Analgesics”. Int J Cancer. 60 (3): 345–9. PMID 7829242.
  8. ↑ Rini BI, Campbell SC, Escudier B (2009). “Renal cell carcinoma”. Lancet. 373 (9669): 1119–32. doi:10.1016/S0140-6736(09)60229-4. PMID 19269025.
Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

There are currently no guidelines for screening for renal cell carcinoma.

Screening

There are currently no guidelines for screening for renal cell carcinoma.

References

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul; Serge Korjian; Rim Halaby, M.D. [2]; Farima Kahe M.D. [3]

Overview

Common complications of renal cell carcinoma include hypertension, hypercalcemia, budd-chiari syndrome, hepatic vein thrombosis, polycythemia, renal failure, metastasis. Prognosis is generally poor, and the 5-year mortality of renal cell carcinoma is approximately 73.2%.

Natural History

  • The symptoms of renal cell carcinoma usually develop in the fifth decade of life, and start with symptoms such as hematuria, flank pain and palpable abdominal mass.[1]
  • If left untreated, 1.3% of patients with renal cell carcinoma may progress to develop metastatic disease.[2]

Complications

The following are possible complications of the primary tumor and its spread, associated paraneoplastic syndromes, or metastasis:[3][4][5][6]

Prognosis

The presence of the following factors may correlate with a poorer prognosis in renal cell carcinoma:[7][8][9]

Other prognostic scoring include the tumor-mode-metastasis (TNM) staging system and the Fuhrman nuclear grade.[7][10][11]

Survival

  • Patients with metastatic renal cell carcinoma have a median age of survival reaching approximately 13 months. Available medical therapy, however, may significantly prolong survival of patients with metastatic disease.[7]
  • Between 2004 and 2010, the 5-year relative survival of patients with kidney cancer was 73.7%.[12]
  • When stratified by age, the 5-year relative survival of patients with kidney cancer was 78% and 65% for patients <65 and ≥ 65 years of age respectively.[12]
  • The survival of patients with kidney cancer varies with the stage of the disease. Shown below is a table depicting the 5-year relative survival by the stage of kidney cancer:[12]
Stage 5-year relative survival (%), (2004-2010)
All stages 72.4%
Localized 91.8%
Regional 64.7%
Distant 12.1%
Unstaged 32.2%
  • Shown below is an image depicting the 5-year conditional relative survival (probability of surviving in the next 5-years given the cohort has already survived 0, 1, 3 years) between 1998 and 2010 of kidney cancer by stage at diagnosis according to SEER. These graphs are adapted from SEER: The Surveillance, Epidemiology, and End Results Program of the National Cancer Institute.[12]

5-year conditional relative survival (probability of surviving in the next 5-years given the cohort has already survived 0, 1, 3 years) between 1998 and 2010 of kidney cancer by stage at diagnosis according to SEER

The following table summarizes the 5-year survival of patients according to cancer staging[7][13]:

Five-Year Survival of Various Stages of Renal Cell Carcinoma[7][13]
Stage Tumor Characteristics Five-Year Survival
Stage I Tumor < 7 cm in greatest dimension, limited to kidney 95%
Stage II Tumor > 7 cm in greatest dimension, limited to kidney 88%
Stage III Tumor in major veins or adrenal glands, tumor within Gerota’s fascia, or 1 regional lymph node involved 59%
Stage IV Tumor beyond Gerota’s fascia or > 1 regional lymph node involved 20%
Adapted from Cohen HT, McGovern FJ. Renal-cell carcinoma. N Engl J Med. 2005; 353:2477-90.

References

  1. ↑ Zhang L, Yao L, Li X, Jewett MA, He Z, Zhou L (June 2016). “Natural history of renal cell carcinoma: An immunohistochemical analysis of growth rate in patients with delayed treatment”. J. Formos. Med. Assoc. 115 (6): 463–9. doi:10.1016/j.jfma.2015.05.003. PMID 26058870.
  2. ↑ Crispen PL, Viterbo R, Boorjian SA, Greenberg RE, Chen DY, Uzzo RG (July 2009). “Natural history, growth kinetics, and outcomes of untreated clinically localized renal tumors under active surveillance”. Cancer. 115 (13): 2844–52. doi:10.1002/cncr.24338. PMC 2860784. PMID 19402168.
  3. ↑ Nielsen OJ, Jespersen FF, Hilden M (August 1988). “Erythropoietin-induced secondary polycythemia in a patient with a renal cell carcinoma. A case report”. APMIS. 96 (8): 688–94. PMID 3046641.
  4. ↑ Shih KL, Yen HH, Su WW, Soon MS, Hsia CH, Lin YM (February 2009). “Fulminant Budd-Chiari syndrome caused by renal cell carcinoma with hepatic vein invasion: report of a case”. Eur J Gastroenterol Hepatol. 21 (2): 222–4. doi:10.1097/MEG.0b013e328305ba06. PMID 19212212.
  5. ↑ Palapattu GS, Kristo B, Rajfer J (2002). “Paraneoplastic syndromes in urologic malignancy: the many faces of renal cell carcinoma”. Rev Urol. 4 (4): 163–70. PMC 1475999. PMID 16985675.
  6. ↑ Pepper K, Jaowattana U, Starsiak MD, Halkar R, Hornaman K, Wang W, Dayamani P, Tangpricha V (July 2007). “Renal cell carcinoma presenting with paraneoplastic hypercalcemic coma: a case report and review of the literature”. J Gen Intern Med. 22 (7): 1042–6. doi:10.1007/s11606-007-0189-1. PMC 2219737. PMID 17443359.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 Cohen HT, McGovern FJ (2005). “Renal-cell carcinoma”. N Engl J Med. 353 (23): 2477–90. doi:10.1056/NEJMra043172. PMID 16339096.
  8. ↑ Motzer RJ, Mazumdar M, Bacik J, Berg W, Amsterdam A, Ferrara J (1999). “Survival and prognostic stratification of 670 patients with advanced renal cell carcinoma”. J Clin Oncol. 17 (8): 2530–40. PMID 10561319.
  9. ↑ Motzer RJ, Bacik J, Schwartz LH, Reuter V, Russo P, Marion S; et al. (2004). “Prognostic factors for survival in previously treated patients with metastatic renal cell carcinoma”. J Clin Oncol. 22 (3): 454–63. doi:10.1200/JCO.2004.06.132. PMID 14752067.
  10. ↑ Zisman A, Pantuck AJ, Dorey F, Said JW, Shvarts O, Quintana D; et al. (2001). “Improved prognostication of renal cell carcinoma using an integrated staging system”. J Clin Oncol. 19 (6): 1649–57. PMID 11250993.
  11. ↑ Patard JJ, Kim HL, Lam JS, Dorey FJ, Pantuck AJ, Zisman A; et al. (2004). “Use of the University of California Los Angeles integrated staging system to predict survival in renal cell carcinoma: an international multicenter study”. J Clin Oncol. 22 (16): 3316–22. doi:10.1200/JCO.2004.09.104. PMID 15310775.
  12. ↑ 12.0 12.1 12.2 12.3 Howlader N, Noone AM, Krapcho M, Garshell J, Miller D, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z,Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2011, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2011/, based on November 2013 SEER data submission, posted to the SEER web site, April 2014.
  13. ↑ 13.0 13.1 Javidan J, Stricker HJ, Tamboli P, Amin MB, Peabody JO, Deshpande A; et al. (1999). “Prognostic significance of the 1997 TNM classification of renal cell carcinoma”. J Urol. 162 (4): 1277–81. PMID 10492179.
Diagnosis

Diagnosis

Staging | History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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