presentation of renal carcinoma

RICHARD E. GRAY, DO, AND GABRIEL T. HARRIS, MD

This is a corrected version of the article that appeared in print.

Am Fam Physician. 2019;99(3):179-184

Related editorial: Stumbling onto Cancer: Avoiding Overdiagnosis of Renal Cell Carcinoma

Author disclosure: No relevant financial affiliations.

Kidney cancer is one of the 10 most common cancers in the United States with 90% being attributed to renal cell carcinoma. Men, especially black men, are more likely to be affected than women. Renal masses, either cystic or solid, are best detected with contrast-enhanced, triple-phase computed tomography. Renal tumors are often detected incidentally during a computed tomography scan of the abdomen or chest that was ordered for unrelated symptoms. Hematuria serves as a warning sign that necessitates further evaluation and imaging leading to a diagnosis and treatment plan. Treatment options include active surveillance, ablation, nephron-sparing tumor excision, nephrectomy, and systemic treatment. Predictors of a poor prognosis include poor functional status and metastasis. In recent years new therapies have improved the prognosis for patients with metastatic disease. The family physician should be aware of risk factors (e.g., hypertension, tobacco use, exposure to trichloroethylene, familial syndromes) and lifestyle and dietary modifications that may reduce risk.

Kidney cancer is one of the 10 most common cancers in the United States. 1 Renal cell carcinoma accounts for 90% of all kidney cancers. 2 Death attributed to renal cell carcinoma accounted for 2% of all cancer deaths or approximately 14,000 persons in 2016. 1 , 2 Men are diagnosed with renal cell carcinoma at almost twice the rate of women, and there is a greater prevalence in black men. 3 Most cases are diagnosed between 60 and 70 years of age. 1 , 2

Renal cell carcinoma is classified in three major histological subtypes: clear cell (75%), papillary (15% to 20%), and chromophobe (5%). 4 Disease-specific survival is worst with clear cell renal cell carcinoma as it tends to be discovered at a more advanced stage. 5

Risk Factors

Risk factors for renal cell carcinoma include hypertension, tobacco use, obesity, and acquired cystic kidney disease in the setting of end-stage renal disease. 1 , 3 , 6 Occupational exposure to trichloroethylene can lead to the development of renal cell carcinoma and increased mortality from renal cell carcinoma. 5 , 7 – 9 The International Agency for Research on Cancer labels trichloroethylene as carcinogenic to humans and specifically associates it with renal cancer. 10 Occupational exposure to trichloroethylene is most commonly encountered by mechanics, dry cleaners, oil processors, polyvinyl chloride manufacturers, and low-nicotine tobacco producers. 8

There are 10 familial syndromes that confer greater risk of developing renal cell carcinoma. 11 The most common of these is von Hippel-Lindau disease which leads to the development of clear cell renal cell carcinoma through the activation of vascular endothelial growth factor (VEGF). 11 Approximately 60% of sporadic clear cell renal cell carcinomas follow the same pathogenesis. This discovery has led to the development of new therapies that inhibit VEGF receptors and are being used to treat heritable and sporadic cases of clear cell renal cell carcinoma. 11 , 12

Screening and Prevention

Screening for renal cell carcinoma is not recommended, except in the setting of a known heritable syndrome associated with the development of renal cell carcinoma. 1 The management of hypertension and obesity, and the avoidance of tobacco use are the only established methods of primary prevention. 8 Evidence from prospective and observational studies suggest that consuming fatty fish (relative risk [RR] = 0.56; 95% confidence interval [CI], 0.35 to 0.91), three or more servings of fruits and vegetables (RR = 0.68; 95% CI, 0.54 to 0.87), and one alcoholic beverage daily (RR = 0.76; 95% CI, 0.68 to 0.85) may reduce the risk of developing renal cell carcinoma. 5 , 13 – 15

Clinical Presentation

More than 50% of patients with renal cell carcinoma are asymptomatic and diagnosed incidentally during thoracoabdominal imaging ordered for unrelated issues. 5 , 16 The history and physical examination triad of gross hematuria, flank pain, and palpable abdominal mass is now an uncommon presentation, and is associated with advanced disease. 6 , 12 , 16 Nonreducing or isolated right-sided varicocele and bilateral lower extremity edema can also be symptoms of advanced disease through occlusion of the right testicular venous system that drains directly to the inferior vena cava [ corrected ]. Similarly, bilateral lower extremity edema can occur from tumor occlusion of the inferior vena cava. Approximately 20% of patients present with paraneoplastic disease, manifested by hypertension, hypercalcemia, and polycythemia. 5 Fever, weight loss, cough, adenopathy, and bone pain may indicate metastatic disease.

CLINICAL EVALUATION

An isolated right-sided varicocele and nonreducing bilateral varicocele should be evaluated with abdominal imaging. Gross hematuria requires computed tomography (CT), urography, and urology consultation for cystoscopy. 17 Signs of paraneoplastic or metastatic disease require evaluation for malignancy, including chest and abdominal imaging.

LABORATORY EVALUATION

Hematuria should be diagnosed by microscopic examination that shows three or more red blood cells per high-powered field, not by urine dipstick alone. The urine should be without pyuria or red blood cell casts, which indicates infection or glomerulonephritis, respectively. If asymptomatic microscopic hematuria is detected, management is recommended per American Urological Association guidelines ( Figure 1 ) . 17 , 18 Benign causes should be ruled out, including infection, recent vigorous exercise, menstruation, and instrumentation. Identified causes should be treated and a repeat urinalysis should be obtained. Further laboratory evaluation includes assessment of urinary sediment, creatinine, C-reactive protein, hemoglobin, erythrocyte sedimentation rate, alkaline phosphatase, and serum calcium. 7 Routine urine cytology is not recommended for the initial evaluation of asymptomatic microscopic hematuria. 17 Patients 35 years or older who have asymptomatic microhematuria should have cystoscopy and imaging with multi-phasic CT urography performed. 17

A contrast-enhanced, triple-phase helical CT scan that images the urinary tract before, during, and after contrast load is the preferred imaging study for evaluating renal masses or persistent microscopic hematuria. 19 , 20 CT detects 90% of renal masses, identifies benign and pathologic features, and evaluates surrounding anatomy to detect lymphadenopathy or an associated thrombus. A contrast-enhanced CT scan will also identify benign masses that do not require further testing.

The Hounsfield unit scale measures a tissue's density or attenuation. Fat has very low attenuation (i.e., −100 to −10 HU), and masses containing fat are almost always benign angiomyolipomas. Homogeneous masses with low attenuation (−10 to +20 HU) can be identified as benign, fluid-filled, simple cysts. Masses with attenuation greater than 20 HU, heterogeneous appearance, septations, or calcifications, may be malignant and require further evaluation 21 ( Figure 2 ) . The differential diagnosis of renal masses is included in Table 1 . 22

For incompletely characterized masses or contraindications to CT, magnetic resonance imaging with and without intravenous contrast is recommended. 21

The management of cystic lesions should be guided by the Bosniak classification system ( Table 2 ) . 21 Shared decision-making between the urologist, the family physician, and the patient is recommended when deciding on a course of treatment. The tumor's stage and characteristics as well as the patient's baseline health and patient preferences should be considered ( Table 3 23 , 24 ) .

Solid tumors are managed according to size. Masses measuring less than 1 cm are observed, and masses greater than 1 cm are usually excised or biopsied. There is an increasing role for renal mass biopsy, instead of partial or radical nephrectomy, because active surveillance is a treatment option for renal cell carcinoma. However, a biopsy has an increased risk of false-negative results. The risk of metastatic spread of cancer cells related to a biopsy is rare and should not preclude the use of biopsy to help clarify a diagnosis and guide treatment. Twenty percent of large (greater than 3 cm) solid masses discovered incidentally will be benign. 5 Metastatic potential increases significantly when the mass is 4 cm or greater. If there is concern for metastatic disease, radiography or CT scan may be necessary based on other risk factors. 5 , 23

INDICATIONS FOR REFERRAL

A urology consultation for further evaluation is indicated for microscopic or gross hematuria without urinary tract infection or other benign causes. 17 , 18 , 25 Patients should also be referred for any Bosniak III or IV cystic lesions, and for selected, low-risk patients with a Bosniak IIF lesion, or any solid mass greater than 1 cm that does not contain fat. 21

INTERVENTION STRATEGIES

The preferred treatment for any nonmetastatic, solid, or Bosniak III or IV complex cystic kidney mass is surgical excision, preferably using a minimally invasive approach. 23 In select patients, nephron-sparing partial nephrectomy is recommended with a priority of achieving negative surgical margins while preserving nephron mass. Radical nephrectomy is indicated in patients with an increased oncologic risk based on clinical indicators (solid masses greater than 3 cm, complex cystic masses, no preexisting chronic kidney disease, normal contralateral kidney and if partial nephrectomy would be challenging) and in patients who plan to undergo targeted pharmaceutical treatment. 12 , 23 Lymph node dissection should be performed for staging purposes in patients with clinically concerning regional lymphadenopathy. Adrenalectomy should be performed in patients where imaging and/or intraoperative indications of adrenal invasion are evident. 23

Other options for treatment of renal masses less than 3 cm include thermal ablation, cryoablation, and radiofrequency ablation. All patients undergoing these treatment options should have a renal mass biopsy (preferably multiple core biopsies) performed to allow histologic diagnosis and guide subsequent surveillance. The patient must also understand the increased risk of local recurrence or persistence of the tumor with these treatment options. 12 , 23

Active surveillance is an acceptable option in some patients when the renal mass measures less than 2 cm (grade C). A plan of active surveillance with repeat imaging every three to six months is acceptable when it is preferred by the patient or when risk of an intervention outweighs the benefits because of complicated comorbidities that decrease life expectancy or increase the risk of death. Renal mass biopsy (preferably performed using a percutaneous approach) should be considered for further risk stratification for patients considering active surveillance. 12 , 23 If expected benefits of the intervention outweigh the benefits of active surveillance, then active treatment is preferred, and patients must clearly understand the risks of surveillance. 23

Approximately 30% of all patients with renal cell carcinoma have metastatic disease at diagnosis. 6 Treatment of metastatic renal cell carcinoma is more complicated and challenging because of the cancer cells' resistance to treatment. 12 Available interventions include various VEGF receptor inhibitors, tyrosine kinase inhibitors, and immunotherapies. First-line treatment for patients with good to intermediate prognosis, who have not been treated previously, includes antiangiogenic VEGF/tyrosine kinase inhibitors (sunitinib [Sutent], pazopanib [Votrient], or bevacizumab [Avastin] with interferon-alpha). Second-line treatment includes another VEGF receptor/tyrosine kinase inhibitor, immunotherapy with nivolumab [Opdivo], and the immunosuppressant everolimus for patients who experience disease progression despite first-line treatment. 26 – 28 Although these interventions may improve overall survival, complete remission is rare in that advanced renal cell carcinoma is a deadly disease. 28

The most significant indicator of prognosis for renal cell carcinoma is based on pathological staging. Patients with stage I or II cancer at the time of diagnosis have a five-year survival rate of 80% to 90%. 23 Poor prognostic indicators include: low functional status scores using the Karnofsky performance scale or Eastern Cooperative Oncology Group Performance Status scale, high levels of serum lactate dehydrogenase, low hemoglobin, high serum corrected calcium levels, and comorbid diabetes mellitus. 12 , 29

Data Sources: Searches were conducted in Essential Evidence Plus, PubMed, Cochrane Database of Systematic Reviews, and the U.S. Preventive Services Task Force using the key terms renal cancer diagnosis and treatment and renal cell carcinoma diagnosis and treatment. The searches included meta-analyses, randomized controlled trials, clinical trials, guidelines, and reviews. Search dates: July to August 2017, and October 2018.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the U.S. Army Medical Department or the U.S. Air Force at large.

American Cancer Society. Cancer Facts & Figures 2016. https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2016/cancer-facts-and-figures-2016.pdf . Accessed August 10, 2017.

Motzer RJ, et al. Kidney cancer, version 2. 2017. NCCN clinical practice guidelines in oncology. J Natl Compr Canc Netw. 2017;15(6):804-834.

Lipworth L, Tarone RE, McLaughlin JK. The epidemiology of renal cell carcinoma. J Urol. 2006;176(6 pt 1):2353-2358.

Ricketts CJ, et al. The cancer genome atlas comprehensive molecular characterization of renal cell carcinoma [published correction appears in Cell Rep . 2018;23(12):3698]. Cell Rep. 2018;23(1):313-326.

Campbell SC, Novick AC, Belldegrun A, et al. Guideline for management of the clinical T1 renal mass. 2009;182(4):1271-1279.

Ljungberg B, Hanbury DC, Kuczyk MA, et al. Renal cell carcinoma guideline. Eur Urol. 2007;51(6):1502-1510.

Alanee S, Clemons J, Zahnd W, Sadowski D, Dynda D. Trichloroethylene is associated with kidney cancer mortality: a population-based analysis. Anticancer Res. 2015;35(7):4009-4013.

Agency for Toxic Substances & Disease Registry. Toxicological profile for trichloroethylene. https://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=173&tid=30 . Accessed August 10, 2017.

Chow WH, Dong LM, Devesa SS. Epidemiology and risk factors for kidney cancer. Nat Rev Urol. 2010;7(5):245-257.

International Agency for Research on Cancer. Trichloroethylene, tetrachloroethylene, and some other chlorinated agents. 2014;106:35-217.

Haas NB, Nathanson KL. Hereditary kidney cancer syndromes. Adv Chronic Kidney Dis. 2014;21(1):81-90.

Cohen HT, McGovern FJ. Renal-cell carcinoma. N Engl J Med. 2005;353(23):2477-2490.

Song DY, Song S, Song Y, Lee JE. Alcohol intake and renal cell cancer risk: a meta-analysis. Br J Cancer. 2012;106(11):1881-1890.

Wolk A, Larsson SC, Johansson JE, Ekman P. Long-term fatty fish consumption and renal cell carcinoma incidence in women. JAMA. 2006;296(11):1371-1376.

Lee JE, et al. Intakes of fruit, vegetables, and carotenoids and renal cell cancer risk. Cancer Epidemiol Biomarkers Prev. 2009;18(6):1730-1739.

Loo RK, Lieberman SF, Slezak JM, et al. Stratifying risk of urinary tract malignant tumors in patients with asymptomatic microscopic hematuria. Mayo Clin Proc. 2013;88(2):129-138.

Davis R, et al. Diagnosis, evaluation, and follow-up of asymptomatic microhematuria (AMH) in adults. J Urol. 2012;188(6 suppl):2473-2481.

Sharp VJ, Barnes KT, Erickson BA. Assessment of asymptomatic microscopic hematuria in adults. Am Fam Physician. 2013;88(11):747-754.

Gray Sears CL, et al. Prospective comparison of computerized tomography and excretory urography in the initial evaluation of asymptomatic microhematuria. J Urol. 2002;168(6):2457-2460.

Kang SK, Chandarana H. Contemporary imaging of the renal mass. Urol Clin North Am. 2012;39(2):161-170.

Herts BR, Silverman SG, Hindman NM, et al. Management of the incidental renal mass on CT. J Am Coll Radiol. 2018;15(2):264-273.

Higgins JC, Fitzgerald JM. Evaluation of incidental renal and adrenal masses. Am Fam Physician. 2001;63(2):288-294.

American Urological Association. Renal mass and localized renal cancer: AUA guideline. 2017. https://www.auanet.org/guidelines/renal-mass-and-localized-renal-cancer-new-(2017) . Accessed September 29, 2017.

American Cancer Society. Survival rates for kidney cancer by stage. 2017. https://www.cancer.org/cancer/kidney-cancer/detection-diagnosis-staging/survival-rates.html . Accessed October 20, 2017.

National Institute for Health and Care Excellence. Suspected cancer. 2017. https://www.nice.org.uk/guidance/ng12/chapter/1-Recommendations-organised-by-site-of-cancer . Accessed August 25, 2017.

Wagstaff J, et al. Treatment patterns and clinical outcomes in patients with renal cell carcinoma in the UK. Ann Oncol. 2016;27(1):159-165.

Molina AM, Motzer RJ. Clinical practice guidelines for the treatment of metastatic renal cell carcinoma. Oncologist. 2011;16(Suppl 2):45-50.

Rodriguez-Vida A, Hutson TE, Bellmunt J, Strijbos MH. New treatment options for metastatic renal cell carcinoma. ESMO Open. 2017;2(2):e000185.

Chen L, Li H, Gu L, et al. The impact of diabetes mellitus on renal cell carcinoma prognosis: a meta-analysis of cohort studies. Medicine (Baltimore). 2015;94(26):e1055.

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INTRODUCTION

The epidemiology, pathology, and pathogenesis of RCC will be reviewed here. The clinical and radiographic presentation, staging methods, prognosis, and management of these tumors are discussed separately. (See "Clinical manifestations, evaluation, and staging of renal cell carcinoma" and "Prognostic factors in patients with renal cell carcinoma" and "Overview of the treatment of renal cell carcinoma" and "Definitive surgical management of renal cell carcinoma" and "Systemic therapy for advanced and metastatic clear cell renal carcinoma" and "Antiangiogenic and molecularly targeted therapy for advanced or metastatic clear cell renal carcinoma" and "The treatment of advanced non-clear cell renal carcinoma" .)

EPIDEMIOLOGY

Incidence  —  Globally, the incidence of renal cell carcinoma (RCC) varies widely from region to region [ 1 ], with the highest rates observed in the Czech Republic and North America [ 2 ]. In the United States, there are approximately 82,000 new cases and almost 15,000 deaths from RCC each year [ 3 ]. Worldwide, there are over 400,000 new cases of RCC and over 170,000 deaths annually due to kidney cancer [ 4 ].

Sex and age  —  RCC is approximately twofold more common in males compared with females [ 3 ]. RCC occurs predominantly in the sixth to eighth decade of life with median age at diagnosis around 64 years of age; it is unusual in patients under 40 years of age and rare in children [ 5-7 ].

Ethnicity  —  Within the United States, Asian American patients or patients of Pacific Islander descent have the lowest incidence of renal cancers, compared with patients of other ethnicities [ 3 ]. The five-year survival rate for Black American patients is similar to that for White American patients (over 75 percent) [ 3 ].

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• What is kidney cancer? An expert explains

Learn more from urologic oncologist Bradley Leibovich, M.D.

I'm Dr. Brad Leibovich, urologic oncologist at Mayo Clinic. In this video, we'll cover the basics of kidney cancer: What is it? Who gets it? The symptoms, diagnosis, and treatment. Whether you're looking for answers for yourself or for someone you love, we're here to give you the best information available. First, let's talk about the kidney. You have two of these bean-shaped organs, each about the size of your fist. They sit right behind your abdominal organs with one on each side of the spine. It's their job to filter excess water, salt, and waste products from your body, turning those substances into urine. Like other organs, kidneys are made up of cellular tissue. Sometimes the cells in this tissue behave irregularly. Changes in their DNA make them grow in abnormal ways, forming tumors. This is how cancer develops. The most common type of kidney cancer is renal cell carcinoma. About nine out of 10 kidney cancers are this type. With improvements in technology, thankfully, come improvements in treatment. So in an encouraging turn, kidney cancer has never been more treatable than it is today.

The average age of those diagnosed with kidney cancer is 64. It is about twice as common in men as it is in women. The exact causes of kidney cancer, like many other cancers, are not known. However, we do know that certain things can increase your chances of developing kidney cancer. Older age, smoking, obesity, high blood pressure, long-term dialysis, and a family history of kidney cancer can all increase your risk.

Unfortunately, kidney cancer is often hard to diagnose, as it doesn't have clear signs or symptoms in its early stages. Over time, the following may develop: Blood in your urine, which may appear pink, red or cola colored. Pain in your back or side that does not go away. Loss of appetite. Unexplained weight loss. Persistent tiredness. Fever. Or night sweats. If you're worried that you may be experiencing these symptoms, please talk to your doctor.

The way doctors evaluate kidney tumors may include one or more of the following tests and procedures: Blood and urine tests. Imaging tests like ultrasounds, x-rays, CT scans and MRIs, which can help visualize the tumor or abnormality. On occasion, your doctor may recommend a biopsy. This involves removing a small sample of tissue from the tumor with a needle for further testing. If it's determined that you have kidney cancer, the next step is staging that cancer. Staging is a medical term to describe how advanced your cancer is. Specific tests for staging could include further CT scans or other imaging tests. Once the doctor has enough information, they'll assign a Roman numeral ranging from 1 to 4 to indicate the stage of your cancer. The lower end means your cancer is confined to the kidney. The higher means the cancer is considered advanced and may have spread to the lymph nodes or other areas of the body.

There are a few small upsides to kidney cancer versus others. The fact that we have two kidneys, and our bodies typically only need one to function normally, means that in many occasions, if the kidney cancer is localized and hasn't spread to other parts of the body, not only are the odds of surviving very good, but typically we do not have any negative impact on quality of life from the treatment for kidney cancer. For most, surgery is the first step. Depending upon the stage and severity of cancer, surgeons may remove the affected kidney altogether - a procedure known as a nephrectomy or radical nephrectomy. Sometimes they may opt to remove the tumor from the kidney. This is known as a partial nephrectomy or kidney-sparing or nephron-sparing surgery. In addition to surgery, some kidney cancers are destroyed by non-surgical methods. Cryoablation is a treatment that freezes and kills cancerous cells. Radiofrequency ablation is a treatment that causes the mutated cells to heat up, in effect disintegrating them. The best treatment for you depends on a handful of factors, including your overall health, the kind of kidney cancer you have, whether the cancer has spread and your preferences for treatment. Together, you and your medical team can decide what's right for you.

Learning you've been diagnosed with cancer is never easy. But there are ways to cope with the daily challenges of processing your disease, treatment and recovery. Learning about your condition can help you feel comfortable when it comes to making decisions. Taking care of yourself is another. Stay active. Sleep well. Eat healthy. And if you feel up to it, keep doing the things you enjoy. Reach out to others. Your doctor can help you find a support group. Don't be afraid to ask for help if you need it. It's normal to feel overwhelmed, depressed or anxious. Sometimes talking to a mental health specialist can make all the difference. Remember, with the right treatment, the right team and the right mindset, there's always a road forward. If you'd like to learn even more about kidney cancer, here are our other related videos or visit mayoclinic.org. We wish you well.

Kidney cancer is cancer that begins in the cells of your kidneys.

Kidney cancer is cancer that begins in the kidneys. Your kidneys are two bean-shaped organs, each about the size of your fist. They're located behind your abdominal organs, with one kidney on each side of your spine.

In adults, renal cell carcinoma is the most common type of kidney cancer. Other less common types of kidney cancer can occur. Young children are more likely to develop a kind of kidney cancer called Wilms' tumor.

The incidence of kidney cancer seems to be increasing. One reason for this may be the fact that imaging techniques such as computerized tomography (CT) scans are being used more often. These tests may lead to the accidental discovery of more kidney cancers. Kidney cancer is often discovered at an early stage, when the cancer is small and confined to the kidney.

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Kidney cancer usually doesn't have signs or symptoms in its early stages. In time, signs and symptoms may develop, including:

• Blood in your urine, which may appear pink, red or cola colored
• Pain in your back or side that doesn't go away
• Loss of appetite
• Unexplained weight loss

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Make an appointment with your doctor if you have any persistent signs or symptoms that worry you.

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It's not clear what causes most kidney cancers.

Doctors know that kidney cancer begins when some kidney cells develop changes (mutations) in their DNA. A cell's DNA contains the instructions that tell a cell what to do. The changes tell the cells to grow and divide rapidly. The accumulating abnormal cells form a tumor that can extend beyond the kidney. Some cells can break off and spread (metastasize) to distant parts of the body.

Risk factors

Factors that can increase the risk of kidney cancer include:

• Older age. Your risk of kidney cancer increases as you age.
• Smoking. Smokers have a greater risk of kidney cancer than nonsmokers do. The risk decreases after you quit.
• Obesity. People who are obese have a higher risk of kidney cancer than people who are considered to have a healthy weight.
• High blood pressure (hypertension). High blood pressure increases your risk of kidney cancer.
• Treatment for kidney failure. People who receive long-term dialysis to treat chronic kidney failure have a greater risk of developing kidney cancer.
• Certain inherited syndromes. People who are born with certain inherited syndromes may have an increased risk of kidney cancer, such as those who have von Hippel-Lindau disease, Birt-Hogg-Dube syndrome, tuberous sclerosis complex, hereditary papillary renal cell carcinoma or familial renal cancer.
• Family history of kidney cancer. The risk of kidney cancer is higher if close family members have had the disease.

Taking steps to improve your health may help reduce your risk of kidney cancer. To reduce your risk, try to:

• Quit smoking. If you smoke, quit. Many options for quitting exist, including support programs, medications and nicotine replacement products. Tell your doctor you want to quit, and discuss your options together.
• Maintain a healthy weight. Work to maintain a healthy weight. If you're overweight or obese, reduce the number of calories you consume each day and try to be physically active most days of the week. Ask your doctor about other healthy strategies to help you lose weight.
• Control high blood pressure. Ask your doctor to check your blood pressure at your next appointment. If your blood pressure is high, you can discuss options for lowering your numbers. Lifestyle measures such as exercise, weight loss and diet changes can help. Some people may need to add medications to lower their blood pressure. Discuss your options with your doctor.

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• Kidney cancer. National Comprehensive Cancer Network. https://www.nccn.org/professionals/physician_gls/default.aspx. Accessed May 8, 2020.
• Partin AW, et al., eds. Malignant renal tumors. In: Campbell-Walsh-Wein Urology. 12th ed. Elsevier; 2021. https://www.clinicalkey.com. Accessed May 8, 2020.
• Niederhuber JE, et al., eds. Cancer of the kidney. In: Abeloff's Clinical Oncology. 6th ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed May 8, 2020.
• Renal cell cancer treatment (PDQ). National Cancer Institute. https://www.cancer.gov/types/kidney/patient/kidney-treatment-pdq. Accessed May 8, 2020.
• Distress management. National Comprehensive Cancer Network. https://www.nccn.org/professionals/physician_gls/default.aspx. Accessed May 8, 2020.
• Alt AL, et al. Survival after complete surgical resection of multiple metastases from renal cell carcinoma. Cancer. 2011; doi:10.1002/cncr.25836.
• Lyon TD, et al. Complete surgical metastasectomy of renal cell carcinoma in the post-cytokine era. The Journal of Urology. 2020; doi:10.1097/JU.0000000000000488.
• Dong H, et al. B7-H1, a third member of the B7 family, co-stimulates T-cell proliferation and interleukin-10 secretion. Nature Medicine. 1999;5:1365.
• Peyronnet B, et al. Impact of hospital volume and surgeon volume on robot-assisted partial nephrectomy outcomes: A multicenter study. BJU International. 2018; doi:10.1111/bju.14175.
• Hsu RCJ, et al. Impact of hospital nephrectomy volume on intermediate- to long-term survival in renal cell carcinoma. BJU International. 2020; doi:10.1111/bju.14848.
• NCCN member institutions. National Comprehensive Cancer Network. https://www.nccn.org/members/network.aspx. Accessed May 20, 2020.
• Locations. Children's Oncology Group. https://www.childrensoncologygroup.org/index.php/locations. Accessed May 20, 2020.
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Associated Procedures

• Ablation therapy
• Biological therapy for cancer
• Computerized tomography (CT) urogram
• Nephrectomy (kidney removal)
• Radiation therapy
• Radiofrequency ablation for cancer

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• Mayo Clinic Minute: How is kidney cancer treated? March 20, 2023, 02:27 p.m. CDT

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Renal Cell Carcinoma

(adenocarcinoma of the kidneys).

• Symptoms and Signs |
• Diagnosis |
• Treatment |
• Prognosis |
• Key Points |

Renal cell carcinoma (RCC) is the most common renal cancer. Symptoms can include hematuria, flank pain, a palpable mass, and fever of unknown origin (FUO). However, symptoms are often absent, so the diagnosis is usually suspected based on incidental findings. Diagnosis is confirmed by CT or MRI and occasionally by biopsy. Treatment is with surgery for early disease and targeted therapy, an experimental protocol, or palliative therapy for advanced disease.

RCC, an adenocarcinoma, accounts for 90 to 95% of primary malignant renal tumors. Less common primary renal tumors include transitional cell carcinoma, Wilms tumor (most often in children), and sarcoma.

In the United States, about 81,800 new cases of RCC and other kidney tumors and 14,890 deaths (2023 estimates) occur each year ( 1 ). RCC occurs more often in men (male:female incidence is about 2:1). People with RCC are usually diagnosed between 65 and 74 years old. Risk factors include the following:

Smoking, which doubles the risk

Hypertension

Excess use of phenacetin

Acquired cystic kidney disease in patients on dialysis

Exposure to certain radiopaque contrast agents, asbestos, cadmium, and leather tanning and petroleum products

Some familial syndromes, particularly von Hippel–Lindau disease and tuberous sclerosis

RCC can trigger thrombus formation in the renal vein, which occasionally propagates into the vena cava. Tumor invasion of the vein wall is uncommon. RCC metastasizes most often to the lymph nodes, lungs, adrenal glands, liver, brain, and bone.

General reference

1. American Cancer Society : Key statistics about kidney cancer. Accessed September 10, 2023.

Signs and Symptoms of Renal Cancer

Symptoms usually do not appear until late, when the tumor may already be large and metastatic. Gross or microscopic hematuria is the most common manifestation, followed by flank pain, fever of unknown origin (FUO), and a palpable mass. Other nonspecific symptoms can include fatigue, weight loss, and early satiety. Sometimes hypertension results from segmental ischemia or pedicle compression. Paraneoplastic syndromes occur in 20% of patients. Polycythemia can result from increased erythropoietin activity. However, anemia may also occur. Hypercalcemia is common and may require treatment. Thrombocytosis, cachexia, or secondary amyloidosis may develop.

Diagnosis of Renal Cancer

CT with contrast or MRI

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Most often, a renal mass is detected incidentally during abdominal or spinal imaging (eg, CT, ultrasonography, MRI) done for other reasons. Otherwise, diagnosis is suggested by clinical findings and confirmed by abdominal CT before and after injection of a radiocontrast agent or by MRI. (See Genitourinary Imaging Tests .) A renal mass that is enhanced by radiocontrast strongly suggests renal cell carcinoma (RCC). CT and MRI also provide information about local extension and nodal and venous involvement. MRI provides further information about extension into the renal vein and vena cava and has replaced inferior vena cavography. Ultrasonography and intravenous urography may show a mass but provide less information about the characteristics of the mass and extent of disease than do CT or MRI.

Often, nonmalignant and malignant masses can be distinguished radiographically, but sometimes biopsy or surgery is needed for confirmation. Needle biopsy does not have sufficient sensitivity when findings are equivocal; it is recommended only when the diagnosis would impact treatment choice, such as when there is an infiltrative pattern instead of a discrete mass, when the renal mass may be a metastasis from another known cancer, or sometimes to confirm a diagnosis before chemotherapy or systemic therapy for metastatic renal masses.

Three-dimensional CT, CT angiography, or magnetic resonance angiography is used before surgery, particularly before nephron-sparing surgery, to define the nature of RCC, to more accurately determine the number of renal arteries present, and to delineate the vascular pattern. (See Genitourinary Imaging Tests .) These imaging techniques have replaced aortography and selective renal artery angiography.

A chest x-ray and liver tests are essential. If chest x-ray is abnormal, chest CT is done. If alkaline phosphatase is elevated, bone scanning is needed. Serum electrolytes, blood urea nitrogen (BUN), creatinine, and calcium are measured. BUN and creatinine are unaffected unless both kidneys are diseased.

Information from the evaluation makes preliminary staging possible. The TNM (tumor, node, metastasis) system has been refined to be precise (see tables AJCC/TNM Staging of Renal Cell Carcinoma and TNM Definitions for Renal Cell Carcinoma ). At diagnosis, RCC is localized in 45%, locally invasive in about 33%, and spread to distant organs in 25% of patients.

Diagnosis reference

1. Roussel E, Capitanio U, Kutikov A, et al : Novel imaging methods for renal mass characterization: A collaborative review. Eur Urol 81(5):476-488, 2022. doi: 10.1016/j.eururo.2022.01.040

Treatment of Renal Cancer

For early renal cell carcinoma (RCC), surgical treatment, active surveillance, or thermal ablation

For advanced RCC, palliative therapies or experimental protocols

Curative treatments

Radical nephrectomy (removal of kidney, perirenal fat, Gerota fascia +/- ipsilateral adrenal gland) is standard treatment for localized RCC and provides a reasonable chance for cure. Results with open or minimally invasive procedures are comparable; recovery is generally easier with minimally invasive procedures. Nephron-sparing surgery (partial nephrectomy) is possible and appropriate for many patients. Partial nephrectomy is gaining popularity because it results in a lower incidence of chronic kidney disease than radical nephrectomy. It is the standard of care for clinically staged T1a tumors (cT1a, < 4 cm) and should be considered in patients with T1b or T2 tumors and those with absolute indications for nephron preservation (eg, bilateral renal masses, CKD, solitary kidney). Radical nephrectomy should be considered in patients with a normal contralateral kidney, normal kidney function, and more advanced primary tumors (cT1b through cT4).

Nonsurgical destruction of renal tumors via freezing (cryosurgery) or thermal energy (radiofrequency ablation), often percutaneously, should be considered for tumors smaller than 3 cm. For small renal masses, active surveillance (with delayed intervention) should be considered a first-line treatment option, particularly if active treatments pose risks and/or patients have significant comorbidities. Decision-making for treatment is complex and multifactorial and typically involves shared decision-making ( 1 ).

For tumors involving the renal vein and vena cava, surgery may be curative if no nodal or distant metastases exist.

If both kidneys are affected, partial nephrectomy of one or both kidneys is preferable to bilateral radical nephrectomy if technically feasible.

2 ). Its use has been limited. The KEYNOTE-564 study ( 3

Palliative treatments

Palliation can include nephrectomy, tumor embolization, external beam radiation therapy and systemic therapy. Resection of metastases offers palliation and, if metastases are limited in number, prolongs life in some patients, particularly those with a long interval between initial treatment (nephrectomy) and development of metastases. Although metastatic RCC is traditionally characterized as radioresistant, radiation therapy can be palliative when RCC is oligometastatic, particularly to the bone.

Other treatments are experimental. They include stem cell transplantation

4 ); however, that trial was criticized for its patient selection (heavily enriched with poor-risk patients with minimal inclusion of intermediate-risk patients).

The current recommendations are to consider cytoreductive nephrectomy in patients with any of the following criteria:

The bulk of the disease burden in the kidney

Symptomatic bleeding or pain from the primary tumor

Presence of a paraneoplastic tumor

Excellent performance status with normal contralateral kidney function

Increased knowledge of genetic subtypes of RCC is leading to evolving management recommendations that are more specific.

Treatment references

1. Chandrasekar T, Boorjian SA, Capitanio U, et al : Collaborative review: Factors influencing treatment decisions for patients with a localized solid renal mass. Eur Urol 80(5):575-588, 2021. doi: 10.1016/j.eururo.2021.01.021

2. Ravaud A, Motzer RJ, Pandha HS et al N Engl J Med  8;375(23):2246-2254, 2016. doi: 10.1056/NEJMoa1611406

3. Choueiri TK, Tomczak P, Park SH, et al for the KEYNOTE-564 Investigators N Engl J Med 385(8):683-694, 2021. doi: 10.1056/NEJMoa2106391

4. Mejean A, Ravaud A, Thezenas S, et al N Eng J Med 379:417-427, 2018. doi: 10.1056/NEJMoa1803675

Prognosis for Renal Cancer

Five-year survival rates ( 1 ) range from about 81% for the American Joint Commission on Cancer (AJCC) stage grouping I (T1 N0 M0) to 8% for stage grouping IV (T4 or M1) ( 1 ). Prognosis is poor for patients with metastatic or recurrent renal cell carcinoma (RCC) because treatments are usually ineffective for cure, although they may be useful for palliation.

Prognosis reference

1. American Cancer Society, Cancer Statistics Center : Kidney and renal pelvis at a glance. Accessed September 29, 2023.

RCC, an adenocarcinoma, accounts for 90 to 95% of primary malignant renal tumors.

Symptoms (most often gross or microscopic hematuria) usually do not develop until the tumor is large or metastatic, so incidental discovery is common.

Diagnose RCC by MRI or contrast-enhanced CT and do a chest x-ray, blood tests (including liver tests) to investigate staging.

Treat most localized RCC by surgery, active surveillance or thermal ablation.

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Renal Cell Carcinoma: Clinical Presentation, Staging, and Prognostic Factors

• First Online: 29 November 2011

Cite this chapter

• Hema Vankayala M.D. 3 ,
• Dongping Shi M.D. 4 &
• Ulka Vaishampayan M.D. 3  

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Renal cell cancer (RCC) accounts for 2–3% of adult malignancies, and the incidence appears to be rising each year. Cigarette smoking, obesity, and hypertension are contributing risk factors, among others. Clear cell RCC is the most common histologic subtype and accounts for approximately 70% of RCC. A small minority (<5%) of RCC cases is considered hereditary. The majority of RCC is initiated by structural alterations in the Von Hippel–Lindau gene. Clinically, only 9% of kidney cancers present with the classic triad of hematuria, flank pain, and fever. About a third of the patients have advanced disease at diagnosis. It has been called one of the “great masqueraders” secondary to its paraneoplastic manifestations: up to 20% of patients present with such. The imaging gold standard for the diagnosis, staging, and surveillance of RCC is the computed tomography scan. Tumor stage and grade are the most important prognostic factors. This chapter highlights the clinical presentation of RCC in both localized and metastatic settings.

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Hema Vankayala M.D. & Ulka Vaishampayan M.D.

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Dongping Shi M.D.

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Vankayala, H., Shi, D., Vaishampayan, U. (2012). Renal Cell Carcinoma: Clinical Presentation, Staging, and Prognostic Factors. In: Lara, Jr., P., Jonasch, E. (eds) Kidney Cancer. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-21858-3_5

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Presentation

Acute exacerbation of chronic abdominal pain. Patient also has early satiety and weight loss.

Patient Data

Large, heterogenous, solid and necrotic exophytic mass arising from the mid to lower pole of the left kidney. There is also a central calcification within the mass. There is a small amount of free fluid adjacent to the mass. There is a conglomerate of enlarged retroperitoneal lymph nodes . There is encasement of the left renal artery by a retroperitoneal lymph node.

Case Discussion

This is a case of sarcomatoid renal cell carcinoma.

The patient underwent a left renal mass and periaortic lymph node biopsy by interventional radiology. Gross pathology of the renal mass demonstrated irregular, soft tan tissue. Both the lymph node and renal mass were positive for AE1/AE3, C-KIT, and PAX-8. These findings support the diagnosis of a sarcomatoid renal cell carcinoma.

Given his age, the patient denied chemoradiation and/or surgery.

Co-author: David Le

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BIOMARKERS SYMPOSIUM Session 1: Biomarker Technologies in RCC

Moderated by toni choueiri, dfci & mahrukh huseni, genentech, genomic dna/rna biomarkers.

Ari Hakimi, Memorial Sloan Kettering

(Video presentation begins at 00:45)

Spatial Biomarkers: Tissue-Based in situ Analyses Including IF for Biomarker Development

High-dimensional/spatial tools for biomarker discovery in rcc, how can ai guide biomarker development and progress in rcc, developing metabolic imaging agents in kidney cancer, ct-based radiomics model for the prediction of genomic alterations in renal cell carcinoma (rcc), circulating and intratumoral immune determinants of response to atezolizumab plus bevacizumab in patients with variant histology or sarcomatoid renal cell carcinoma.

Note presentation time stamps to locate specific speakers.

Biomarkers Session One Q&A begins at 1:10:55.

BIOMARKERS SYMPOSIUM Session 2: Clinical Biomarkers: Trial Data and Directions

Moderated by medhi mollapour, state university of new york, and tom powles, barts cancer centre, emerging biomarkers for the ipi/nivo: new data from prism.

Tom Powles , Barts Cancer Centre

(Video presentation begins at 01:06)

Learning from the Atezolizumab Biomarker Program in RCC: Lessons for Future Trial Designs

David McDermott , Beth Israel Deaconess Medical Center

(Video presentation begins at 11:20)

Biomarkers for PD-1 Based Therapies in RCC

Saurabh Gupta , Bristol Myers Squibb

(Video presentation begins at 23:15)

Designing Clinical Trials in the Perioperative Setting in RCC

Axel Bex , Royal Free Hospital London

(Video presentation begins at 35:40)

Development and Clinical Application of ctDNA in RCC

Sylvan Baca , Dana-Farber Cancer Institute

(Video presentation begins at 46:20)

Biomarkers of Toxicity to Immune Checkpoint Blockers

Alexander Gusev , Dana-Farber Cancer Institute

(Video presentation begins at 56:05)

KIM 1 and Kidney Cancer: Multiple Setting or an Ideal Setting?

Wenxin (Vincent) Xu , Dana-Farber Cancer Institute

(Video presentation begins at 1:07:05)

Utilization of ctDNA for RCC Disease Monitoring and Treatment Response

Adam ElNaggar , Natera

(Video presentation begins at 1:18:35)

Biomarkers Session Two Q&A begins at 1:28:30.

MENTORSHIP & SPONSORSHIP Challenges and Opportunities

Moderated by hans hammers, utsw, and tom powles, barts cancer centre.

Session 1: Modulating Tumor Microenvironment in Kidney Cancer

The bone metastasis immunological niche: unraveling its complexity and role in therapy response and resistance.

Eleonora Dondossola , MD Anderson Cancer Center

(Video presentation begins at 01:35)

Metabolic Demands and Determinants in the RCC Tumor Microenvironment

Kimryn Rathmell , Vanderbilt University Medical Center

(Video presentation begins at 14:55)

Identifying Novel Immune Evasion Tumor Immune Networks as Targets for ccRCC Immunotherapy

Hartland Jackson , Samuel Lunenfeld Research Institute

(Video presentation begins at 32:30)

Targeting a Combined VHL and 3p Chromatin Remodeler Deficit in Renal Cell Carcinoma

Ruhee Dere , Baylor College of Medicine

(Video presentation begins at 46:10)

Session 2: Biology of Non-Clear Cell Subtypes

Defining cellular and genetic factors for renal cell carcinoma subtypes.

Jung Wook Park , Duke Cancer Institute

(Video presentation begins at 00:35)

Targeting GPNMB in Renal Tumors in Tuberous Sclerosis Complex and Translocation Renal Cell Carcinoma

Kaushal Asrani , Johns Hopkins University

(Video presentation begins at 16:15)

Deep Functional Characterization of MiT/TFE Fusions in Translocation Renal Cell Carcinoma

Srinivas Viswanathan , Dana-Farber Cancer Institute

(Video presentation begins at 29:40)

Targeting TFEB and TFE3 in Renal Tumorigenesis

Elizabeth Henske , Brigham and Women’s Hospital

(Video presentation begins at 45:15)

Session 3: Trials in Progress: Moving the Needle

Zanzalintinib in combination with immune checkpoint inhibitors: design of the renal cell carcinoma expansion stage cohorts in stellar-002.

Neil Shah , Memorial Sloan Kettering

(Video presentation begins at 00:50)

LITESPARK-024: A Randomized Phase 1/2 Study of Belzutifan with or without Palbociclib for Previously Treated Advanced Renal Cell Carcinoma

David McDermott , Beth Israel

(Video presentation begins at 05:40)

SAMETA: A Phase III Study of Savolitinib + Durvalumab vs Sunitinib and Durvalumab Monotherapy in Patients with MET-Driven, Unresectable, Locally Advanced/Metastatic Papillary Renal Cell Carcinoma

Toni Choueiri , Dana-Farber Cancer Institute

(Video presentation begins at 09:00)

A Phase 1/2, Open Label Dose-Escalation and Expansion Trial of NKT2152, an Orally Administered HIF2α Inhibitor, to Investigate Safety, PK, PD and Clinical Activity in Patients with Advanced ccRCC

(Video presentation begins at 14:15)

NRG-GU012: Randomized Phase II Stereotactic Ablative Radiation Therapy (SABR) for Metastatic Unresected Renal Cell Carcinoma (RCC) Receiving Immunotherapy (SAMURAI)

Rana McKay , UC San Diego

(Video presentation begins at 17:05)

STARLITE 1: Phase 1b/2 Study of Combination 177Lu Girentuximab Plus Cabozantinib and Nivolumab in Treatment Naïve Patients with Advanced Clear Cell RCC

Eric Jonasch , MD Anderson

(Video presentation begins at 22:45)

Phase 1/2 Study of PRO1160, a CD70-Directed Antibody-drug Conjugate, in Patients with Advanced Solid Tumors and Hematologic Malignancies

(Video presentation begins at 26:35)

Phase 1b/2 Trial of Ipilimumab, Nivolumab, and Ciforadenant (INC) (Adenosine A2a Receptor Antagonist) in First-Line Advanced Renal Cell Carcinoma

Katy Beckermann , Vanderbilt University Medical Center

(Video presentation begins at 29:30)

Optimal Treatment by Invoking Biologic Clusters in Renal Cell Carcinoma (OPTIC RCC)

(Video presentation begins at 33:15)

Session Three Q&A begins at 37:20.

BREAKING BARRIERS TO TRIAL ENROLLMENT Special Session Four

Moderated by michael atkins, georgetown lombardi comprehensive cancer center.

The panelists discussed the challenges and opportunities in clinical trial enrollment, focusing on how to decrease barriers of entry for kidney cancer patients. They explored strategies to make clinical trials more inclusive for all kidney cancer patients, regardless of race, age, location, or gender, which are all currently limiting access. The panelists also shared their insights on the role of regulatory bodies, pharmaceutical companies, and healthcare providers in facilitating trial enrollment.

FEATURED SPEAKER: New Directions in Basic Kidney Cancer Research

New directions in basic kidney cancer research.

SESSION 5: Clinical and Scientific Updates in Kidney Cancer

Front line systemic therapy sessions, subsequent line treatments for advanced disease.

Robert Motzer , Memorial Sloan Kettering Cancer Center

(Video presentation begins at 13:00)

Adjuvant Treatment Options

Bradley McGregor , Dana-Farber Cancer Institute

(Video presentation begins at 28:15)

Radiation Therapy Strategies in RCC

Raquibul Hannan , UTSW

(Video presentation begins at 38:30)

Strategies for Patients with Non-Clear Cell RCC

Chung-Han Lee , Memorial Sloan Kettering Cancer Center

(Video presentation begins at 49:40)

Novel Therapies Outside Immunotherapy

Rana McKay , University of California (San Diego)

(Video presentation begins at 1:00:45)

Novel Immunotherapy Strategies

David Braun , Yale 

(Video presentation begins at 1:15:10)

Session Five Q&A begins at 1:24:30.

SESSION 6: Immunotherapy Advances and Research

Car t therapies for rcc: what we've learned.

Avery Posey , Penn Medicine

Targeting Interleukin-1beta to Overcome Adaptive Immune Resistance in Renal Cell Carcinoma

Matthew Dallos , MSKCC

(Video presentation begins at 25:00)

Targeting RNA Sensing to Enhance Immunotherapy Responses in Kidney Cancer

John Wilson , Vanderbilt

(Video presentation begins at 40:55)

A Novel STAT3 Antisense Oligonucleotide-Based Immunotherapy for Renal Cell Carcinoma

Marice Alcantara , City of Hope

(Video presentation begins at 52:55)

Derepression of Human Endogenous Retrovirus and Implications for Immunotherapy for Clear Cell Renal Cell Carcinoma

Qinqin Jiang , DFCI

(Video presentation begins at 1:04:30)

SESSION 7: Oral Abstract Presentations

Final database lock results of the phase 2 cohort of lenvatinib + pembrolizumab for progressive disease after a pd-1/pd-l1-containing therapy in metastatic clear cell renal cell carcinoma.

Chung-Han Lee , MSKCC

(Video presentation begins at 01:20)

ORCHID: A Phase II Study of Olaparib in Metastatic Renal Cell Carcinoma Patients HarborIng a BAP1 or Other DNA Repair Gene Mutations

Yasser Ged , Johns Hopkins

(Video presentation begins at 09:15)

Circulating KIM-1 is a Minimally Invasive Biomarker Correlated with Treatment Response to Nivolumab in Patients with Metastatic Renal Cell Carcinoma

Wenxin (Vincent) Xu , DFCI 

(Video presentation begins at 28:55)

Functional and Translational Consequences of Immunometabolic Coevolution in ccRCC

Ed Reznik , MSKCC

(Video presentation begins at 36:15)

Host Immune Signatures as Predictors of Response to Immunotherapy-Based Regimens in Patients with Metastatic Renal Cell Carcinoma (mRCC)

Eddy Saad , DFCI

(Video presentation begins at 57:45)

Spatial Proteomics Enables Identification of Prognostic Biomarkers in Papillary Renal Cell Carcinoma

Anupama Reddy , Vindhya Data Science Inc.

(Video presentation begins at 1:06:00)

Session Seven is structured with two presentations, followed by Q&A, then two more presentations, etc. The Q&A sessions are at 18:00, 44:20, and 1:15:30.

SESSION 8: Rapid Abstract Presentations

Moderated by:  Sumanta Pal, City of Hope & Deepak Kilari, Medical College of Wisconsin

Dissection of Tumor-Intrinsic and Tumor-Extrinsic Features of MiT/TFE Translocation Renal Cell Carcinoma Via Single-Cell RNA Sequencing

Prathyusha Konda , DFCI

Characterization of the Cellular Origin and Oncogenic Mechanisms of Chromophobe Renal Cell Carcinoma (ChRCC) and Renal Oncocytic Neoplasms

Chris Labaki , DFCI

(Video presentation begins at 06:00)

Epigenomic Profiling Nominates Master Transcription Factors (TFs) Driving Sarcomatoid Differentiation (SD) of Renal Cell Carcinoma (RCC)

Karl Semaan , DFCI

(Video presentation begins at 10:45)

A Modified IL-18 Drug in Combination with CTLA-4 Blockade Enhances Anti-Tumor Efficacy in Preclinical Models of Renal Cell Carcinoma

David Schoenfeld , Yale 

(Video presentation begins at 22:35)

The Identification of a Novel Orally Available Ferroptosis Inducer for the Treatment of Clear Cell Renal Carcinoma

Mei Koh , Kuda Therapeutics, Inc.

(Video presentation begins at 28:25)

The Impact of Insurance Status on Progression-Free Survival (PFS) and Overall Survival (OS) in Patients with Metastatic Renal Cell Carcinoma (mRCC)

Daniela Castro , City of Hope

(Video presentation begins at 38:20)

Examining Trends in Kidney Cancer Mortality by Gender and Race in the United States: A 20-Year AnalysisccRCC

Chinmay Jani , Univ. of Miami

(Video presentation begins at 44:35)

Impact of Time to Metastasis (Synchronous vs. Metachronous) on Outcomes in Metastatic Renal Cell Carcinoma Patients Treated with First Line Immune-Checkpoint Inhibitors (ICI)-based Combinations

George Gebrael , Huntsman

(Video presentation begins at 50:00)

Session Eight is structured with three presentations, followed by Q&A, then more presentations, etc. The Q&A sessions are at 15:55, 34:40, and 54:40.

Special Session for Investigators: Expert Insights on the Research Funding Landscape

Writing a grant: the nci perspective, cdmrp grant proposals: tips for the first time applicant, arpa-h opportunities for research funding.

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The unusual first sign of presentation of renal cell carcinoma: a rare case report

Rocco morra.

1 Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy;

Antonio D’Ambrosio

Erica pietroluongo, pietro de placido, liliana montella.

2 Oncology Operative Unit, “Santa Maria delle Grazie” Hospital (ASL NA 2 NORD), Pozzuoli, Italy;

Vitantonio Del Deo

3 Azienda Ospdaliera Universitaria Federico II of Naples, Clinical Department of Oncology and Hematology, Naples, Italy;

Marianna Tortora

4 Coordinating Rare Tumors Reference Center of Campania Region (CRCTR), Clinical Department of Oncology and Hematology, Azienda Ospdaliera Universitaria Federico II of Naples, Naples, Italy

Elide Matano

Vincenzo damiano, giovannella palmieri, sabino de placido, mario giuliano, associated data.

The article’s supplementary files as

Renal cell carcinoma (RCC) usually is characterized by a slow pattern of growth, although with an unpredictable evolution and metastatic potential, favored by its extensive vascularity and related high angioinvasive profile. The most common sites of metastases from kidney cancer are lung, lymph nodes, bone and liver; whereas orbital metastases are very uncommon. In more than 25% of cases, orbital metastases are the first manifestation of a primary tumor of unknown origin. The clinical features of orbital metastases from kidney cancer are non-specific and could divert attention from the real problem.

Case Description

In this article, we describe the case of a 72-year-old male patient reporting a painful mass on the right orbit, with exophthalmos and ptosis, as the first and unique signs of a previously undetected advanced RCC. Due to the clinical conditions, the patient underwent palliative radiation therapy delivered to the orbital lesion with the scope to relieve pain; subsequently started systemic therapy with pazopanib at the dose of 800 mg daily. Unfortunately, he did not achieve any benefit from systemic therapy, his conditions progressively worsened, and he finally passed away after four months of treatment due to rapid disease progression.

Conclusions

Despite its rarity, differential diagnosis of an orbital lesion should always consider the possibility of metastasis from RCC, performing an appropriate radiological evaluation.

Introduction

Kidney cancer is estimated to account for approximately 5% of new cancer diagnoses in men and 3% of new cancer diagnoses in women in the US in 2020 ( 1 ). Renal cell carcinoma (RCC) accounts for approximately 90% of kidney cancers, while clear cell, papillary and chromophobe subtypes account for approximately 90% of renal cell cancers ( 2 ). The peak of RCC incidence is in the sixth decade with nearly twice incidence in men as compared with women. The incidental detection of RCC is about 50% of cases; in fact, nowadays, the classic triad of presenting symptoms for renal cancer (hematuria, flank pain, and palpable mass) is a rare finding, usually observed in case of advanced disease ( 3 ). At the time of diagnosis, about 54% of patients present organ-confined disease, 20% locally advanced disease, and the remaining 25% have metastatic disease ( 4 ). The most common sites of metastases are lung (45%), lymph nodes (22%), bones (30%), and liver (20%) ( 5 ). RCC ranks as the third neoplasm among the malignancies that metastasize most commonly to anatomic sites of head and neck, after breast and lung cancer ( 6 ). Orbital and intraocular metastases of RCC are rare, accounting together for less than 2% of all ophthalmic metastasis. In individual series, the eye is involved in 2% to 5% of cases of metastatic disease, whereas the orbit is involved in 1% to 5%, representing sometimes the first clinical manifestation of kidney cancer ( 7 ).

This article aimed to present a patient with ptosis and exophthalmos, due to orbital metastasis, as the first manifestation of a previously undetected RCC. We present the following case in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-22-16/rc ).

Case presentation

A 72-year-old man, presented to our ophthalmology department reporting a mass in the right eye accompanied by throbbing pain and vision loss. Past medical history was notable for type II diabetes mellitus, gouty tophus, essential hypertension, chronic kidney disease, a third-degree atrioventricular block that required a pacemaker implant. He had neither personal nor family history of cancer. The physical examination revealed third-grade exophthalmos on the right eye and a firm and fixed mass on the right superior orbit on palpation ( Figure 1 ). Palpebral ptosis and conjunctival hyperemia, with vision loss and slightly limited right eye movements, were also present. Ultrasonography of the right eye showed the presence of a large mass arising from the lacrimal gland, extending to the temporal lobe and occupying I/II/III Benedikt’s space, compatible with lymphoma ( Figure 2 ). Cranial computed tomography scan (CT scan) with contrast demonstrated the presence of an expansive lesion, with a maximum diameter of 50×30 mm on axial plane, located at the upper outer portion of the right orbit, right anterior clinoid process, and right lesser wing of the sphenoid bone. The lesion infiltrated the right lateral rectus muscle and part of the right superior rectus muscle and caused the medial displacement of the right optic nerve, with initial signs of pachymeningeal enhancement in the right front-orbital area ( Figure 3 ). Tumor mass showed irregular contrast enhancement. To obtain tumor tissue for pathology assessment, the patient underwent an orbitotomy. A subsequent 18-fluorodeoxyglucose-positron emission tomography/computerized tomography scan (18F-FDG PET/CT scan) showed a lesion on the right orbit measuring approximately 25×38 mm, with diffuse tracer uptake in the right orbit (SUVmax 5.5), lateral and posterior wall erosion of orbit and with extra-orbital extension, subcentimetric multiple lung nodules, the greater located on inferior lobe (SUVmax 3.9), a hyperdense lesion enclosing hypodense necrotic areas in the lower third of right kidney with a maximum diameter of 50 mm (SUVmax 12.3), and disseminated bone involvement with mixed lytic and sclerotic bone metastases ( Figure 4 ). We finally got the histological examination that proved the presence of a malignant lesion, likely epithelial, highly suggestive of a secondary lesion from renal cell carcinoma. Immunohistochemistry showed positivity for paired-box gene 8 ( PAX8 ) , cytokeratin 19 (CK 19) and renal cell carcinoma marker (RCC-Ma) and negativity for S100, thyroid transcription factor-1 (TTF1), human melanoma black -45 (HMB45), p63, cytokeratin 7 (CK 7), placental alkaline phosphatase (PLAP) and GATA binding protein 3 (GATA 3) ( Figures 5-7 ​ 5-7 ​ ). ). Therefore, the patient underwent palliative radiation therapy delivered to the orbital lesion with the scope to relieve pain, with a total dose of 20 Gy in 5 fractions. He subsequently started systemic therapy with pazopanib, a multi-target tyrosine kinase inhibitor (TKI) used routinely in the treatment of advanced renal cancer, at the dose of 800 mg daily. Unfortunately, he did not achieve any benefit from systemic therapy, his conditions progressively worsened, and he finally passed away after four months of treatment due to rapid progression of disease. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent for the publication of this case report, including radiographic images and patient picture was obtained from the patient’s daughter. A copy of the written consent is available for review by the editorial office of this journal.

Patient’s clinical appearance at the first presentation, showing right palpebral ptosis and exophthalmos. This image is published with the patient’s daughter’s consent.

Ocular ultrasonography of the right eye. Red circles show a large mass arising from the lacrimal gland, reaching the temporal lobe.

Cranio-facial computed tomography scan (CT scan) showing the lesion located at the upper outer portion of right orbit, with bone erosion, muscle and pachymeningeal infiltration.

Coronal fusion images of 18F-FDG PET/CT scan showing 18 F-FDG uptake in the right orbit, multiple FDG-positive pulmonary nodules, bone metastasis and a lesion with a maximum diameter of 50 mm in the right kidney. 18F-FDG PET/CT, 18-fluorodeoxyglucose-positron emission tomography/computerized tomography.

Hematoxylin and eosin staining. Magnification ×2.

Immunohistochemical staining for RCC-Ma. Magnification ×2.8. RCC-Ma, renal cell carcinoma marker.

Immunohistochemical staining for PAX8. Magnification ×2. PAX8, paired-box gene 8.

Overall, metastatic dissemination to the orbit is uncommon in cancer patients; indeed, only 2–5% of them will develop a secondary lesion in this anatomic site ( 8 , 9 ). Moreover, about only 1% to 13% of orbital mass lesions are represented by metastases. Secondary orbital lesions, as reported in clinical cases, are typically found in advanced cancer patients with an age between 51 and 60 years old and occur 19 months to 7 years after the primary tumor diagnosis ( 8 ). The most frequent malignancies spreading to the orbit are breast, lung, and prostate cancers, as well as melanoma and skin cancers. In more than 25% of cases, orbital metastases are the first manifestation of a primary tumor of unknown origin ( 10 ). Generally, orbital metastases can occur with 5 different clinical patterns: mass effect, infiltrative tumor growth pattern, functional impact, signs of inflammation or no symptoms ( 11 ). Some of these clinical manifestations can coexist. Kidney cancer is usually a well-encapsulated tumor, with a clinical behavior characterized by slow growth, although it often presents an unpredictable evolution and displays metastatic potential ( 12 ). The most common sites of kidney cancer metastases are lung (45%), lymph nodes (22%), bone (30%), and liver (20%) ( 5 ). Metastases to the head and neck region have been found in 15% of cases, most frequently involving the nose, paranasal sinuses, and oral cavity. Ocular metastases from kidney cancer usually involve the iris, ciliary body, and choroids, although eyelid and lacrimal sac involvement have also been described ( 13 ). Therefore, orbital metastases from kidney cancer are very rare.

The clinical features of orbital metastases from kidney cancer are non-specific and could divert attention from the real problem. Indeed, ophthalmologic symptoms, like ptosis, diplopia, vision loss, epiphora, strabismus, and cataract, could rely on many factors, such as size, type, and location of metastasis and are not suggestive of the nature and origin of the primary tumor ( 6 ). Hence, in the absence of pathognomonic symptoms of kidney cancer, imaging is crucial. A total body CT scan is necessary to orient the diagnosis, rule out other secondary lesions and identify the ideal site for tissue biopsy. In this case, the orbital biopsy was essential to identify the malignant nature of the lesion, as well as its histological features.

The mechanism by which kidney cancer metastasizes to the orbit is still unknown. One potential mechanism of tumor diffusion to the orbital area is a hematogenous spread of circulating tumor cells, as the eye has no lymphatic channels. Thereby, tumor cells reach the orbit by entering the circulatory system and spreading to the lung first. Tumor cells migration with retrograde venous flow through the vertebral-basilar plexus is another potential mechanism ( 14 ).

During the last decades, many advances have been made for the treatment of metastatic RCC. The drastic change happened when the new combinations of immune checkpoint inhibitors (ICIs) with tyrosine kinase inhibitors (TKIs) or the association of anti-PD-1 plus anti CTLA-4 improved the therapeutic portfolio, especially for patients with intermediate and poor risk class.

Indeed, as emerged from the Keynote 426 study, the combination of Pembrolizumab plus Axitinib, or from the CLEAR and Checkmate ER trials, the combination of Pembrolizumab plus Lenvatinib and Nivolumab plus Cabozantinib, respectively, demonstrated to be more effective as compared to sunitinib monotherapy. At the same time, the combination of Nivolumab and Ipilimumab showed significantly superior overall survival (OS) and overall response rate (ORR) compared to sunitinib for intermediate and poor risk patients ( Table 1 ).

PFS, progression-free survival; OS, overall survival; ITT, intention-to-treat; IMDC, International mRCC Database Consortium; HR, hazard ratio; mo, months; NR, not reached; I/P, intermediate/poor risk; NE, could not be estimated.

Despite all the recent progress in anticancer therapy, patient prognosis is still poor in the presence of orbital metastases, maybe due to the high systemic cancer burden and/or to a particularly aggressive disease. Indeed, there are currently no available data demonstrating a clear clinical benefit achieved by combination therapies in the management of patients with orbital metastases from kidney cancer. However, the combination of TKI plus anti PD-1 might be the preferred option when a rapid tumor response is needed due to disease burden and related symptoms, given considering the reported response rates, which were greater than those obtained with ipilimumab plus nivolumab ( 15 , 16 ).

A recent review showed a median OS of 6 months (range, 0.2–144 months), and a 2-year survival rate of 29% for all cases of cancer patients with orbital metastases ( 17 ). Long-term outcome has not significantly improved over time and systemic and locoregional treatments are mostly palliative ( 8 ).

Despite the diagnostic delay, due to the unusual clinical presentation, this case suggests a poor efficacy of TKI monotherapy, as patient survival was only 4 months from treatment start.

The radiotherapy treatment resulted in the greatest clinical benefit achieving a pain reduction.

In summary, we described here a rare case of orbital metastasis, as the first and unique sign of a previously undetected RCC. Since ophthalmic signs and symptoms are not pathognomonic of any cancer type, their occurrence can suggest different clinical conditions resulting in delayed diagnosis and treatment. Therefore, despite its rarity, differential diagnosis of an orbital lesion should always consider the possibility of metastasis from kidney cancer.

Supplementary

Acknowledgments.

This report was part of research activity of the Rare Tumors Coordinating Center of Campania Region (CRCTR) recognized as full member of the European Reference Network (ERN-EURACAN). The authors would like to acknowledge the ERN-EURACAN as a powerful resource for transnational collaboration in rare cancers.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent for the publication of this case report, including radiographic images and patient picture was obtained from the patient’s daughter. A copy of the written consent is available for review by the editorial office of this journal.

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-22-16/rc

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-22-16/coif ). SDP reports consulting fees for Consulting or advisory Role: GSK, MSD, Seagen, Daiichi Sankyo, Lilly, Clovis, Celgene, Astrazeneca, Novartis, Pfizer, Roche; and Speaker’s Bureau: Celgene, Astrazeneca, Novartis, Pfizer, Roche. MG reports consulting fees for Consulting or advisory Role: Astrazeneca, MSD, Seagen, Daiichi Sankyo, Lilly, Celgene, Novartis, Pfizer; Speaker’s Bureau: Lilly, Celgene, Novartis, Pfizer, Istituto Gentili, Eisai Europe Ltd., Roche; Travel, accommodation, expenses: Novartis, Pfizer, Roche. The other authors have no conflicts of interest to declare.

Renal cell carcinoma histologic subtypes exhibit distinct transcriptional profiles

Affiliations.

• 1 Department of Internal Medicine, University Hospitals Seidman Cancer Center, Cleveland, United States of America.
• 2 Division of Hematology and Oncology, Department of Internal Medicine, UC Davis Comprehensive Cancer Center, Sacramento, United States of America.
• 3 Clinical and Translational Research/Medical Affairs, Caris Life Sciences, Irving, United States of America.
• 4 UT Southwestern Kidney Cancer Program, UT Southwestern Medical Center, Dallas, United States of America.
• 5 Department of Internal Medicine, Levine Cancer Institute Atrium Health, Charlotte, United States of America.
• 6 Department of Medicine, Division of Oncology, Albert Einstein College of Medicine, Bronx, United States of America.
• 7 Clinical Genomics, Hoag Memorial Hospital Presbyterian, Newport Beach, United States of America.
• 8 Winship Cancer Institute, Emory University School of Medicine, Atlanta, United States of America.
• 9 Department of Medical Oncology, University of Alabama, Birmingham, United States of America.
• 10 Department of Medical Oncology, Fox Chase Cancer Center, Philadelphia, United States of America.
• 11 Department of Internal Medicine, Georgetown University Lombardi Comprehensive Cancer Center, Washington D.C., United States of America.
• 12 Department of Internal Medicine, Fox Chase Cancer Center, Philadelphia, United States of America.
• 13 Department of Pathology, Fox Chase Cancer Center, Philadelphia, United States of America.
• 14 Medical School, University of Minnesota, Minneapolis, United States of America.
• 15 Barbara Ann Karmanos Cancer Institute, Wayne State University, Detroit, United States of America.
• 16 Department of Molecular Biology, Caris LifeSciences, Irving, United States of America.
• 17 Chairman of the Caris Precision Oncology Alliance, Caris LifeSciences, Phoenix, United States of America.
• 18 Moores Cancer Center, UCSD, San Diego, United States of America.
• PMID: 38652565
• DOI: 10.1172/JCI178915

Molecular profiling of clear cell RCC (ccRCC) tumors of clinical trial patients has identified distinct transcriptomic signatures with predictive value, yet data in non-clear cell variants (nccRCC) are lacking. We examined the transcriptional profiles of RCC tumors representing key molecular pathways, from a multi-institutional, real-world patient cohort, including ccRCC (n = 508) and centrally-reviewed nccRCC (n = 149) samples. ccRCC had increased angiogenesis signature scores compared to the heterogeneous group of nccRCC tumors (mean z-score 0.37 vs -0.99, P < 0.001), while cell cycle, fatty acid oxidation (FAO)/AMPK signaling, fatty acid synthesis (FAS)/pentose phosphate signature scores were increased in one or more nccRCC subtypes. Among both ccRCC and nccRCC tumors, T-effector scores statistically correlated with increased immune cell infiltration and were more commonly associated with immunotherapy-related markers (PD-L1+/TMB-High/MSI-High). In conclusion, this study provides evidence of differential gene transcriptional profiles among ccRCC vs nccRCC tumors, providing new insights for optimizing personalized and histology-specific therapeutic strategies for patients with advanced RCC.

Keywords: Cancer; Genetics; Molecular genetics; Oncology; Urology.

UCLA Health urologists will showcase groundbreaking research at the 2024 American Urological Association Annual Meeting

The ucla department of urology will deliver over 70 presentations showcasing new discoveries and innovations in urologic research.

Newswise — Faculty, scientists, and urologists from  UCLA Health Urology  will present research data on the latest discoveries and innovations in urology at the 2024 American Urological Association’s (AUA) Annual Meeting in San Antonio, Texas, May 3-6.

The conference will feature over 70 presentations from UCLA Health physicians and scientists, including abstracts and podium presentations, highlighting topics impacting the field of urology.

These studies review cutting-edge topics, including novel evaluation techniques for Peyronie’s disease, using AI to help plan focal prostate cancer therapy, and evaluating the role of endourology innovations in low-resource communities.

According to the AUA, the annual meeting is the largest gathering of urologists globally – offering researchers in the field access to groundbreaking research, new guidelines, and the latest advances in urologic medicine.  

“The AUA Meeting is always an exciting opportunity for our entire department, as it allows us to share our research with professionals across the world, as well as to learn from presentations from other leading academic centers,” said  Christopher Saigal, MD, MPH, Professor and Executive Vice Chair  of  Urology  at the  UCLA David Geffen School of Medicine . “Collectively as a department, we take pride in the fact that over 70 presentations from  UCLA Urology  researchers will be featured, demonstrating our commitment to providing new solutions to the most challenging dilemmas faced by patients with urologic diseases.”

Abstracts from UCLA Health researchers and urologists will include:   

Bacteria Trigger Calcium Oxalate Crystal Formation  

Kymora Scotland, MD, PhD , will present a poster on kidney stone pathogenesis.  Her research reveals that approximately 80% of kidney stones are composed of calcium oxalate (CaOx), and recent studies suggest the potential involvement of bacteria in CaOx nephrolithiasis. The study aims to identify evidence of bacteria within kidney stones and investigate biofilm-forming bacteria's impact on the formation and growth of CaOx crystals.

Endourology in Resource Limited Areas  

Additionally, Dr. Kymora Scotland will also deliver multiple invited talks, including one on endourology in low-resource communities.

Effect of 3-dimensional, virtual reality models for surgical planning of robotic prostatectomy on trifecta outcomes: A randomized clinical trial   

Joseph Shirk, MD , will present research on utilizing virtual three-dimensional (3D) models in planning robotic-assisted laparoscopic radical prostatectomy (RALP). Traditionally, surgeons review two-dimensional Magnetic Resonance Imaging (MRI) images and pathology results to understand the three-dimensional anatomy. The study aims to evaluate the impact of virtual 3D models on the trifecta of cancer control, continence, and erectile function in patients undergoing RALP.  

Novel Evaluation Techniques for  Peyronie’s  Disease   

Sriram  Eleswarapu , MD, PhD , will discuss the current state of diagnosis for  Peyronie’s  disease by evaluating newer technologies.   

Metrics of Treatment Outcome Following Partial Gland Ablation for Prostate Cancer  

Wayne Brisbane, MD , will present an evaluation of the outcomes of treating prostate cancer in men who do not fully meet the standard inclusion criteria recommended by the focal therapy community.  

Software to Determine Extent of Tumor Margins in Focal Therapy of Prostate Cancer  

Wayne Brisbane, MD , will also present on the challenge of poorly defined margins of prostate cancer by MRI imaging, emphasizing the importance of treating these margins for complete ablation. The objective of the study is to assess the efficacy of Unfold-AI™, a recently FDA-cleared software, in enhancing the definition of tumor margins and guiding focal therapy.   

“In presenting these diverse scientific findings, our goal is to illuminate what is happening at the forefront of urologic research and that research’s significant implications for patient care,” said Dr. Saigal. “From novel evaluation techniques for  Peyronie’s  disease to AI-based approaches that are revolutionizing prostate cancer therapy, each presentation reflects our dedication to pushing boundaries, improving outcomes, and enhancing the lives of our patients.”   

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