Renal Cell Carcinoma: Diagnosis and Management

Total Page:16

File Type:pdf, Size:1020Kb

Renal Cell Carcinoma: Diagnosis and Management Renal Cell Carcinoma: Diagnosis and Management Richard E. Gray, DO, and Gabriel T. Harris, MD, Uniformed Services University of the Health Sciences, Bethesda, Maryland Kidney cancer is one of the 10 most common cancers in the United States with 90% being attributed to renal cell carci- noma. 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. (Am Fam Physician. 2019; 99(3): 179-184. Copyright © 2019 American Academy of Family Physicians.) Kidney cancer is one of the 10 most common cancers in most commonly encountered by mechanics, dry cleaners, the United States.1 Renal cell carcinoma accounts for 90% of oil processors, polyvinyl chloride manufacturers, and low- all kidney cancers.2 Death attributed to renal cell carcinoma nicotine tobacco producers.8 accounted for 2% of all cancer deaths or approximately There are 10 familial syndromes that confer greater risk 14,000 persons in 2016.1,2 Men are diagnosed with renal cell of developing renal cell carcinoma.11 The most common carcinoma at almost twice the rate of women, and there is a of these is von Hippel-Lindau disease which leads to the greater prevalence in black men.3 Most cases are diagnosed development of clear cell renal cell carcinoma through the between 60 and 70 years of age.1,2 activation of vascular endothelial growth factor (VEGF).11 Renal cell carcinoma is classified in three major histolog- Approximately 60% of sporadic clear cell renal cell carcino- ical subtypes: clear cell (75%), papillary (15% to 20%), and mas follow the same pathogenesis. This discovery has led to chromophobe (5%).4 Disease-specific survival is worst with the development of new therapies that inhibit VEGF recep- clear cell renal cell carcinoma as it tends to be discovered at tors and are being used to treat heritable and sporadic cases a more advanced stage.5 of clear cell renal cell carcinoma.11,12 Risk Factors Screening and Prevention Risk factors for renal cell carcinoma include hypertension, Screening for renal cell carcinoma is not recommended, except tobacco use, obesity, and acquired cystic kidney disease in the setting of a known heritable syndrome associated with in the setting of end-stage renal disease.1,3,6 Occupational the development of renal cell carcinoma.1 The management exposure to trichloroethylene can lead to the develop- of hypertension and obesity, and the avoidance of tobacco ment of renal cell carcinoma and increased mortality from use are the only established methods of primary prevention.8 renal cell carcinoma.5,7-9 The International Agency for Evidence from prospective and observational studies suggest Research on Cancer labels trichloroethylene as carcino- that consuming fatty fish (relative risk [RR] = 0.56;​​ 95% con- genic to humans and specifically associates it with renal fidence interval [CI], 0.35 to 0.91), three or more servings of cancer.10 Occupational exposure to trichloroethylene is 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) 5,13-15 See related editorial on page 145. may reduce the risk of developing renal cell carcinoma. CME This clinical content conforms to AAFP criteria for con- tinuing medical education (CME). See CME Quiz on page 157. Clinical Presentation Author disclosure: No relevant financial affiliations. More than 50% of patients with renal cell carcinoma are asymptomatic and diagnosed incidentally during Downloaded from the American Family Physician website at www.aafp.org/afp. Copyright © 2018 American Academy of Family Physicians. For the private, noncom- Downloaded from the American Family Physician website at www.aafp.org/afp. Copyright © 2018 American Academy of Family Physicians. For the private, noncom- ◆ 179 mercial use of one individual user of the website. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. Februarymercial 1,use 2019 of one Volume individual 99, user Number of the website.3 All other rightswww.aafp.org/afp reserved. Contact [email protected] for copyright questionsAmerican and/or Family permission Physician requests. RENAL CELL CARCINOMA SORT: KEY RECOMMENDATIONS FOR PRACTICE Evidence Clinical recommendation rating References Comments Patients 35 years or older who have asymptomatic microhematuria C 17 Recommendation from should have cystoscopy and imaging with multiphasic computed consensus guideline based tomography urography performed. on observational studies Refer for a urology consultation for gross hematuria without urinary C 25 Recommendation from tract infection, especially if the patient is older than 45 years. consensus guideline based on observational studies Refer for a urology consultation for any mass with Bosniak III or IV C 21 Recommendation from classification and for selected, low-risk patients with IIF classification, consensus guideline based or any solid mass greater than 1 cm. on observational studies A = consistent, good-quality patient-oriented evidence;​​ B = inconsistent or limited-quality patient-oriented evidence;​​ C = consensus, disease- oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https:// www.aafp. org/afpsort. thoracoabdominal imaging ordered for unrelated issues.5,16 creatinine, C-reactive protein, hemoglobin, erythrocyte The history and physical examination triad of gross hema- sedimentation rate, alkaline phosphatase, and serum cal- turia, flank pain, and palpable abdominal mass is now an cium.7 Routine urine cytology is not recommended for the uncommon presentation, and is associated with advanced initial evaluation of asymptomatic microscopic hematuria.17 disease.6,12,16 Nonreducing or isolated right-sided varicocele Patients 35 years or older who have asymptomatic microhe- and bilateral lower extremity edema can also be symptoms maturia should have cystoscopy and imaging with multi- of advanced disease through occlusion of the right testicu- phasic CT urography performed.17 lar venous system that drains directly to the right renal vein. Similarly, bilateral lower extremity edema can occur from IMAGING tumor occlusion of the inferior vena cava. Approximately A contrast-enhanced, triple-phase helical CT scan that images 20% of patients present with paraneoplastic disease, mani- the urinary tract before, during, and after contrast load is the fested by hypertension, hypercalcemia, and polycythemia.5 preferred imaging study for evaluating renal masses or per- Fever, weight loss, cough, adenopathy, and bone pain may sistent microscopic hematuria.19,20 CT detects 90% of renal indicate metastatic disease. masses, identifies benign and pathologic features, and evalu- ates surrounding anatomy to detect lymphadenopathy or an Diagnosis associated thrombus. A contrast-enhanced CT scan will also CLINICAL EVALUATION identify benign masses that do not require further testing. An isolated right-sided varicocele and nonreducing bilat- The Hounsfield unit scale measures a tissue’s density eral varicocele should be evaluated with abdominal imag- or attenuation. Fat has very low attenuation (i.e., –100 to ing. Gross hematuria requires computed tomography (CT), –10 HU), and masses containing fat are almost always urography, and urology consultation for cystoscopy.17 Signs benign angiomyolipomas. Homogeneous masses with low of paraneoplastic or metastatic disease require evaluation attenuation (–10 to +20 HU) can be identified as benign, for malignancy, including chest and abdominal imaging. fluid-filled, simple cysts. Masses with attenuation greater than 20 HU, heterogeneous appearance, septations, or cal- LABORATORY EVALUATION cifications, may be malignant and require further evalua- Hematuria should be diagnosed by microscopic exam- tion21 (Figure 2). The differential diagnosis of renal masses ination that shows three or more red blood cells per is included in Table 1.22 high-powered field, not by urine dipstick alone. The urine For incompletely characterized masses or contraindica- should be without pyuria or red blood cell casts, which tions to CT, magnetic resonance imaging with and without indicates infection or glomerulonephritis, respectively. If intravenous contrast is recommended.21 asymptomatic microscopic hematuria is detected, manage- ment is recommended per American Urological Association Management guidelines (Figure 1).17,18 Benign causes should be ruled out, The management of cystic lesions should be guided by the including infection, recent vigorous exercise, menstruation, Bosniak classification system (Table 2).21 Shared decision- and instrumentation. Identified
Recommended publications
  • Cholangiocarcinoma 2020: the Next Horizon in Mechanisms and Management
    CONSENSUS STATEMENT Cholangiocarcinoma 2020: the next horizon in mechanisms and management Jesus M. Banales 1,2,3 ✉ , Jose J. G. Marin 2,4, Angela Lamarca 5,6, Pedro M. Rodrigues 1, Shahid A. Khan7, Lewis R. Roberts 8, Vincenzo Cardinale9, Guido Carpino 10, Jesper B. Andersen 11, Chiara Braconi 12, Diego F. Calvisi13, Maria J. Perugorria1,2, Luca Fabris 14,15, Luke Boulter 16, Rocio I. R. Macias 2,4, Eugenio Gaudio17, Domenico Alvaro18, Sergio A. Gradilone19, Mario Strazzabosco 14,15, Marco Marzioni20, Cédric Coulouarn21, Laura Fouassier 22, Chiara Raggi23, Pietro Invernizzi 24, Joachim C. Mertens25, Anja Moncsek25, Sumera Rizvi8, Julie Heimbach26, Bas Groot Koerkamp 27, Jordi Bruix2,28, Alejandro Forner 2,28, John Bridgewater 29, Juan W. Valle 5,6 and Gregory J. Gores 8 Abstract | Cholangiocarcinoma (CCA) includes a cluster of highly heterogeneous biliary malignant tumours that can arise at any point of the biliary tree. Their incidence is increasing globally, currently accounting for ~15% of all primary liver cancers and ~3% of gastrointestinal malignancies. The silent presentation of these tumours combined with their highly aggressive nature and refractoriness to chemotherapy contribute to their alarming mortality, representing ~2% of all cancer-related deaths worldwide yearly. The current diagnosis of CCA by non-invasive approaches is not accurate enough, and histological confirmation is necessary. Furthermore, the high heterogeneity of CCAs at the genomic, epigenetic and molecular levels severely compromises the efficacy of the available therapies. In the past decade, increasing efforts have been made to understand the complexity of these tumours and to develop new diagnostic tools and therapies that might help to improve patient outcomes.
    [Show full text]
  • The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Inherited Polyposis Syndromes Daniel Herzig, M.D
    CLINICAL PRACTICE GUIDELINES The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Inherited Polyposis Syndromes Daniel Herzig, M.D. • Karin Hardimann, M.D. • Martin Weiser, M.D. • Nancy Yu, M.D. Ian Paquette, M.D. • Daniel L. Feingold, M.D. • Scott R. Steele, M.D. Prepared by the Clinical Practice Guidelines Committee of The American Society of Colon and Rectal Surgeons he American Society of Colon and Rectal Surgeons METHODOLOGY (ASCRS) is dedicated to ensuring high-quality pa- tient care by advancing the science, prevention, and These guidelines are built on the last set of the ASCRS T Practice Parameters for the Identification and Testing of management of disorders and diseases of the colon, rectum, Patients at Risk for Dominantly Inherited Colorectal Can- and anus. The Clinical Practice Guidelines Committee is 1 composed of society members who are chosen because they cer published in 2003. An organized search of MEDLINE have demonstrated expertise in the specialty of colon and (1946 to December week 1, 2016) was performed from rectal surgery. This committee was created to lead interna- 1946 through week 4 of September 2016 (Fig. 1). Subject tional efforts in defining quality care for conditions related headings for “adenomatous polyposis coli” (4203 results) to the colon, rectum, and anus, in addition to the devel- and “intestinal polyposis” (445 results) were included, us- opment of Clinical Practice Guidelines based on the best ing focused search. The results were combined (4629 re- available evidence. These guidelines are inclusive and not sults) and limited to English language (3981 results), then prescriptive.
    [Show full text]
  • Germline Fumarate Hydratase Mutations in Patients with Ovarian Mucinous Cystadenoma
    European Journal of Human Genetics (2006) 14, 880–883 & 2006 Nature Publishing Group All rights reserved 1018-4813/06 $30.00 www.nature.com/ejhg SHORT REPORT Germline fumarate hydratase mutations in patients with ovarian mucinous cystadenoma Sanna K Ylisaukko-oja1, Cezary Cybulski2, Rainer Lehtonen1, Maija Kiuru1, Joanna Matyjasik2, Anna Szyman˜ska2, Jolanta Szyman˜ska-Pasternak2, Lars Dyrskjot3, Ralf Butzow4, Torben F Orntoft3, Virpi Launonen1, Jan Lubin˜ski2 and Lauri A Aaltonen*,1 1Department of Medical Genetics, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland; 2International Hereditary Cancer Center, Department of Genetics and Pathology, Pomeranian Medical University, Szczecin, Poland; 3Department of Clinical Biochemistry, Aarhus University Hospital, Skejby, Denmark; 4Pathology and Obstetrics and Gynecology, University of Helsinki, Helsinki, Finland Germline mutations in the fumarate hydratase (FH) gene were recently shown to predispose to the dominantly inherited syndrome, hereditary leiomyomatosis and renal cell cancer (HLRCC). HLRCC is characterized by benign leiomyomas of the skin and the uterus, renal cell carcinoma, and uterine leiomyosarcoma. The aim of this study was to identify new families with FH mutations, and to further examine the tumor spectrum associated with FH mutations. FH germline mutations were screened from 89 patients with RCC, skin leiomyomas or ovarian tumors. Subsequently, 13 ovarian and 48 bladder carcinomas were analyzed for somatic FH mutations. Two patients diagnosed with ovarian mucinous cystadenoma (two out of 33, 6%) were found to be FH germline mutation carriers. One of the changes was a novel mutation (Ala231Thr) and the other one (435insAAA) was previously described in FH deficiency families. These results suggest that benign ovarian tumors may be associated with HLRCC.
    [Show full text]
  • HPV-Negative Penile Squamous Cell Carcinoma
    Modern Pathology (2017) 30, 1013–1020 © 2017 USCAP, Inc All rights reserved 0893-3952/17 $32.00 1013 HPV-negative penile squamous cell carcinoma: disruptive mutations in the TP53 gene are common Karl Kashofer, Elke Winter, Iris Halbwedl, Andrea Thueringer, Marisa Kreiner, Stefan Sauer and Sigrid Regauer Institute of Pathology, Medical University of Graz, Graz, Austria The majority of penile squamous cell carcinomas is caused by transforming human papilloma virus (HPV) infection. The etiology of HPV-negative cancers is unclear, but TP53 mutations have been implicated. Archival tissues of 108 invasive squamous cell carcinoma from a single pathology institution in a low-incidence area were analyzed for HPV-DNA and p16ink4a overexpression and for TP53 mutations by ion torrent next-generation sequencing. Library preparation failed in 32/108 squamous cell carcinomas. Institutional review board approval was obtained. Thirty of 76 squamous cell carcinomas (43%; average 63 years) were HPV-negative with 8/33 squamous cell carcinomas being TP53 wild-type (24%; average 63 years). Twenty-five of 33 squamous cell carcinomas (76%; average 65 years) showed 32 different somatic TP53 mutations (23 missense mutations in exons 5–8, 6 nonsense, 1 frameshift and 2 splice-site mutations). Several hotspot mutations were detected multiple times (R175H, R248, R282, and R273). Eighteen of 19 squamous cell carcinomas with TP53 expression in immunohistochemistry had TP53 mutations. Fifty percent of TP53-negative squamous cell carcinomas showed mostly truncating loss-of-function TP53 mutations. Patients without mutations had longer survival (5 years: 86% vs 61%; 10 years: 60% vs 22%), but valid clinically relevant conclusions cannot be drawn due to different tumor stages and heterogeneous treatment of the cases presented in this study.
    [Show full text]
  • Lung Equivalent Terms, Definitions, Charts, Tables and Illustrations C340-C349 (Excludes Lymphoma and Leukemia M9590-9989 and Kaposi Sarcoma M9140)
    Lung Equivalent Terms, Definitions, Charts, Tables and Illustrations C340-C349 (Excludes lymphoma and leukemia M9590-9989 and Kaposi sarcoma M9140) Introduction Use these rules only for cases with primary lung cancer. Lung carcinomas may be broadly grouped into two categories, small cell and non-small cell carcinoma. Frequently a patient may have two or more tumors in one lung and may have one or more tumors in the contralateral lung. The physician may biopsy only one of the tumors. Code the case as a single primary (See Rule M1, Note 2) unless one of the tumors is proven to be a different histology. It is irrelevant whether the other tumors are identified as cancer, primary tumors, or metastases. Equivalent or Equal Terms • Low grade neuroendocrine carcinoma, carcinoid • Tumor, mass, lesion, neoplasm (for multiple primary and histology coding rules only) • Type, subtype, predominantly, with features of, major, or with ___differentiation Obsolete Terms for Small Cell Carcinoma (Terms that are no longer recognized) • Intermediate cell carcinoma (8044) • Mixed small cell/large cell carcinoma (8045) (Code is still used; however current accepted terminology is combined small cell carcinoma) • Oat cell carcinoma (8042) • Small cell anaplastic carcinoma (No ICD-O-3 code) • Undifferentiated small cell carcinoma (No ICD-O-3 code) Definitions Adenocarcinoma with mixed subtypes (8255): A mixture of two or more of the subtypes of adenocarcinoma such as acinar, papillary, bronchoalveolar, or solid with mucin formation. Adenosquamous carcinoma (8560): A single histology in a single tumor composed of both squamous cell carcinoma and adenocarcinoma. Bilateral lung cancer: This phrase simply means that there is at least one malignancy in the right lung and at least one malignancy in the left lung.
    [Show full text]
  • What Are Basal and Squamous Cell Skin Cancers?
    cancer.org | 1.800.227.2345 About Basal and Squamous Cell Skin Cancer Overview If you have been diagnosed with basal or squamous cell skin cancer or are worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Are Basal and Squamous Cell Skin Cancers? Research and Statistics See the latest estimates for new cases of basal and squamous cell skin cancer and deaths in the US and what research is currently being done. ● Key Statistics for Basal and Squamous Cell Skin Cancers ● What’s New in Basal and Squamous Cell Skin Cancer Research? What Are Basal and Squamous Cell Skin Cancers? Basal and squamous cell skin cancers are the most common types of skin cancer. They start in the top layer of skin (the epidermis), and are often related to sun exposure. 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Cancer starts when cells in the body begin to grow out of control. Cells in nearly any part of the body can become cancer cells. To learn more about cancer and how it starts and spreads, see What Is Cancer?1 Where do skin cancers start? Most skin cancers start in the top layer of skin, called the epidermis. There are 3 main types of cells in this layer: ● Squamous cells: These are flat cells in the upper (outer) part of the epidermis, which are constantly shed as new ones form. When these cells grow out of control, they can develop into squamous cell skin cancer (also called squamous cell carcinoma).
    [Show full text]
  • Immunohistochemical Differential Diagnosis Between Thymic Carcinoma and Type B3 Thymoma: Diagnostic Utility of Hypoxic Marker, GLUT-1, in Thymic Epithelial Neoplasms
    Modern Pathology (2009) 22, 1341–1350 & 2009 USCAP, Inc. All rights reserved 0893-3952/09 $32.00 1341 Immunohistochemical differential diagnosis between thymic carcinoma and type B3 thymoma: diagnostic utility of hypoxic marker, GLUT-1, in thymic epithelial neoplasms Masakazu Kojika1,2, Genichiro Ishii1, Junji Yoshida2, Mituyo Nishimura2, Tomoyuki Hishida2, Shu-ji Ota1, Yukinori Murata1, Kanji Nagai2 and Atsushi Ochiai1 1Pathology Division, Research Center for Innovative Oncology, National Cancer Center Hospital East, Kashiwa, Chiba, Japan and 2Thoracic Surgery Division, National Cancer Center Hospital East, Kashiwa, Chiba, Japan There are only a few immunohistochemical markers that are useful for differentiating thymic carcinomas from type B3 thymomas. The purpose of this study is to examine the additional markers that would be useful for differentiating between thymic carcinoma and thymoma type B3. We performed a tissue microarray analysis of surgically resected thymic tumor specimens from12 cases of thymic carcinoma, 7 cases of type B3 thymoma, and 68 cases of other types of thymoma. Immunostaining using 49 antibodies was scored based on staining intensity and the percentage of cells that stained positive. Seven proteins that were selected by the staining scores, namely, GLUT-1 (167 vs 4), CA-IX (110 vs 15), c-kit (162 vs 44), CD5 (33 vs 0), MUC-1 (54 vs 0), CEA (42 vs 0), and CK18 (110 vs 42), were significantly higher in the thymic carcinomas than in the type B3 thymomas. The staining sensitivity and specificity of the antibodies for thymic carcinoma were GLUT-1, sensitivity 72% and specificity 100%; CA-IX, 58 and 71%; c-kit, 72 and 85%; CD5, 33 and 100%; CK18, 58 and 71%; MUC-1, 25 and 100%; and CEA, 33 and 100%.
    [Show full text]
  • Pathology and Classification of SCLC
    cancers Review Pathology and Classification of SCLC Maria Gabriela Raso * , Neus Bota-Rabassedas and Ignacio I. Wistuba * Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; [email protected] * Correspondence: [email protected] (M.G.R.); [email protected] (I.I.W.); Tel.: +1-713-834-6026 (M.G.R.); +1-713-563-9184 (I.I.W.) Simple Summary: Small cell lung carcinoma (SCLC), is a high-grade neuroendocrine carcinoma defined by its aggressiveness, poor differentiation, and somber prognosis. This review highlights cur- rent pathological concepts including classification, immunohistochemistry features, and differential diagnosis. Additionally, we summarize the current knowledge of the immune tumor microenvi- ronment, tumor heterogeneity, and genetic variations of SCLC. Recent comprehensive genomic research has improved our understanding of the diverse biological processes that occur in this tumor type, suggesting that a new era of molecular-driven treatment decisions is finally foreseeable for SCLC patients. Abstract: Lung cancer is consistently the leading cause of cancer-related death worldwide, and it ranks as the second most frequent type of new cancer cases diagnosed in the United States, both in males and females. One subtype of lung cancer, small cell lung carcinoma (SCLC), is an aggressive, poorly differentiated, and high-grade neuroendocrine carcinoma that accounts for 13% of all lung carcinomas. SCLC is the most frequent neuroendocrine lung tumor, and it is commonly presented as an advanced stage disease in heavy smokers. Due to its clinical presentation, it is typically diagnosed in small biopsies or cytology specimens, with routine immunostaining only. However, Citation: Raso, M.G.; immunohistochemistry markers are extremely valuable in demonstrating neuroendocrine features of Bota-Rabassedas, N.; Wistuba, I.I.
    [Show full text]
  • Primary Renal Carcinoid Tumor: a Radiologic Review
    Radiology Case Reports Volume 9, Issue 2, 2014 Primary renal carcinoid tumor: A radiologic review Leslie Lamb, MD, Msc, Bsc; Wael Shaban, MBBCH, MD, PhD Carcinoid tumor is the classic famous anonym of neuroendocrine neoplasms. Primary renal carcinoid tumors are extremely rare, first described by Resnick and colleagues in 1966, with fewer than a total of 100 cases reported in the literature. Thus, given the paucity of cases, the clinical and histological behav- ior is not well understood, impairing the ability to predict prognosis. Computed tomography and (occa- sionally) octreotide studies are used in the diagnosis and followup of these rare entites. A review of 85 cases in the literature shows that no distinctive imaging features differentiate them from other primary renal masses. The lesions tend to demonstrate a hypodense appearance and do not usually enhance in the arterial phases, but can occasionally calcify. Octreotide scans do not seem to help in the diagnosis; however, they are more commonly used in the postoperative followup. In addition, we report a new case of primary renal carcinoid in a horseshoe kidney. Case report Imaging findings 40-year-old male initially presented to a community hos- pital with a 20-lb weight loss over a few months. In retro- CT of the abdomen and pelvis, done in the portal ve- spect, the patient recalled mild left-flank discomfort and nous phase, demonstrated a solid, hypodense, 4.5-cm renal fatigue, but denied any hematuria. Blood work revealed an mass containing calcifications, located in the posterior as- elevated serum glucose, and he was diagnosed with type 2 pect of the medial diabetes.
    [Show full text]
  • Solitary Duodenal Metastasis from Renal Cell Carcinoma with Metachronous Pancreatic Neuroendocrine Tumor: Review of Literature with a Case Discussion
    Published online: 2021-05-24 Practitioner Section Solitary Duodenal Metastasis from Renal Cell Carcinoma with Metachronous Pancreatic Neuroendocrine Tumor: Review of Literature with a Case Discussion Abstract Saphalta Baghmar, Renal cell cancinoma (RCC) is a unique malignancy with features of late recurrences, metastasis S M Shasthry1, to any organ, and frequent association with second malignancy. It most commonly metastasizes Rajesh Singla, to the lungs, bones, liver, renal fossa, and brain although metastases can occur anywhere. RCC 2 metastatic to the duodenum is especially rare, with only few cases reported in the literature. Herein, Yashwant Patidar , 3 we review literature of all the reported cases of solitary duodenal metastasis from RCC and cases Chhagan B Bihari , of neuroendocrine tumor (NET) as synchronous/metachronous malignancy with RCC. Along with S K Sarin1 this, we have described a unique case of an 84‑year‑old man who had recurrence of RCC as solitary Departments of Medical duodenal metastasis after 37 years of radical nephrectomy and metachronous pancreatic NET. Oncology, 1Hepatology, 2Radiology and 3Pathology, Keywords: Late recurrence, pancreatic neuroendocrine tumor, renal cell carcinoma, second Institute of Liver and Biliary malignancy, solitary duodenal metastasis Sciences, New Delhi, India Introduction Case Presentation Renal cell carcinoma (RCC) is unique An 84‑year‑old man with a medical history to have many unusual features such as notable for hypertension and RCC, 37 years metastasis to almost every organ in the body, postright radical nephrectomy status, late recurrences, and frequent association presented to his primary care physician with second malignancy. The most common with fatigue. When found to be anemic, sites of metastasis are the lung, lymph he was treated with iron supplementation nodes, liver, bone, adrenal glands, kidney, and blood transfusions.
    [Show full text]
  • (NCCN Guidelines®) Thymomas and Thymic Carcinomas
    NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Thymomas and Thymic Carcinomas Version 2.2019 — March 11, 2019 NCCN.org Continue Version 2.2019, 03/11/19 © 2019 National Comprehensive Cancer Network® (NCCN®), All rights reserved. NCCN Guidelines® and this illustration may not be reproduced in any form without the express written permission of NCCN. NCCN Guidelines Index NCCN Guidelines Version 2.2019 Table of Contents Thymomas and Thymic Carcinomas Discussion *David S. Ettinger, MD/Chair † Ramaswamy Govindan, MD † Sandip P. Patel, MD ‡ † Þ The Sidney Kimmel Comprehensive Siteman Cancer Center at Barnes- UC San Diego Moores Cancer Center Cancer Center at Johns Hopkins Jewish Hospital and Washingtn University School of Medicine Karen Reckamp, MD, MS † ‡ *Douglas E. Wood, MD/Vice Chair ¶ City of Hope National Medical Center Fred Hutchinson Cancer Research Matthew A. Gubens, MD, MS † Center/Seattle Cancer Care Alliance UCSF Helen Diller Family Gregory J. Riely, MD, PhD † Þ Comprehensive Cancer Center Memorial Sloan Kettering Cancer Center Dara L. Aisner, MD, PhD ≠ University of Colorado Cancer Center Mark Hennon, MD ¶ Steven E. Schild, MD § Roswell Park Cancer Institute Mayo Clinic Cancer Center Wallace Akerley, MD † Huntsman Cancer Institute Leora Horn, MD, MSc † Theresa A. Shapiro, MD, PhD Þ at the University of Utah Vanderbilt-Ingram Cancer Center The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins Jessica Bauman, MD ‡ † Rudy P. Lackner, MD ¶ Fox Chase Cancer Center Fred & Pamela Buffett Cancer Center James Stevenson, MD † Case Comprehensive Cancer Center/ Ankit Bharat, MD ¶ Michael Lanuti, MD ¶ University Hospitals Seidman Cancer Center Robert H. Lurie Comprehensive Cancer Massachusetts General Hospital Cancer Center and Cleveland Clinic Taussig Cancer Institute Center of Northwestern University Ticiana A.
    [Show full text]
  • HCC/RCC Referral Form
    Date Shipment Needed: Ship To: Patient Prescriber Nursing needed; Training needed ►All the supplies including syringes and needles will be dispensed if needed. HEPATOCELLULAR CARCINOMA (HCC) Phone: 866.892.1580 • Fax: 866.892.2363 RENAL CELL CARCINOMA (RCC) REFERRAL FORM PATIENT INFORMATION Patient Name: DOB: Sex: M F Weight: lbs. kg. SSN: Phone: Allergies: Address: City: State: Zip: Emergency Contact: Phone: Please attach demographic information PRESCRIBER INFORMATION Prescriber: NPI: DEA: State Lic: Supervising Physician: Practice Name: Address: City: State: Zip: Phone: Fax: Key Office Contact: Phone: DIAGNOSIS INFORMATION / MEDICAL ASSESMENT Primary Diagnosis: C22.0 Hepatocellular Carcinoma (HCC) C22.2; C22.7; C22.8; C64.9 Renal Cell Carcinoma (RCC) Other________________________________ . Has patient been treated previously for this condition? Yes No Medication(s): __________________________________________________________________ . Cancer Stage: Stage 0 Stage I Stage II Stage III Stage IV Other: ______________________________________________________________________ . Is patient currently on therapy? Yes No Medication(s): ____________________________________________________________________________________ . Will patient stop taking the above medication(s) before starting the new medication? Yes No If yes: _________________________________________________ . How long should patient wait before starting the new medication? ________________________________________________________________________________ . Other medications patient is
    [Show full text]