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• W2616948211 abstract "The objective of this review is to explore the available literature on solid renal masses (SRMs) in transplant allograft kidneys to better understand the epidemiology and management of these tumors. A literature review using PubMed was performed according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) methodology. Fifty-six relevant studies were identified from 1988 to 2015. A total of 174 SRMs in 163 patients were identified, with a mean tumor size of 2.75 cm (range 0.5–9.0 cm). Tumor histology was available for 164 (94.3%) tumors: clear cell renal cell carcinoma (RCC; 45.7%), papillary RCC (42.1%), chromophobe RCC (3%), and others (9.1%). Tumors were managed by partial nephrectomy (67.5%), radical nephrectomy (19.4%), percutaneous radiofrequency ablation (10.4%), and percutaneous cryoablation (2.4%). Of the 131 patients (80.3%) who underwent nephron-sparing interventions, 10 (7.6%) returned to dialysis and eight (6.1%) developed tumor recurrence over a mean follow-up of 2.85 years. Of the 110 patients (67.5%) who underwent partial nephrectomy, 3.6% developed a local recurrence during a mean follow-up of 3.12 years. The current management of SRMs in allograft kidneys mirrors management in the nontransplant population, with notable findings including an increased rate of papillary RCC and similar recurrence rates after partial nephrectomy in the transplant population despite complex surgical anatomy. The objective of this review is to explore the available literature on solid renal masses (SRMs) in transplant allograft kidneys to better understand the epidemiology and management of these tumors. A literature review using PubMed was performed according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) methodology. Fifty-six relevant studies were identified from 1988 to 2015. A total of 174 SRMs in 163 patients were identified, with a mean tumor size of 2.75 cm (range 0.5–9.0 cm). Tumor histology was available for 164 (94.3%) tumors: clear cell renal cell carcinoma (RCC; 45.7%), papillary RCC (42.1%), chromophobe RCC (3%), and others (9.1%). Tumors were managed by partial nephrectomy (67.5%), radical nephrectomy (19.4%), percutaneous radiofrequency ablation (10.4%), and percutaneous cryoablation (2.4%). Of the 131 patients (80.3%) who underwent nephron-sparing interventions, 10 (7.6%) returned to dialysis and eight (6.1%) developed tumor recurrence over a mean follow-up of 2.85 years. Of the 110 patients (67.5%) who underwent partial nephrectomy, 3.6% developed a local recurrence during a mean follow-up of 3.12 years. The current management of SRMs in allograft kidneys mirrors management in the nontransplant population, with notable findings including an increased rate of papillary RCC and similar recurrence rates after partial nephrectomy in the transplant population despite complex surgical anatomy. Renal transplantation has emerged as the gold standard treatment for end-stage renal disease (ESRD). Among patients who have undergone renal transplantation, the long-term mortality rate is 48–82% lower than those remaining on the transplant waitlist (1Wolfe RA Ashby VB Milford EL et al.Comparison of mortality in all patients on dialysis, patients on dialysis awaiting transplantation, and recipients of a first cadaveric transplant.N Engl J Med. 1999; 341: 1725Crossref PubMed Scopus (3975) Google Scholar). These patients, however, are at a twofold increased risk of developing a malignancy compared with the general healthy population (2Engels EA Pfeiffer RM Fraumeni Jr, JF et al.Spectrum of cancer risk among US solid organ transplant recipients.JAMA. 2011; 306: 1891-1901Crossref PubMed Scopus (990) Google Scholar). The incidence of renal cell carcinoma (RCC) in allograft kidneys is low (0.19–0.5%) (3Tillou X Guleryuz K Doerfler A et al.Nephron sparing surgery for de novo kidney graft tumor: Results from a multicenter national study.Am J Transplant. 2014; 14: 2120-2125Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar,4Ploussard G Chambade D Meria P et al.Biopsy-confirmed de novo renal cell carcinoma in renal grafts: A single-centre management experience in a 2396 recipient cohort.BJU Int. 2012; 109: 195-199Crossref PubMed Scopus (38) Google Scholar), but compared with the general population (0.017%) (5Nepple KG Tang L Grubb 3rd, RL Strope SA Population based analysis of the increasing incidence of kidney cancer in the United States: Evaluation of age specific trends from 1975 to 2006.J Urol. 2012; 187: 32-38Crossref PubMed Scopus (45) Google Scholar), there is an approximately 10-fold increased risk of development of this solid malignancy. The etiology of this increased risk of RCC is unknown but may be linked to the chronic immunosuppressive state of transplanted patients (2Engels EA Pfeiffer RM Fraumeni Jr, JF et al.Spectrum of cancer risk among US solid organ transplant recipients.JAMA. 2011; 306: 1891-1901Crossref PubMed Scopus (990) Google Scholar). Although growing literature shows that RCC is more prevalent in kidneys of patients with ESRD and the native kidneys of transplanted patients, there is a paucity of data on the epidemiology and management of solid renal masses (SRMs) in renal transplant allografts (6Terasawa Y Suzuki Y Morita M Kato M Suzuki K Sekino H Ultrasonic diagnosis of renal cell carcinoma in hemodialysis patients.J Urol. 1994; 152: 846-851Crossref PubMed Scopus (36) Google Scholar). In this review, we present a summary of the available literature on the incidence of and management patterns for SRMs in allograft kidneys. A literature review using keyword searches in PubMed was performed according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) methodology (7Moher D Liberati A Tetzlaff J Altman DG PRISMA GroupPreferred reporting items for systematic reviews and met-analyses: The PRISMA statement.Ann Intern Med. 2009; 104: 1363Google Scholar). Keywords used to identify relevant studies included renal mass, renal cell carcinoma, renal cancer, renal transplant, renal allograft, and kidney or renal transplantation. An abstract review was then performed to identify pertinent studies. Article references were used to further identify all relevant published articles. Studies were defined as pertinent for inclusion if they explored the topic of SRMs in transplant allograft kidneys. All identified, pertinent studies were included in this analysis, including retrospective multi-institutional case series, single-institution case series, and case reports. An individual review of each article was performed, with patient and tumor characteristics extracted for cumulative analysis. If available, the following data points were collected: number of kidney transplants performed at the institution, number of patients with SRMs in allograft kidney, number of SRMs identified, deceased or living donor transplant, size of SRM, how mass was diagnosed, immunosuppressive regimen prior to diagnosis, modifications in immunosuppressive regimen following diagnosis, histologic diagnosis, American Joint Committee on Cancer (AJCC) 2010 staging classification, Fuhrman grade, type of intervention performed, allograft function after treatment, cancer-specific survival, and length of follow-up. Descriptive statistics including frequencies, means, and ranges were calculated from the pooled data. Mean values are reported rather than medians because individual values were not reported by every study reviewed, and thus median values could not be calculated. Cumulative incidence was calculated using the studies that reported the total number of renal transplants performed over the same period in which SRMs were diagnosed in the allograft kidney. From 1988 to 2016, a total of 56 studies were found reporting on SRMs in transplanted allograft kidneys (3Tillou X Guleryuz K Doerfler A et al.Nephron sparing surgery for de novo kidney graft tumor: Results from a multicenter national study.Am J Transplant. 2014; 14: 2120-2125Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar,4Ploussard G Chambade D Meria P et al.Biopsy-confirmed de novo renal cell carcinoma in renal grafts: A single-centre management experience in a 2396 recipient cohort.BJU Int. 2012; 109: 195-199Crossref PubMed Scopus (38) Google Scholar,8Vegso G Toronyi E Deak PA Doros A Langer RM Detection and management of renal cell carcinoma in the renal allograft.Int Urol Nephrol. 2013; 45: 93-98Crossref PubMed Scopus (23) Google Scholar, 9Swords DC Al-Geizawi SM Farney AC et al.Treatment options for renal cell carcinoma in renal allografts: A case series from a single institution.Clin Transplant. 2013; 27: E199-E205Crossref PubMed Scopus (22) Google Scholar, 10Leveridge M Musquera M Evans E et al.Renal cell carcinoma in the native and allograft kidneys of renal transplant recipients.J Urol. 2011; 186: 219-223Crossref PubMed Scopus (48) Google Scholar, 11Hevia V Gomez V Diez Nicolas V et al.Development of urologic de novo malignancies after renal transplantation.Transplant Proc. 2014; 46: 170-175Crossref PubMed Scopus (24) Google Scholar, 12Viart L Surga N Collon S Jaureguy M Elalouf V Tillou X The high rate of de novo graft carcinomas in renal transplant recipients.Am J Nephrol. 2013; 37: 91-96Crossref PubMed Scopus (21) Google Scholar, 13Saleeb R Faragalla H Yousef GM Stewart R Streutker CJ Malignancies arising in allograft kidneys, with a first reported translocation RCC post-transplantation: a case series.Pathol Res Pract. 2015; 211: 584-587Crossref PubMed Scopus (14) Google Scholar, 14Kaouk JH Spana G Hillyer SP White MA Haber GP Goldfarb D Robotic-assisted laparoscopic partial nephrectomy for a 7-cm mass in a renal allograft.Am J Transplant. 2011; 11: 2242-2246Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar, 15Aron M Hegarty NJ Remer E O’Malley C Goldfarb D Kouk JH Percutaneous radiofrequency ablation of tumor in transplanted kidney.Urology. 2007; 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Our literature search yielded one multicenter retrospective case series, 19 single-institution case series, and 36 case reports. Fourteen studies reported on the total number of renal transplants performed over the same study period in which the SRMs were diagnosed, allowing for an overall calculated cumulative incidence of RCC in allografts from these studies of 0.23% (152 of 65 667). A total of 174 SRMs in allograft kidneys were identified in 163 patients. All but four patients had clinically localized disease at diagnosis, and all patients with metastases underwent transplant nephrectomies. The mean tumor size of these 174 masses was 2.75 cm (range 0.5–9.0 cm). Information regarding radiographic tumor detection was available in 133 of 163 patients (81.6%). Of these, 105 of 133 patients (79%) were initially diagnosed on routine screening ultrasound, 24 of 133 (18%) were symptomatic, and three of 133 (2.3%) were discovered incidentally on transplant nephrectomy. Symptoms that prompted imaging included hematuria (seven of 24, 29%), acute kidney injury (six of 24, 25%), pain (five of 24, 21%), constitutional symptoms (four of 24, 17%), hypertension (one of 24, 4%), and recurrent urinary tract infections (one of 24, 4%; Table 1). Preintervention immunosuppressive regimens were reported in 133 of 163 patients (81.6%), with only one patient reported to have received induction immunosuppression with thymoglobulin. Moreover, 123 of 133 (92.5%) included a calcineurin inhibitor (CNI), whereas the remaining 10 patients were on an antimetabolite and corticosteroid immunosuppressive regimen. The origin of the transplanted allograft in which the SRM occurred (deceased or living donor) was available for 62 of 163 patients (38%). Of these, 46 of 62 patients (74.2%) received an allograft from a deceased donor and 16 of 62 (25.8%) received an allograft from a living donor. Tumor histology was available for 164 of 174 tumors (94.3%) and included clear cell (45.7%), papillary (42.1%), chromophobe (3%), and other variant histologies (oncocytomas, mixed histologies, angiomyolipomas, benign fibrous tumors, and spindle cell carcinoma; 9.1%). A Fuhrman grade designation was available for 127 of 174 tumors (73%): grade I (18.9%), grade II (63.7%), grade III (15.7%), and grade IV (1.6%). Donor origin of the malignant cells was documented through DNA assay in 15 of 163 patients (9.2%). The AJCC 2010 staging classification was available for 154 of 163 patients (94.5%). The majority of patients were pT1a (87%), whereas 9%, 1.3%, and 2.6% were pT1b, pT2a, and pT3a, respectively. In our review of the literature, we did not identify any reports of pT2b, pT3b, pT3c, or pT4 tumors (Table 2).Table 1:Presenting symptoms prompting identification of the solid renal mass in transplanted allograft kidneySymptomNumber of patients (n = 24)Percentage of patients, %Hematuria729Acute kidney injury625Pain521Constitutional symptoms417Hypertension14Recurrent urinary tract infections14 Open table in a new tab Table 2:Tumor characteristics and interventionsCharacteristicResultPatients, n163Renal masses, n174Tumor size, cm, mean (range)2.75 (0.5–9.0)Tumor histology, n/N (%)163/174 (93.4)Clear cell, %45.70Papillary, %42.10Chromophobe, %3Other, %9.10Fuhrman grade, n/N (%)127/174 (73.0)I, %18.90II, %63.70III, %15.70IV, %1.60AJCC 2010 staging, n/N (%)155/174 (89.1)T1a, %87T1b, %9T2a, %1.30T2b, %0T3a, %2.60T3b, %0T3c, %0T4, %0Intervention, n/N (%)163/163 (100)Partial nephrectomy, %67.50Radical nephrectomy, %19.40Radiofrequency ablation, %10.40Cryoablation, %2.40 Open table in a new tab The treatment modality for management of SRM was reported for all 163 patients. Partial nephrectomy was performed in 110 patients (67.5%), transplant nephrectomy was performed in 32 (19.4%), radiofrequency ablation (RFA) was performed in 17 (10.4%), and cryoablation was performed in four (2.4%) (Table 2). Of the 131 patients who underwent nephron-sparing interventions, 7.6% returned to hemodialysis and 6.1% developed tumor recurrence in the allograft over a mean follow-up of 2.85 years. Immunosuppression was altered in 29 patients after nephron-sparing interventions, of which 20 of these changes were to include a mammalian target of rapamycin (mTOR) inhibitor. Of the 110 patients who underwent partial nephrectomy, 3.6% developed local recurrence during a mean follow-up of 3.12 years, and all of these patients ultimately underwent completion transplant nephrectomy. Over a mean follow-up of 1.83 years, three of 17 patients (17.6%) had persistent mass enhancement after RFA, with all residual tumors treated with repeat RFA without evidence of recurrence on follow-up. One patient had decreased renal function prior to RFA that worsened following the procedure and required a return to dialysis. Notably, one patient underwent RFA of two biopsy-proven synchronous clear cell renal carcinomas within a transplanted allograft kidney with no evidence of disease progression at 33-mo follow-up (16Su MZ Campbell NA Lau H Management of renal masses in transplant allografts at an Australian kidney-pancreas transplant unit.Transplantation. 2014; 97: 654-659Crossref PubMed Scopus (19) Google Scholar). In the four patients treated with cryotherapy, none experienced local recurrence or return to dialysis during the short mean follow-up of 4.25 mo. Of the 32 patients who underwent primary transplant nephrectomy, 28 had clinically localized disease at time of surgical intervention, with no reports of disease recurrence or metastases following nephrectomy during the available follow-up. Of nine reported deaths, two were renal cancer–specific (8Vegso G Toronyi E Deak PA Doros A Langer RM Detection and management of renal cell carcinoma in the renal allograft.Int Urol Nephrol. 2013; 45: 93-98Crossref PubMed Scopus (23) Google Scholar,42Akioka K Masuda K Harada S et al.How long should we follow the post-transplantation after graft loss? A case report of renal cancer in the grafted kidney that occurred 16 years after graft loss.Transplant Proc. 2014; 46: 626-629Crossref PubMed Scopus (4) Google Scholar). This report is the largest cumulative review of available literature exploring the tumor characteristics and management of SRMs in transplant allograft kidneys. As reported in 2013 by the Scientific Registry of Transplant Recipients, 10-year overall graft survival for living and deceased donors increased from 35–40% to 55–60% compared with the previous decade (62Matas AJ Smith JM Skeans MA et al.OPTN/SRTR 2013 Annual data report: Kidney.Am J Transplant. 2015; 15: 1Abstract Full Text Full Text PDF PubMed Scopus (334) Google Scholar). Although our literature review identified a total of only 163 affected patients, we suspect that this increase in overall survival will likely lead to an increased incidence of renal masses in the allograft kidney. Consequently, an increasing number of transplant surgeons and urologists will be faced with this difficult clinical scenario that requires maximizing preservation of renal function while ensuring adequate cancer control. Immunosuppression has been identified as a risk factor for developing both infectious-mediated malignancies and those without underlying infectious etiology. It is hypothesized that this may be secondary to the immune system having a decreased ability to identify and destroy cancer cells. Although minimal literature links immunosuppression to the development of RCC in the transplanted allograft, a wide body of literature supports the role of immunosuppression in the development of other malignancies, particularly related to oncogenic viruses and nonmelanoma skin cancer (63Krisl JC Doan VP Chemotherapy and transplantation: The role of immunosuppression in malignancy and a review of antineoplastic agents in solid organ transplant recipients.Am J Transplant. 2017; ([E-pub ahead of print].)Abstract Full Text Full Text PDF PubMed Scopus (51) Google Scholar). The role of CNIs in the development of malignancy has been explored, with increased levels of VEGF and TGF-β1 identified with CNI use (64Engels EA Jennings L Kemp TJ et al.Circulating TGF-β1 and VEGF and risk of cancer among liver transplant recipients.Cancer Med. 2015; 4: 1252Crossref PubMed Scopus (18) Google Scholar). This upregulation may result in proliferation of malignant cells in patients on CNIs, which the majority of our reviewed patients used prior to diagnosis of SRM. A dose-dependent increase in circulating TGF- β1 has been identified in both in vitro and in vivo analyses (65Maluccio M Sharma V Shefali V Yang H Li B Suthanthiran M Tacrolimus enhances transforming growth factor-β1 expression and promotes tumor progression.Transplantation. 2003; 76: 597Crossref PubMed Scopus (211) Google Scholar). Although the use of low-dose CNI regimens has been associated with a decreased risk of malignancy, an increased risk of acute rejection was seen with lower dose suppression (66Dantal J Hourmant M Cantarovich D et al.Effect of long-term immunosuppression in kidney-graft recipients on cancer incidence: Randomized comparison of two cyclosporin regimens.Lancet. 1998; 351: 623Abstract Full Text Full Text PDF PubMed Scopus (623) Google Scholar). Less literature supports an increased malignant potential with other immunosuppressive agents such antimetabolites, corticosteroids, and induction therapies; however, this is an area of continuing active research. The utilization of mTOR inhibitors for immunosuppression after transplantation has been shown to lower the rates of de novo malignancy; however, this approach is associated with significant adverse affects leading to discontinuation (67Schena F Pascoe M Alberu J et al.Conversion from calcineurin inhibitors to sirolimus maintenance therapy in renal allograft recipients: 24-month efficacy and sfety results from the CONVERT trial.Transplantation. 2009; 87: 233Crossref PubMed Scopus (484) Google Scholar). After diagnosis of malignancy after transplantation, alterations to the immunosuppressive regimen could include altering the medications used, lowering the dos" @default.
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• W2616948211 title "Solid Renal Masses in Transplanted Allograft Kidneys: A Closer Look at the Epidemiology and Management" @default.
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