Elrggal, Mohamed Essam MD1; Gokcay Bek, Sibel MD2; Shendi, Ali M MD3; Tannor, Elliot Koranteng MD4; Nlandu, Yannick Mayamba MD5; Gaipov, Abduzhappar MD6
doi : 10.1097/TP.0000000000003585
November 2021 - Volume 105 - Issue 11 - p 2325-2329
Chronic kidney disease (CKD) is a global health problem with nearly 0.1% of the world’s population suffering from end-stage kidney disease (ESKD).1 The availability and accessibility to treatments for ESKD differ around the globe because of variations in healthcare budgets and availability of treatments. Although the prevalence of ESKD in low-income countries (LICs, 0.05%) and lower middle–income countries (L-MICs, 0.07%) is estimated to be lower than in high-income countries (HICs, 0.2%), or potentially underdiagnosed, the proportion of patients who are not receiving effective treatment is much higher in LICs (96%) and L-MICs (90%) compared with upper middle–income countries (U-MICs, 70%) and HICs (40%).2 In some L-MICs, it is impossible to support hemodialysis treatment for every ESKD patient, and most patients are unable to pay for dialysis out of pocket.2
Schroder, Paul M. MD, PhD1; Luo, Xunrong MD, PhD2
doi : 10.1097/TP.0000000000003956
November 2021 - Volume 105 - Issue 11 - p 2330-2331
Peloso, Andrea MD, PhD1,2
doi : 10.1097/TP.0000000000003909
November 2021 - Volume 105 - Issue 11 - p 2332-2333
Choubey, Ankur P. BA1; Reilly, Margaret MD1; Bullock, Brenna BA1; Ireland, Megan BA1; Brown, Meghan MD1; Ortiz, Alejandro BA2; Pai, Kavya BA1; Sureddi, Sriya BA1; Khan, Samar A. BA1; Mishra, Anil BA1; Koizumi, Naoru PhD3; Pearson, Terra MD4; Ortiz, Jorge MD2
doi : 10.1097/TP.0000000000003748
November 2021 - Volume 105 - Issue 11 - p 2334-2336
Turgeon, Nicole A. MD1
doi : 10.1097/TP.0000000000003800
November 2021 - Volume 105 - Issue 11 - p 2337-2339
Howell, Martin PhD1,2
doi : 10.1097/TP.0000000000003558
November 2021 - Volume 105 - Issue 11 - p 2340-2341
Samstein, Benjamin MD1
doi : 10.1097/TP.0000000000003560
November 2021 - Volume 105 - Issue 11 - p 2342-2343
Wagener, Gebhard MD1
doi : 10.1097/TP.0000000000003506
November 2021 - Volume 105 - Issue 11 - p 2344-2345
Pesavento, Todd E. MD1
doi : 10.1097/TP.0000000000003885
November 2021 - Volume 105 - Issue 11 - p 2346-2347
Nankivell, Brian J. MD, PhD, FRACP1
doi : 10.1097/TP.0000000000003571
November 2021 - Volume 105 - Issue 11 - p 2348-2349
Immenschuh, Stephan MD1
doi : 10.1097/TP.0000000000003742
November 2021 - Volume 105 - Issue 11 - p e154-e155
Wang, Carol MD1; Garg, Amit X. MD, PhD1,2
doi : 10.1097/TP.0000000000003644
November 2021 - Volume 105 - Issue 11 - p 2350-2351
Macdonald, Peter MD1,2,3
doi : 10.1097/TP.0000000000003692
November 2021 - Volume 105 - Issue 11 - p 2352-2361
Frailty has been defined as a state of increased vulnerability due to a decline in the reserve and function of multiple physiological systems. Initially conceived as a geriatric syndrome indicative of physiological aging, it is now apparent that frailty can also be observed as a manifestation of chronic disease states including heart failure. Estimates of the prevalence of frailty in heart failure vary according to the age of the study population and the frailty instrument used; however, multiple studies have identified frailty to be prevalent in patients with advanced heart failure including those who are referred for heart transplantation. Frailty is emerging as an independent predictor of mortality both before and after bridge-to-transplant ventricular assist device implantation and heart transplantation. Frailty is also predictive of prolonged hospitalization following these procedures. Heart failure–associated frailty is a dynamic state. While reversibility of frailty can be anticipated in younger heart failure patients, predicting the reversibility of frailty is more challenging in older patients who often have multiple comorbidities that may contribute to the frailty syndrome. Prehabilitation is a promising approach to both preventing and reversing frailty however more research is urgently needed to establish its effectiveness in mitigating the adverse impacts of frailty on postventricular assist device and posttransplant morbidity and mortality.
Shi, Shaojun MD1; Wang, Ling MSc2; van der Laan, Luc J.W. PhD1; Pan, Qiuwei PhD2; Verstegen, Monique M. A. PhD1
doi : 10.1097/TP.0000000000003691
November 2021 - Volume 105 - Issue 11 - p 2362-2373
Mitochondria are essential organelles for cellular energy and metabolism. Like with any organ, the liver highly depends on the function of these cellular powerhouses. Hepatotoxic insults often lead to an impairment of mitochondrial activity and an increase in oxidative stress, thereby compromising the metabolic and synthetic functions. Mitochondria play a critical role in ATP synthesis and the production or scavenging of free radicals. Mitochondria orchestrate many cellular signaling pathways involved in the regulation of cell death, metabolism, cell division, and progenitor cell differentiation. Mitochondrial dysfunction and oxidative stress are closely associated with ischemia-reperfusion injury during organ transplantation and with different liver diseases, including cholestasis, steatosis, viral hepatitis, and drug-induced liver injury. To develop novel mitochondria-targeting therapies or interventions, a better understanding of mitochondrial dysfunction and oxidative stress in hepatic pathogenesis is very much needed. Therapies targeting mitochondria impairment and oxidative imbalance in liver diseases have been extensively studied in preclinical and clinical research. In this review, we provide an overview of how oxidative stress and mitochondrial dysfunction affect liver diseases and liver transplantation. Furthermore, we summarize recent developments of antioxidant and mitochondria-targeted interventions.
Charreau, Béatrice PhD1
doi : 10.1097/TP.0000000000003741
November 2021 - Volume 105 - Issue 11 - p e156-e167
Graft endothelial cell (EC) injury is central to the pathogenesis of antibody-mediated rejection (AMR). The ability of donor-specific antibodies (DSA) to bind C1q and activate the classical complement pathway is an efficient predictor of graft rejection highlighting complement-dependent cytotoxicity as a key process operating during AMR. In the past 5 y, clinical studies further established the cellular and molecular signatures of AMR revealing the key contribution of other, IgG-dependent and -independent, effector mechanisms mediated by infiltrating NK cells and macrophages. Beyond binding to alloantigens, DSA IgG can activate NK cells and mediate antibody-dependent cell cytotoxicity through interacting with Fc? receptors (Fc?Rs) such as Fc?RIIIa (CD16a). FcRn, a nonconventional Fc?R that allows IgG recycling, is highly expressed on ECs and may contribute to the long-term persistence of DSA in blood. Activation of NK cells and macrophages results in the production of proinflammatory cytokines such as TNF and IFN? that induce transient and reversible changes in the EC phenotype and functions promoting coagulation, inflammation, vascular permeability, leukocyte trafficking. MHC class I mismatch between transplant donor and recipient can create a situation of “missing self” allowing NK cells to kill graft ECs. Depending on the microenvironment, cellular proximity with ECs may participate in macrophage polarization toward an M1 proinflammatory or an M2 phenotype favoring inflammation or vascular repair. Monocytes/macrophages participate in the loss of endothelial specificity in the process of endothelial-to-mesenchymal transition involved in renal and cardiac fibrosis and AMR and may differentiate into ECs enabling vessel and graft (re)-endothelialization.
Louis, Kevin MD, PhD1,2,3; Macedo, Camila MD1; Metes, Diana MD1,4
doi : 10.1097/TP.0000000000003776
November 2021 - Volume 105 - Issue 11 - p e168-e180
Humoral allogeneic immunity driven by anti-HLA donor-specific antibodies and antibody-mediated rejection (AMR) significantly impede prolonged survival of organ allografts after transplantation. Although the importance of T follicular helper (TFH) cells in controlling antibody responses has been long established, their role in directing donor-specific antibody generation leading to AMR was only recently appreciated in the clinical setting of organ transplantation. In this review, we provide a comprehensive summary of the current knowledge on the biology of human TFH cells as well as their circulating counterparts and describe their pivotal role in driving humoral alloimmunity. In addition, we discuss the intrinsic effects of current induction therapies and maintenance immunosuppressive drugs as well as of biotherapies on TFH cells and provide future directions and novel opportunities of biotherapeutic targeting of TFH cells that have the potential of bringing the prophylactic and curative treatments of AMR toward personalized and precision medicine.
Filippone, Edward J. MD, FASN1; Farber, John L. MD2
doi : 10.1097/TP.0000000000003797
November 2021 - Volume 105 - Issue 11 - p e181-e190
Histologic antibody-mediated rejection (hAMR) is defined as a kidney allograft biopsy satisfying the first 2 Banff criteria for diagnosing AMR: tissue injury and evidence of current/recent antibody interaction with the endothelium. In approximately one-half of such cases, circulating human leukocyte antigen (HLA) donor-specific antibodies (DSA) are not detectable by current methodology at the time of biopsy. Some studies indicated a better prognosis for HLA-DSA-negative cases of hAMR compared to those with detectable HLA-DSA, whereas others found equally poor survival compared to hAMR-negative cases. We reviewed the literature regarding the pathophysiology of HLA-DSA-negative hAMR. We find 3 nonmutually exclusive possibilities: (1) HLA-DSA are involved, but just not detected; (2) non-HLA-DSA (allo or autoantibodies) are pathogenically involved; and/or (3) antibody-independent NK cell activation is mediating the process through “missing-self” or other activating mechanisms. These possibilities are discussed in detail. Recommendations regarding the approach to such patients are made. Clearly, more research is necessary regarding the measurement of non-HLA antibodies, recipient/donor NK cell genotyping, and the use of antibody reduction therapy or other immunosuppression in any subset of patients with HLA-DSA-negative hAMR.
Tran, Danh T. BS1,2; Sundararaj, Kamala PhD1,2,3; Atkinson, Carl PhD1,2,3; Nadig, Satish N. MD, PhD1,2,3
doi : 10.1097/TP.0000000000003767
November 2021 - Volume 105 - Issue 11 - p e191-e201
Although solid-organ transplantation has evolved steadily with many breakthroughs in the past 110 y, many problems remain to be addressed, and advanced therapeutic strategies need to be considered. T-cell immunometabolism is a rapidly advancing field that has gathered much attention recently, providing ample mechanistic insight from which many novel therapeutic approaches have been developed. Applications from the field include antitumor and antimicrobial therapies, as well as for reversing graft-versus-host disease and autoimmune diseases. However, the immunometabolism of T cells remains underexplored in solid-organ transplantation. In this review, we will highlight key findings from hallmark studies centered around various metabolic modes preferred by different T-cell subtypes (categorized into naive, effector, regulatory, and memory T cells), including glycolysis, glutaminolysis, oxidative phosphorylation, fatty acid synthesis, and oxidation. This review will discuss the underlying cellular signaling components that affect these processes, including the transcription factors myelocytomatosis oncogene, hypoxia-inducible factor 1-alpha, estrogen-related receptor alpha, and sterol regulatory element-binding proteins, along with the mechanistic target of rapamycin and adenosine monophosphate–activated protein kinase signaling. We will also explore potential therapeutic strategies targeting these pathways, as applied to the potential for tolerance induction in solid-organ transplantation.
Hosgood, Sarah A. PhD1; Brown, Rachel J. BSc1; Nicholson, Michael L. DSc1
doi : 10.1097/TP.0000000000003679
November 2021 - Volume 105 - Issue 11 - p e202-e214
The use of cold preservation solutions to rapidly flush and cool the kidney followed by static cold storage in ice has been the standard kidney preservation technique for the last 50 y. Nonetheless, changing donor demographics that include organs from extended criteria donors and donation after circulatory death donors have led to the adoption of more diverse techniques of preservation. Comparison of hypothermic machine perfusion and static cold storage techniques for deceased donor kidneys has long been debated and is still contested by some. The recent modification of hypothermic machine perfusion techniques with the addition of oxygen or perfusion at subnormothermic or near-normothermic temperatures are promising strategies that are emerging in clinical practice. In addition, the use of normothermic regional perfusion to resuscitate abdominal organs of donation after circulatory death donors in situ before cold flushing is also increasingly being utilized. This review provides a synopsis of the different types of preservation techniques including their mechanistic effects and the outcome of their application in clinical practice for different types of donor kidney.
Xu, Min MD1; Zhou, Fangyu MD1; Ahmed, Ola MD1; Upadhya, Gundumi A. PhD1; Jia, Jianluo MD1; Lee, Choonghee MS1; Xing, Jianwei MS1; Ye, Li MS1; Shim, So Hee PhD1; Zhang, Zhengyan MD, PhD1; Byrnes, Kathleen MD2; Wong, Brian PhD1; Kim, Jae-Sung PhD1; Lin, Yiing MD, PhD1; Chapman, William C. MD1
doi : 10.1097/TP.0000000000003675
November 2021 - Volume 105 - Issue 11 - p e215-e225
Hepatic steatosis is now the leading cause of liver discards in deceased donors. Previous studies [Yarmush formula (Y) defatting] have successfully reduced the fat content by treating rat steatotic livers on extracorporeal normothermic machine perfusion (NMP) with a multidrug combination including the GW compounds that were linked to an increased risk of carcinogenesis.
Halloran, Philip F. MD, PhD1,2; Madill-Thomsen, Katelynn S. PhD1; Böhmig, Georg A. MD3; Myslak, Marek MD4; Gupta, Gaurav MD5; Kumar, Dhiren MD5; Viklicky, Ondrej MD, PhD6; Perkowska-Ptasinska, Agnieszka MD7; Famulski, Konrad S. PhD1
doi : 10.1097/TP.0000000000003884
November 2021 - Volume 105 - Issue 11 - p 2374-2384
BK nephropathy (BKN) in kidney transplants diagnosed by histology is challenging because it involves damage from both virus activity and cognate T cell–mediated inflammation, directed against alloantigens (rejection) or viral antigens. The present study of indication biopsies from the Integrated Diagnostic System in the International Collaborative Microarray Study Extension study measured major capsid viral protein 2 (VP2) mRNA to assess virus activity and a T cell–mediated rejection (TCMR) classifier to assess cognate T cell–mediated inflammation.
De Carlis, Riccardo MD1; Schlegel, Andrea MD2; Frassoni, Samuele MSc3; Olivieri, Tiziana MD4; Ravaioli, Matteo PhD5; Camagni, Stefania MD6; Patrono, Damiano PhD7; Bassi, Domenico MD8; Pagano, Duilio PhD9; Di Sandro, Stefano PhD4; Lauterio, Andrea MD1; Bagnardi, Vincenzo PhD3; Gruttadauria, Salvatore MD9; Cillo, Umberto MD8; Romagnoli, Renato MD7; Colledan, Michele MD6; Cescon, Matteo MD5; Di Benedetto, Fabrizio MD4; Muiesan, Paolo MD2,10; De Carlis, Luciano MD1,11
doi : 10.1097/TP.0000000000003595
November 2021 - Volume 105 - Issue 11 - p 2385-2396
Donation after circulatory death (DCD) in Italy, given its 20-min stand-off period, provides a unique bench test for normothermic regional perfusion (NRP) and dual hypothermic oxygenated machine perfusion (D-HOPE).
Zuckerman, Jesse MD, CM1; Gorgen, Andre MD2; Acuna, Sergio A. PhD1; Abreu, Phillipe MD2; Goldaracena, Nicolas MD2; Galvin, Zita MD2; Cattral, Mark S. MD2; Ghanekar, Anand PhD2; McGilvray, Ian D. MD2; Lilly, Les B. MD1; Selzner, Nazia PhD2; Grant, David R. MD2; Sapisochin, Gonzalo PhD2
doi : 10.1097/TP.0000000000003559
November 2021 - Volume 105 - Issue 11 - p 2397-2403
The main concern with live donor liver transplantation (LDLT) is the risk to the donor. Given the potential risk of liver insufficiency, most centers will only accept candidates with future liver remnants (FLR) >30%. We aimed to compare postoperative outcomes of donors who underwent LDLT with FLR ?30% and >30%.
Verhelst, Xavier PhD1,2,3; Geerts, Anja PhD1,2,3; Colman, Roos MSc4; Vanlander, Aude MD5; Degroote, Helena MD1,2,3; Abreu de Carvalho, Luis MD5; Meuris, Leander PhD6; Berrevoet, Frederik PhD5; Rogiers, Xavier PhD5,†; Callewaert, Nico PhD6; Van Vlierberghe, Hans PhD1,2,3
doi : 10.1097/TP.0000000000003567
November 2021 - Volume 105 - Issue 11 - p 2404-2410
Prediction of outcome after liver transplantation (LT) is limited by the lack of robust predictors of graft failure. In this prospective study, we aimed to define a serum glycomic signature in the first week after LT that is associated with graft loss at 3 mo after LT.
Niazi, Shehzad K. MD, FRCPC1,2; Vargas, Emily MPH2,3; Spaulding, Aaron PhD2,3; Crook, Julia PhD3; Keaveny, Andrew P. MD, FRCPI4; Schneekloth, Terry MD5; Rummans, Teresa MD1,5; Taner, C. Burcin MD4
doi : 10.1097/TP.0000000000003557
November 2021 - Volume 105 - Issue 11 - p 2411-2419
There is limited information concerning whether social determinants of health affect postliver transplant (LT) outcomes. This study aims to understand to what extent the health of LT recipients’ counties of residence influence long-term LT outcomes.
Cullaro, Giuseppe MD, MAS1; Rubin, Jessica MD, MPH1; Mehta, Neil MD1; Yao, Francis MD1; Verna, Elizabeth C. MD, MSc2; Lai, Jennifer C. MD, MBA1
doi : 10.1097/TP.0000000000003575
November 2021 - Volume 105 - Issue 11 - p 2420-2426
Women with chronic liver disease have lower rates of hepatocellular carcinoma (HCC) as compared to men; it is unknown if there are sex-based differences in HCC recurrence postliver transplant.
Singh, Nina MD1; Winston, Drew J. MD2; Razonable, Raymund R. MD3; Lyon, G. Marshall MD4; Huang, Meei-Li PhD5; Jerome, Keith R. MD, PhD5,6; Silveira, Fernanda P. MD7; Wagener, Marilyn M. MD1; Limaye, Ajit P. MD5
doi : 10.1097/TP.0000000000003604
November 2021 - Volume 105 - Issue 11 - p 2427-2434
Risk factors, virological parameters, and outcomes associated with HHV-6 viremia in high-risk donor CMV-seropositive and recipient CMV-seronegative (D+R–) liver transplant recipients in the current era are incompletely defined.
Ivanics, Tommy MD1,2; Salinas-Miranda, Emmanuel MD3,4; Abreu, Phillipe MD, MSc, PhD1; Khalvati, Farzad PhD3,4; Namdar, Khashayar MSc3; Dong, Xin MSc3; Deniffel, Dominik MD3,4; Gorgen, Andre MD, MSc1; Erdman, Lauren MSc5; Jhaveri, Kartik MD4; Haider, Masoom MD2,4; Veit-Haibach, Patrick MD4; Sapisochin, Gonzalo MD, PhD, MSc1
doi : 10.1097/TP.0000000000003605
November 2021 - Volume 105 - Issue 11 - p 2435-2444
Despite transarterial chemoembolization (TACE) for hepatocellular carcinoma (HCC), a significant number of patients will develop progression on the liver transplant (LT) waiting list or disease recurrence post-LT. We sought to evaluate the feasibility of a pre-TACE radiomics model, an imaging-based tool to predict these adverse outcomes.
Benoit, Thibaut MD1; Prudhomme, Thomas MD2; Adypagavane, Aurélien MD3; Malavaud, Bernard MD, PhD4; Soulié, Michel MD, PhD2; Gamé, Xavier MD, PhD2; Kamar, Nassim MD, PhD5; Dariane, Charles MD, PhD3; Legendre, Christophe MD, PhD6; Méjean, Arnaud MD, PhD3; Roumiguié, Mathieu MD2; Timsit, Marc Olivier MD, PhD3,7
doi : 10.1097/TP.0000000000003643
November 2021 - Volume 105 - Issue 11 - p 2445-2450
Transplantation from living donor nephrectomy (LDN) is the best treatment for end-stage renal disease but observed decrease in donor renal function is a major concern. The aim of this study was to externally validate a predictive model to estimate 1-y postdonation estimated glomerular filtration rate (eGFR) and risk of chronic kidney disease (CKD) in living donors.
Grande, Joseph P. MD, PhD1; Helgeson, Erika S. PhD2; Matas, Arthur J. MD3
doi : 10.1097/TP.0000000000003570
November 2021 - Volume 105 - Issue 11 - p 2451-2460
Glomerular size in renal allografts is impacted by donor–recipient factors and response to injury. In serial biopsies of patients with well-functioning grafts, increased glomerular size correlates with better survival. However, no previous study has addressed the association of glomerular size at the time of a for-cause biopsy and clinical/histopathologic markers of injury, or effect on long-term graft outcome.
Echterdiek, Fabian MD1; Latus, Joerg MD1; Döhler, Bernd PhD2; Schwenger, Vedat MD1; Süsal, Caner MD2
doi : 10.1097/TP.0000000000003629
November 2021 - Volume 105 - Issue 11 - p 2461-2469
The use of kidney allografts from ?70-y-old donors has increased persistently over the last 20 y. Prolonged cold ischemia time (CIT) is well known to increase graft failure risk. However, despite their growing importance, no data are available on the impact of CIT, specifically on survival of allografts from ?70-y-old donors.
Haskin, Orly MD1,2; Ashkenazi-Hoffnung, Liat MD2,3; Ziv, Noa MD2,4; Borovitz, Yael MD1; Dagan, Amit MD1,2; Levi, Shelly MD1,2; Koren, Gili1; Hamdani, Gilad MD1; Levi-Erez, Daniella MD1,2; Landau, Daniel MD1,2; Alfandary, Hadas MD1,2
doi : 10.1097/TP.0000000000003922
November 2021 - Volume 105 - Issue 11 - p e226-e233
Initial reports in adult kidney transplant recipients (KTR) indicate low immunogenicity after 2 doses of the BNT162b2 COVID-19 mRNA vaccine. We describe the immunogenicity of this vaccine compared to the serologic response in naturally infected COVID-19 positive adolescent and young adult KTR.
Hod, Tammy MD1,2,3; Ben-David, Aharon MD1,2,3; Olmer, Liraz4; Levy, Itzchak MD3,5; Ghinea, Ronen MD1,3; Mor, Eytan MD1,3; Lustig, Yaniv PhD3,6; Rahav, Galia MD, PhD3,5
doi : 10.1097/TP.0000000000003889
November 2021 - Volume 105 - Issue 11 - p e234-e243
Data about SARS-CoV-2 vaccines efficacy in renal transplant recipients (RTR) are lacking.
D’Costa, Matthew R. MD1,2; Bentall, Andrew MD1,2; Denic, Aleksandar PhD1; Schinstock, Carrie A. MD1,2; Merzkani, Massini A. MD1,2; Park, Walter D. BS3; Ryan, Margaret S. MD4; Alexander, Mariam P. MD5; Smith, Byron H. PhD2,6; Gandhi, Manish J. MD2,7; Stegall, Mark D. MD2,3,8
doi : 10.1097/TP.0000000000003579
November 2021 - Volume 105 - Issue 11 - p e244-e256
At 5 and 10 y after kidney transplantation, chronic histologic changes such as arteriolar hyalinosis and mesangial expansion are common; however, determining cause is difficult. We compared surveillance biopsies in living donor kidney transplants (LDKTx) from HLA-matched siblings (termed HLA-identical [HLA-ID]) with HLA non-ID to investigate which histologic changes were likely due to alloimmune injury and which were due to nonalloimmune injury.
Lim, Wai H. PhD1,2; Lok, Charmaine E. MD3,4; Kim, S. Joseph MD3; Knoll, Greg MD5,6; Shah, Baiju R. PhD7,8,9; Naylor, Kyla PhD9; Luo, Bin PhD9; Vinegar, Marlee MPH9; Dixon, Stephanie N. PhD9,10; Hawley, Carmel FRACP11,12,13; Ooi, Esther PhD2,14; Viecelli, Andrea PhD11,12; Wong, Germaine PhD15,16,17
doi : 10.1097/TP.0000000000003639
November 2021 - Volume 105 - Issue 11 - p 2470-2481
Pretransplant diabetes and new-onset diabetes after transplant (NODAT) are known risk factors for vascular events after kidney transplantation, but the incidence and magnitude of the risk of major adverse cardiovascular events (MACE) and cardiac deaths remain uncertain in recent era.
Fujisaki, Tomohiro MD1; Mikami, Takahisa MD2,3; Kuno, Toshiki MD, PhD2; Moss, Noah MD4; Itagaki, Shinobu MD, MSc5
doi : 10.1097/TP.0000000000003638
November 2021 - Volume 105 - Issue 11 - p 2482-2489
The effect of hepatitis C virus (HCV) infection in recipients or donors on heart transplants is less known in the current era after the introduction of direct-acting antiviral agents (DAAs) in 2011.
Rios, Paola MD1; Baidal, David MD1,2; Lemos, Joana PhD1; Camhi, Stephanie S. BS1; Infante, Marco MD1; Padilla, Nathalia MD1; Alvarez Gil, Ana M. APRN1; Fuenmayor, Virginia MD1; Ambut, Jonathan MD1; Qasmi, Fatima A. MD1; Mantero, Alejandro M. PhD3; Cayetano, Shari Messinger PhD3; Ruiz, Phillip MD, PhD4; Ricordi, Camillo MD1,5; Alejandro, Rodolfo MD1,2
doi : 10.1097/TP.0000000000003635
November 2021 - Volume 105 - Issue 11 - p 2490-2498
Allosensitization has been reported after discontinuation of immunosuppression following graft failure in islet transplantation (ITx) recipients, though duration of its persistence is unknown.
Boucher, Alexander A. MD1,2; Wastvedt, Solvejg BA3; Hodges, James S. PhD3; Beilman, Gregory J. MD4; Kirchner, Varvara A. MD4; Pruett, Timothy L. MD4; Hering, Bernhard J. MD4; Schwarzenberg, Sarah J. MD1; Downs, Elissa MD1; Freeman, Martin MD2; Trikudanathan, Guru MBBS2; Chinnakotla, Srinath MD1,4; Bellin, Melena D. MD1,4
doi : 10.1097/TP.0000000000003624
November 2021 - Volume 105 - Issue 11 - p 2499-2506
Total pancreatectomy with islet autotransplantation (TPIAT) involves pancreatectomy, splenectomy, and reinjection of the patient’s pancreatic islets into the portal vein. This process triggers a local inflammatory reaction and increase in portal pressure, threatening islet survival and potentially causing portal vein thrombosis. Recent research has highlighted a high frequency of extreme thrombocytosis (platelets ?1000?×?109/L) after TPIAT, but its cause and association with thrombotic risk remain unclear.
Fernandes, Guillaume MD1; Devresse, Arnaud PhD1,2; Scohy, Anais PharmD3; Yombi, Jean Cyr MD2,4; Belkhir, Leila PhD2,4; De Greef, Julien MD2,4; De Meyer, Martine MD2,5; Mourad, Michel PhD2,5; Darius, Tom PhD2,5; Buemi, Antoine MD2,5; Kabamba, Benoit MD2,4; Goffin, Eric MD1,2; Kanaan, Nada MD1,2
doi : 10.1097/TP.0000000000003910
November 2021 - Volume 105 - Issue 11 - p e257-e258
Noble, Johan MD1,2; Langello, Antoine St.1,*; Bouchut, William St.1,*; Lupo, Julien MD3; Lombardo, Dorothee MD1; Rostaing, Lionel MD, PhD1,2
doi : 10.1097/TP.0000000000003923
November 2021 - Volume 105 - Issue 11 - p e259-e260
Vinson, Amanda J. MD1; Chong, Anita S. PhD2; Clegg, Deborah PhD3; Falk, Christine PhD4; Foster, Bethany J. MD5,6; Halpin, Anne MSc6,7,8,9; Mannon, Roslyn B. MD10; Oertelt-Prigione, Sabine MD11,12; Palmer, Biff F. MD13; Sapir-Pichhadze, Ruth MD6,14,15; West, Lori J. MD6,9,16,17,18; Wong, Germaine MD19
doi : 10.1097/TP.0000000000003967
November 2021 - Volume 105 - Issue 11 - p e261-e262
Ravanan, Rommel FRCP1; Mumford, Lisa MSc1; Ushiro-Lumb, Ines FRCPath1; Callaghan, Chris FRCS1; Pettigrew, Gavin FRCS1; Thorburn, Douglas FRCP1; Gardiner, Dale FFICM1; Forsythe, John FRCS1
doi : 10.1097/TP.0000000000003908
November 2021 - Volume 105 - Issue 11 - p e263-e264
Solid organ and islet transplant (SOT) recipients have higher risk of death following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.1,2 Trials investigating SARS-CoV-2 vaccine efficacy excluded SOT recipients.3 As seen with other vaccines, immunosuppression may reduce SARS-CoV-2 vaccine efficacy. Emerging data indicate lower spike protein antibody levels following vaccination in SOT recipients.4
Qin, Caroline X. BS1; Moore, Linda W. PhD2; Anjan, Shweta MD3; Rahamimov, Ruth MD4; Sifri, Costi D. MD5; Ali, Nicole M. MD6; Morales, Megan K. MD7; Tsapepas, Demetra S. PharmD8; Basic-Jukic, Nikolina MD, PhD9; Miller, Rachel A. MD10; van Duin, David MD, PhD11; Santella, Robert N. MD12; Wadei, Hani M. MD13; Shah, Pali D. MD14; Gage, Nikki RN15; Malinis, Maricar MD16; Aslam, Saima MD, MS17; Todesco, Eve PhD18; Werbel, William A. MD14; Avery, Robin K. MD14; Segev, Dorry L. MD, PhD1
doi : 10.1097/TP.0000000000003907
November 2021 - Volume 105 - Issue 11 - p e265-e266
It is well established at this point that solid organ transplant recipients (SOTRs) have substantially diminished antibody responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines.1,2 The correlation of this suboptimal antibody response to disease susceptibility is clinically important but poorly understood. In this multicenter study, we estimated the breakthrough infection rates after SARS-CoV-2 mRNA vaccination in SOTRs and compared them with rates reported in the general population.
Stumpf, Julian MD1,2; Tonnus, Wulf1; Paliege, Alexander MD1,2; Rettig, Ronny MD1; Steglich, Anne PhD1; Gembardt, Florian PhD1; Kessel, Friederike MSc1; Kröger, Hannah MSc1; Arndt, Patrick MSc1; Sradnick, Jan PhD1; Frank, Kerstin MSc3; Tonn, Torsten MD4,5; Hugo, Christian MD1,2
doi : 10.1097/TP.0000000000003903
November 2021 - Volume 105 - Issue 11 - p e267-e269
Kidney transplant recipients (KTRs) have an increased risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mortality1 and a markedly decreased immune response after 2 doses of mRNA vaccination.2 The optimal vaccination strategy for KTRs without sufficient immune response after standard vaccination protocols remains unknown. Here, we report combined cellular and humoral response rates after a third dose of the BNT162b2 mRNA vaccine (Tozinameran; Pfizer–BioNTech COVID-19 vaccine).
Boyarsky, Brian J. MD, PhD1; Barbur, Iulia BSE1; Chiang, Teresa Po-Yu MD1; Ou, Michael T. BS1; Greenberg, Ross S. BS1; Teles, Aura T. BS1; Krach, Michelle R. MS1; López, Julia I. BA1; Garonzik-Wang, Jacqueline M. MD, PhD1; Avery, Robin K. MD2; Massie, Allan B. PhD1; Segev, Dorry L. MD, PhD1,3; Werbel, William A. MD2
doi : 10.1097/TP.0000000000003900
November 2021 - Volume 105 - Issue 11 - p e270-e271
Zhang, Xiaohai PhD1; Li, Fang PhD1; Jordan, Stanley C. MD2
doi : 10.1097/TP.0000000000003849
November 2021 - Volume 105 - Issue 11 - p e272-e273
Chen, Chen MD1; Gu, Lihong MD2; Zhou, Tao MD1; Gu, Guangxiang MD, PhD1; Xia, Qiang MD1
doi : 10.1097/TP.0000000000003848
November 2021 - Volume 105 - Issue 11 - p e274-e275
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