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The authors compare the risk of end-stage renal disease (ESRD) in 96217 kidney donors in the United States, followed for a median of 7.6 years with that of a healthy cohort of 20024 nondonors, followed for a median of 15 years of who are at equally low risk of renal disease and free of contraindications to live donation. Live kidney donors who are supposed to be “super healthy”; on average have excellent quality of life compared with healthy control individuals in the population. The authors were able to use a very healthy population of their country as a comparison group. However most analyses have included control groups less healthy than the living donor population and have had relatively short follow-up periods. Previously we didn’t have accurate information about a live donor’s lifetime risk of needing dialysis. The authors found that live kidney donors have an elevated relative risk of developing ESRD. However, the risk of reaching ESRD in the donor’s lifetime is very low. In this study estimated risk for ESRD would be less than 1% at 15 years for the donors in the United States. Nonetheless, that the risk for ESRD for live kidney donors remain lower than the risk for the average person in the population, but the risks are probably higher than if these “super healthy” people had never donated a kidney. These findings allowed us to have a precise understanding of the risks related to live kidney donation and may help to inform people better considering this option as a gift of life.

There is a significant shortage of donor kidneys. As a result, kidney transplant candidates wait for prolonged periods of time for an organ, and over eight die every day while awaiting a kidney transplant. To improve this situation, the transplant community has actively sought creative solutions to the organ shortage. Many patients have willing live donors who are excluded from donation due to a positive crossmatch or blood group incompatibility. Plasmapheresis and intravenous immunoglobulin in combination can efficiently remove antibodies against donor tissue and blood group antigens and prevent these antibodies from returning after transplantation. Both strategies are complex but have good success rates and provide an opportunity for transplantation to those who might wait years for an organ or die waiting on the list Knowledge of these novel protocols is essential for the nephrology nurse who is often the first health care provider to discuss transplantation with end stage renal disease (ESRD) patients. [ABSTRACT FROM AUTHOR]

Competing Interests: The author declares no funding or conflict of interest.

Background: Imlifidase is an IgG-cleaving endopeptidase conditionally approved in Europe for desensitization of highly sensitized patients before kidney transplantation. We present 5-y outcomes and donor-specific antibody (DSA) levels for clinical trial participants from a single site who received imlifidase for desensitization before incompatible transplantation (NCT02790437)., Methods: Imlifidase was administered up to 24 h before living or deceased donor kidney transplantation. DSAs were monitored before transplantation, at days 7 and 28, and at 5 y posttransplant., Results: At 5 y, 7 of 8 participants were alive. One of these 7 had suboptimal graft function secondary to donor-derived disease but remained dialysis independent. Three participants had antibody-mediated rejection (AMR), which occurred in the first 30 d in all cases and was successfully treated. No new episodes of suspected or biopsy-proven AMR occurred after 30 d posttransplant. Seven participants had DSA rebound. DSAs commonly persisted 5 y posttransplant, although they were generally lower strength compared with pre-imlifidase. Dilution studies of sensitized serum enabled the identification of lower AMR risk phenotypes for persisting DSAs. Severe and/or opportunistic infections were not observed at greater than expected frequency., Conclusions: Five-year outcomes of imlifidase-enabled incompatible transplants are overall favorable. DSA rebound is common, but antibody strength lessens in the long term, and longitudinally persisting DSAs did not lead to premature graft failure., (Copyright © 2025 The Author(s). Transplantation Direct. Published by Wolters Kluwer Health, Inc.)

High human leukocyte antigen (HLA) sensitization limits access to compatible transplantation. New CD38-targeting agents have been shown to reduce anti-HLA antibodies, although with important interpatient variability. Thus, pretreatment identification of responder and nonresponder (NR) patients is needed for treatment decision-making. We analyzed 26 highly sensitized (HS) patients from 2 desensitization trials using anti-CD38 monoclonal antibodies. Hierarchical clustering identified 3 serologic responder groups: high responders, low responders, and NR. Spectral flow cytometry and functional HLA-specific memory B cell (mBC) assessment were first conducted on peripheral blood mononuclear cells and bone marrow samples from 16 patients treated with isatuximab (NCT04294459). Isatuximab effectively depleted bone marrow plasma cells, peripheral CD38-expressing plasmablasts, plasma cells, transitional B cells, and class-switch mBCs, ultimately reducing frequencies of HLA-specific immunoglobulin G (IgG)-producing mBCs. Multidimensional spectral flow cytometry with partial least squares discriminant analysis revealed that pretreatment abundance of specific circulating mBC phenotypes, especially CD38neg class-switch mBCs, accurately distinguished between high serologic responders and low responders or NR (AUC 0.958, 0.860-1.000, P = .009), who also displayed significantly lower frequencies of HLA-specific IgG-producing mBCs (P < .0001). This phenotypical mBC signature predicting response to therapy was validated in an external HS patient cohort (n = 10) receiving daratumumab (NCT04204980). This study identifies critical circulating mBC subset phenotypes that distinguish HS patients with successful serologic responses to CD38-targeting desensitization therapies, potentially guiding treatment decision-making., Competing Interests: Declaration of competing interest The authors of this manuscript have conflicts of interest to disclose as described by the American Journal of Transplantation. H. Lee is a Sanofi employee and may hold stock/stock options in the company. O. Bestard reports patents or royalties from Oxford Immunotec. All the remaining authors have nothing to disclose related to this study., (Copyright © 2024 American Society of Transplantation & American Society of Transplant Surgeons. Published by Elsevier Inc. All rights reserved.)

Photosynthetic acclimation to both warming and elevated CO 2 of boreal trees remains a key uncertainty in modelling the response of photosynthesis to future climates. We investigated the impact of increased growth temperature and elevated CO 2 on photosynthetic capacity (V cmax and J max ) in mature trees of two North American boreal conifers, tamarack and black spruce. We show that V cmax and J max at a standard temperature of 25°C did not change with warming, while V cmax and J max at their thermal optima (T opt ) and growth temperature (T g ) increased. Moreover, V cmax and J max at either 25°C, T opt or T g decreased with elevated CO 2 . The J max /V cmax ratio decreased with warming when assessed at both T opt and T g but did not significantly vary at 25°C. The J max /V cmax increased with elevated CO 2 at either reference temperature. We found no significant interaction between warming and elevated CO 2 on all traits. If this lack of interaction between warming and elevated CO 2 on the V cmax , J max and J max /V cmax ratio is a general trend, it would have significant implications for improving photosynthesis representation in vegetation models. However, future research is required to investigate the widespread nature of this response in a larger number of species and biomes., (© 2024 The Author(s). Plant, Cell & Environment published by John Wiley & Sons Ltd.)

The degree of immunological compatibility between donors and recipients greatly impacts allograft survival. In the United States kidney allocation system, HLA antigen-level matching has been shown to cause ethnic disparities and thus, has been de-emphasised. However, priority points are still awarded for antigen-level zero-ABDR matching, zero-DR matching and one-DR matching. Recently, the degree of HLA molecular (eplet) mismatch has emerged as a more accurate measure of immunological risk, and eplet mismatch load has gained attention as a possible biomarker to improve HLA compatibility. However, little is known about the frequency of eplets in population groups, which is a necessary step to ensure that candidates from any ethnical background can have similar chances at a well-matched organ. Eplet frequencies were estimated using HLA alleles in the Common, Intermediate and Well-Documented (CIWD) 3.0.0 catalogue for six population groups: African-American (AFA), Asian-Pacific Islander (API), European/European descent (EURO), Middle East/North Coast of Africa (MENA), Hispanic/Latino (HIS) and Native-American (NAM). We determined that 98.6% (484 out of 491) of HLA eplets are expressed by the common HLA alleles in all population groups. Of the seven eplets that were expressed by less common HLA alleles, six were Class I eplets and one was expressed by HLA-DQB1 alleles and most were expressed by HLA alleles that were more commonly observed in European/European descent populations. Our observations indicate that HLA eplets will not cause any significant disparity if applied to HLA molecular compatibility, regardless of the ethnic origin of both recipients and donors., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Hypothesis: Hepatitis C virus (HCV) positive-to-negative kidney transplants (KT) require direct acting antiviral therapy, but the optimal timing and duration remain unclear. We hypothesized that 14-day prophylactic course of glecaprevir/pibrentasvir 300/120 mg (GLE/PIB) would be safe and effective at treating donor-derived HCV viremia., Methods: This was a prospective, single-center, single-arm, open-label pilot study. 20 adult HCV negative recipients of HCV nucleic acid amplification test positive deceased-donor kidneys (HCV positive-to-negative) received a 14-day course of GLE/PIB, with the first dose pre-transplant. HCV RNA viral loads (VL) were monitored on post-operative days (POD) 1, 3, 7, and 13. If VL was undetectable on POD 13, GLE/PIB was stopped, and if detectable, GLE/PIB was continued to complete an 8-week course. Surveillance monitoring continued after treatment to ensure sustained viral response (SVR). The primary outcome was efficacy of 14-day prophylactic GLE/PIB. Secondary outcomes included patient and allograft survival, the incidence, timing, and clearance of HCV viremia, and safety events., Results: 7/20 subjects (35%) never developed detectable HCV viremia. Only one subject had a detectable, but nonquantifiable, VL on POD 13 and completed an 8-week course. All subjects achieved SVR 12 weeks post-treatment with no relapses through 1-year follow-up. Mean time to undetectable HCV RNA VL was 10.5 (±4.7) days and mean peak VL was 371 (±715) copies/mL. 6-month and 1-year patient and allograft survival were 100% and 95%., Conclusion: A 14-day course of prophylactic GLE/PIB is safe and effective for HCV positive-to-negative KT and may prevent HCV transmission or significantly reduce the VL for those with detectable transmission allowing for rapid clearance within 2 weeks., (© The Author(s) 2024. Published by Oxford University Press on behalf of the ERA.)

Optimizing immunologic compatibility in organ transplantation extends beyond the conventional approach of Human Leukocyte Antigen (HLA) antigen matching, which exhibits significant limitations. A broader comprehension of the roles of classical and non-classical HLA genes in transplantation is imperative for enhancing long-term graft survival. High-resolution molecular HLA genotyping, despite its inherent challenges, has emerged as the cornerstone for precise patient-donor compatibility assessment. Leveraging understanding of eplet biology and indirect immune activation, eplet mismatch calculators and the PIRCHE-II algorithm surpass traditional methods in predicting allograft rejection. Understanding minor histocompatibility antigens may also present an opportunity to personalize the compatibility process. While the application of molecular matching in deceased donor organ allocation presents multiple technical, logistical, and conceptual barriers, rendering it premature for mainstream use, several other areas of donor-recipient matching and post-transplant management are ready to incorporate molecular matching. Provision of molecular mismatch scores to physicians during potential organ offer evaluations could potentially amplify long-term outcomes. The implementation of molecular matching in living organ donation and kidney paired exchange programs is similarly viable. This article will explore the current understanding of immunologic matching in transplantation and the potential applications of epitope and non-epitope molecular biology and genetics in clinical transplantation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Mattoo, Jaffe, Keating, Montgomery and Mangiola.)

Human-wildlife interactions are situated within dynamic systems, characterized by social and ecological complexity. Human-wildlife coexistence research, however, typically focuses on one component of these systems in isolation. We inadvertently followed this norm while carrying out semi-structured interviews of livestock-owners in Northern Tanzania. As existing literature highlighted that this area was a hotspot for livestock depredation, our research questions focused on human interactions with carnivores. Interestingly, almost three quarters (72%, n = 72 of 100) of study participants independently raised African elephants (Loxodonta africana) as presenting the greatest impediments to coexistence. By centering our interviews on carnivores, we omitted vital components of this complex system. To counteract the effects of this oversimplification, we changed our intended analytical process after data collection. Instead of conducting a quantitative analysis of rates of livestock depredation and perceptions of risk posed by a suite of sympatric carnivores, we applied a grounded theory approach to assess interactions across multiple dimensions of this complex system. Through this transparent effort to realign our approaches with the complexity of the study system, we highlight the importance of designing research approaches that effectively reflect the complexities inherent to human-wildlife coexistence., (© 2024. The Author(s).)

Large mammals respond to human hunting via proactive and reactive responses, which can induce subsequent nonconsumptive effects (NCEs). Thus, there is evidence that large mammals exhibit considerable behavioral plasticity in response to human hunting risk. Currently, however, it is unclear which cues of human hunting large mammals may be responding to. We conducted a literature review to quantify the large mammal behavioral responses induced by the cues of human hunting. We detected 106 studies published between 1978 and 2022 of which 34 (32%) included at least one measure of cue, typically visual ( n = 26 of 106, 25%) or auditory ( n = 11 of 106, 10%). Space use ( n = 37 of 106, 35%) and flight ( n = 31 of 106, 29%) were the most common behavioral responses studied. Among the 34 studies that assessed at least one cue, six (18%) measured large mammal behavioral responses in relation to proxies of human hunting (e.g. hunting site or season). Only 14% ( n = 15 of 106) of the studies quantified an NCE associated with an animal's response to human hunting. Moreover, the association between cues measured and antipredator behaviors is unclear due to a consistent lack of controls. Thus, while human hunting can shape animal populations via consumptive effects, the cues triggering these responses are poorly understood. There hence remains a need to link cues, responses, NCEs, and the dynamics of large mammal populations. Human activities can then be adjusted accordingly to prevent both overexploitation and unintended NCEs in animal populations., (© The Author(s) 2024. Published by Oxford University Press on behalf of National Academy of Sciences.)

Background: Xenotransplantation of genetically engineered porcine organs has the potential to address the challenge of organ donor shortage. Two cases of porcine-to-human kidney xenotransplantation were performed, yet the physiological effects on the xenografts and the recipients' immune responses remain largely uncharacterized., Methods: We performed single-cell RNA sequencing (scRNA-seq) and longitudinal RNA-seq analyses of the porcine kidneys to dissect xenotransplantation-associated cellular dynamics and xenograft-recipient interactions. We additionally performed longitudinal scRNA-seq of the peripheral blood mononuclear cells (PBMCs) to detect recipient immune responses across time., Findings: Although no hyperacute rejection signals were detected, scRNA-seq analyses of the xenografts found evidence of endothelial cell and immune response activation, indicating early signs of antibody-mediated rejection. Tracing the cells' species origin, we found human immune cell infiltration in both xenografts. Human transcripts in the longitudinal bulk RNA-seq revealed that human immune cell infiltration and the activation of interferon-gamma-induced chemokine expression occurred by 12 and 48 h post-xenotransplantation, respectively. Concordantly, longitudinal scRNA-seq of PBMCs also revealed two phases of the recipients' immune responses at 12 and 48-53 h. Lastly, we observed global expression signatures of xenotransplantation-associated kidney tissue damage in the xenografts. Surprisingly, we detected a rapid increase of proliferative cells in both xenografts, indicating the activation of the porcine tissue repair program., Conclusions: Longitudinal and single-cell transcriptomic analyses of porcine kidneys and the recipient's PBMCs revealed time-resolved cellular dynamics of xenograft-recipient interactions during xenotransplantation. These cues can be leveraged for designing gene edits and immunosuppression regimens to optimize xenotransplantation outcomes., Funding: This work was supported by NIH RM1HG009491 and DP5OD033430., Competing Interests: Declaration of interests J.D.B. is a founder and director of CDI Labs, Inc.; a founder of and consultant to Opentrons LabWorks/Neochromosome, Inc.; and serves or served on the scientific advisory boards of the following: CZ Biohub New York, LLC; Logomix, Inc.; Modern Meadow, Inc.; Rome Therapeutics, Inc.; Sangamo, Inc.; Tessera Therapeutics, Inc.; and the Wyss Institute. R.A.M. is on scientific advisory boards for eGenesis, Sanofi, Regeneron, CareDx, and Hansa Biopharma; is a consultant to Recombinetics; reports consulting fees from Hansa Medical, Regeneron, Thermo Fisher Scientific, Genentech, CareDx, One Lambda, ITB Med, Sanofi, and PPD Development; and reports grant support from Hansa Biopharma, all unrelated to the present work. R.A.M. also reports grant support from United Therapeutics Corporation, PBC. All other authors have no competing interests., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Xenotransplantation offers the potential to meet the critical need for heart and lung transplantation presently constrained by the current human donor organ supply. Much was learned over the past decades regarding gene editing to prevent the immune activation and inflammation that cause early organ injury, and strategies for maintenance of immunosuppression to promote longer-term xenograft survival. However, many scientific questions remain regarding further requirements for genetic modification of donor organs, appropriate contexts for xenotransplantation research (including nonhuman primates, recently deceased humans, and living human recipients), and risk of xenozoonotic disease transmission. Related ethical questions include the appropriate selection of clinical trial participants, challenges with obtaining informed consent, animal rights and welfare considerations, and cost. Research involving recently deceased humans has also emerged as a potentially novel way to understand how xeno-organs will impact the human body. Clinical xenotransplantation and research involving decedents also raise ethical questions and will require consensus regarding regulatory oversight and protocol review. These considerations and the related opportunities for xenotransplantation research were discussed in a workshop sponsored by the National Heart, Lung, and Blood Institute, and are summarized in this meeting report., Competing Interests: Declaration of competing interest The authors of this manuscript have conflicts of interest to disclose as described by the American Journal of Transplantation. Kiran K. Khush: recipient of NHLBI research grant on donor heart evaluation for transplantation (R01HL125303). Brendan Parent: recipient of Applebaum Foundation grant to study ethics of xenotransplantation. Karen J. Maschke and Michael Gusmano: recipients of NCATS research grant on ethical translation of xenotransplantation clinical trials (1R01TR003844-0). The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services., (Copyright © 2024 American Society of Transplantation & American Society of Transplant Surgeons. Published by Elsevier Inc. All rights reserved.)

In a previous study, heart xenografts from 10-gene-edited pigs transplanted into two human decedents did not show evidence of acute-onset cellular- or antibody-mediated rejection. Here, to better understand the detailed molecular landscape following xenotransplantation, we carried out bulk and single-cell transcriptomics, lipidomics, proteomics and metabolomics on blood samples obtained from the transplanted decedents every 6 h, as well as histological and transcriptomic tissue profiling. We observed substantial early immune responses in peripheral blood mononuclear cells and xenograft tissue obtained from decedent 1 (male), associated with downstream T cell and natural killer cell activity. Longitudinal analyses indicated the presence of ischemia reperfusion injury, exacerbated by inadequate immunosuppression of T cells, consistent with previous findings of perioperative cardiac xenograft dysfunction in pig-to-nonhuman primate studies. Moreover, at 42 h after transplantation, substantial alterations in cellular metabolism and liver-damage pathways occurred, correlating with profound organ-wide physiological dysfunction. By contrast, relatively minor changes in RNA, protein, lipid and metabolism profiles were observed in decedent 2 (female) as compared to decedent 1. Overall, these multi-omics analyses delineate distinct responses to cardiac xenotransplantation in the two human decedents and reveal new insights into early molecular and immune responses after xenotransplantation. These findings may aid in the development of targeted therapeutic approaches to limit ischemia reperfusion injury-related phenotypes and improve outcomes., (© 2024. The Author(s), under exclusive licence to Springer Nature America, Inc.)

The first 2 living recipients of pig hearts died unexpectedly within 2 months, despite both recipients receiving what over 30 years of nonhuman primate (NHP) research would suggest were the optimal gene edits and immunosuppression to ensure success. These results prompt us to question how faithfully data from the NHP model translate into human outcomes. Before attempting any further heart xenotransplants in living humans, it is highly advisable to gain a more comprehensive understanding of why the promising preclinical NHP data did not accurately predict outcomes in humans. It is also unlikely that additional NHP data will provide more information that would de-risk a xenoheart clinical trial because these cases were based on the best practices from the most successful NHP results to date. Although imperfect, the decedent model offers a complementary avenue to determine appropriate treatment regimens to control the human immune response to xenografts and better understand the biologic differences between humans and NHP that could lead to such starkly contrasting outcomes. Herein, we explore the potential benefits and drawbacks of the decedent model and contrast it to the advantages and disadvantages of the extensive body of data generated in the NHP xenoheart transplantation model., Competing Interests: Declaration of competing interests The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation., (Copyright © 2024 American Society of Transplantation & American Society of Transplant Surgeons. Published by Elsevier Inc. All rights reserved.)

Significance Statement: There is no standardized desensitization regimen for kidney transplant candidates. CD38, expressed by plasma cells, could be targeted for desensitization to deplete plasma cells producing alloantibodies and donor-specific antibodies. Few studies and case reports are available regarding the use of CD38 antibodies for desensitization in patients awaiting kidney transplant. This study shows that isatuximab, a CD38-targeting therapy, was well tolerated in kidney transplant candidates, with a durable decrease in anti-HLA antibodies and partial desensitization activity. The short treatment period and long follow-up of this study allowed for the understanding of the mechanism and timing for any antibody rebound. Isatuximab could be further investigated as an option for adjunct therapy to existing desensitization for patients on the kidney transplant waitlist., Background: Patients with calculated panel reactive antibody (cPRA) ≥80.00%, particularly those with cPRA ≥99.90%, are considered highly sensitized and underserved by the Kidney Allocation System. Desensitization removes circulating reactive antibodies and/or suppresses antibody production to increase the chances of a negative crossmatch. CD38 is expressed highly on plasma cells, thus is a potential target for desensitization., Methods: This was an open-label single-arm phase 1/2 study investigating the safety, pharmacokinetics, and preliminary efficacy of isatuximab in patients awaiting kidney transplantation. There were two cohorts, cohorts A and B, which enrolled cPRA ≥99.90% and 80.00% to <99.90%, respectively., Results: Twenty-three patients (12 cohort A, 11 cohort B) received isatuximab 10 mg/kg weekly for 4 weeks then every 2 weeks for 8 weeks. Isatuximab was well tolerated with pharmacokinetic and pharmacodynamic profiles that indicated similar exposure to multiple myeloma trials. It resulted in decreases in CD38 + plasmablasts, plasma cells, and NK cells and significant reductions in HLA-specific IgG-producing memory B cells. Overall response rate, on the basis of a predefined composite desensitization end point, was 83.3% and 81.8% in cohorts A and B. Most responders had decreases in anti-HLA antibodies that were maintained for 26 weeks after the last dose. Overall, cPRA values were minimally affected, however, with only 9/23 patients (39%) having cPRA decreases to target levels. By study cutoff (median follow-up of 68 weeks), six patients received transplant offers, of which four were accepted., Conclusions: In this open-label trial, isatuximab was well tolerated and resulted in a durable decrease in anti-HLA antibodies with partial desensitization activity., Clinical Trial Registration Number: NCT04294459 ., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Society of Nephrology.)

The XVIth Banff Meeting for Allograft Pathology was held in Banff, Alberta, Canada, from September 19 to 23, 2022, as a joint meeting with the Canadian Society of Transplantation. In addition to a key focus on the impact of microvascular inflammation and biopsy-based transcript analysis on the Banff Classification, further sessions were devoted to other aspects of kidney transplant pathology, in particular T cell-mediated rejection, activity and chronicity indices, digital pathology, xenotransplantation, clinical trials, and surrogate endpoints. Although the output of these sessions has not led to any changes in the classification, the key role of Banff Working Groups in phrasing unanswered questions, and coordinating and disseminating results of investigations addressing these unanswered questions was emphasized. This paper summarizes the key Banff Meeting 2022 sessions not covered in the Banff Kidney Meeting 2022 Report paper and also provides an update on other Banff Working Group activities relevant to kidney allografts., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Obesity is a chronic, relapsing disease that increases the risks of living kidney donation; at the same time, transplant centers have liberalized body mass index constraints for donors. With the increasing number of antiobesity medications available, the treatment of obesity with antiobesity medications may increase the pool of potential donors and enhance donor safety. Antiobesity medications are intended for long-term use given the chronic nature of obesity. Cessation of treatment can be expected to lead to weight regain and increase the risk of comorbidity rebound/development. In addition, antiobesity medications are meant to be used in conjunction with-rather than in replacement of-diet and physical activity optimization. Antiobesity medication management includes selecting medications that may ameliorate any coexisting medical conditions, avoiding those that are contraindicated in such conditions, and being sensitive to any out-of-pocket expenses that may be incurred by the potential donor. A number of questions remain regarding who will and should shoulder the costs of long-term obesity treatment for donors. In addition, future studies are needed to quantify the degree of weight loss and duration of weight loss maintenance needed to normalize the risk of adverse kidney outcomes relative to comparable nondonors and lower-weight donors., (Copyright © 2023 American Society of Transplantation & American Society of Transplant Surgeons. Published by Elsevier Inc. All rights reserved.)

Introduction: Thoracoabdominal normothermic regional perfusion (TA-NRP) following cardiac death is an emerging multivisceral organ procurement technique. Recent national studies on outcomes of presumptive TA-NRP-procured organs are limited by potential misclassification since TA-NRP is not differentiated from donation after cardiac death (DCD) in registry data., Methods: We studied 22 donors whose designees consented to TA-NRP and organ procurement performed at our institution between January 20, 2020 and July 3, 2022. We identified these donors in SRTR to describe organ utilization and recipient outcomes and compared them to recipients of traditional DCD (tDCD) and donation after brain death (DBD) organs during the same timeframe., Results: All 22 donors progressed to cardiac arrest and underwent TA-NRP followed by heart, lung, kidney, and/or liver procurement. Median donor age was 41 years, 55% had anoxic brain injury, 45% were hypertensive, 0% were diabetic, and median kidney donor profile index was 40%. TA-NRP utilization was high across all organ types (88%-100%), with a higher percentage of kidneys procured via TA-NRP compared to tDCD (88% vs. 72%, p = .02). Recipient and graft survival ranged from 89% to 100% and were comparable to tDCD and DBD recipients (p ≥ .2). Delayed graft function was lower for kidneys procured from TA-NRP compared to tDCD donors (27% vs. 44%, p = .045)., Conclusion: Procurement from TA-NRP donors yielded high organ utilization, with outcomes comparable to tDCD and DBD recipients across organ types. Further large-scale study of TA-NRP donors, facilitated by its capture in the national registry, will be critical to fully understand its impact as an organ procurement technique., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Tree mortality due to global change-including range expansion of invasive pests and pathogens-is a paramount threat to forest ecosystems. Oak forests are among the most prevalent and valuable ecosystems both ecologically and economically in the United States. There is increasing interest in monitoring oak decline and death due to both drought and the oak wilt pathogen ( Bretziella fagacearum ). We combined anatomical and ecophysiological measurements with spectroscopy at leaf, canopy, and airborne levels to enable differentiation of oak wilt and drought, and detection prior to visible symptom appearance. We performed an outdoor potted experiment with Quercus rubra saplings subjected to drought stress and/or artificially inoculated with the pathogen. Models developed from spectral reflectance accurately predicted ecophysiological indicators of oak wilt and drought decline in both potted and field experiments with naturally grown saplings. Both oak wilt and drought resulted in blocked water transport through xylem conduits. However, oak wilt impaired conduits in localized regions of the xylem due to formation of tyloses instead of emboli. The localized tylose formation resulted in more variable canopy photosynthesis and water content in diseased trees than drought-stressed ones. Reflectance signatures of plant photosynthesis, water content, and cellular damage detected oak wilt and drought 12 d before visual symptoms appeared. Our results show that leaf spectral reflectance models predict ecophysiological processes relevant to detection and differentiation of disease and drought. Coupling spectral models that detect physiological change with spatial information enhances capacity to differentiate plant stress types such as oak wilt and drought., Competing Interests: Competing interests statement:The authors declare no competing interest.

Background: Understanding immunogenicity and alloimmune risk following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination in kidney transplant recipients is imperative to understanding the correlates of protection and to inform clinical guidelines., Methods: We studied 50 kidney transplant recipients following SARS-CoV-2 vaccination and quantified their anti-spike protein antibody, donor-derived cell-free DNA (dd-cfDNA), gene expression profiling (GEP), and alloantibody formation., Results: Participants were stratified using nucleocapsid testing as either SARS-CoV-2-naïve or experienced prior to vaccination. One of 34 (3%) SARS-CoV-2 naïve participants developed anti-spike protein antibodies. In contrast, the odds ratio for the association of a prior history of SARS-CoV-2 infection with vaccine response was 18.3 (95% confidence interval 3.2, 105.0, p < 0.01). Pre- and post-vaccination levels did not change for median dd-cfDNA (0.23% vs. 0.21% respectively, p = 0.13), GEP scores (9.85 vs. 10.4 respectively, p = 0.45), calculated panel reactive antibody, de-novo donor specific antibody status, or estimated glomerular filtration rate., Conclusions: SARS-CoV-2 vaccines do not appear to trigger alloimmunity in kidney transplant recipients. The degree of vaccine immunogenicity was associated most strongly with a prior history of SARS-CoV-2 infection., (© 2023 Wiley Periodicals LLC.)