Kidney transplantation has emerged as the optimal treatment for end-stage renal disease. However, the occurrence of atypical hemolytic uremic syndrome (aHUS) following renal transplantation is extremely uncommon and associated with adverse outcomes, often resulting in early graft loss, thus warranting heightened awareness. This report details a case of successful management of a patient who developed post-transplant aHUS following retransplantation. The patient had previously suffered graft failure shortly after the first kidney transplantation due to unexplained non-rejection mechanisms. Following the second transplantation, the individual presented with new-onset anemia, thrombocytopenia, acute kidney injury, and elevated lactate dehydrogenase levels within a short time frame, all manifesting undetermined etiology. A comprehensive assessment of dynamic changes in hemoglobin, platelet count, serum creatinine, and lactate dehydrogenase, alongside pathological examinations, culminated in a definitive diagnosis of aHUS. After undergoing four treatments with eculizumab, there was a sustained improvement in hemoglobin, platelet count, serum creatinine, and lactate dehydrogenase levels, thereby preserving the function of the transplanted kidney. Timely diagnosis and early application of eculizumab in treating aHUS are crucial. Furthermore, comprehensive pre-transplant evaluations of patients to exclude aHUS risk factors are essential.

Background Fibronectin glomerulopathy (FNG) is a rare autosomal dominant glomerulonephritis characterized by proteinuria, hematuria, and progressive kidney dysfunction. FNG treatment includes kidney transplantation; however, chronic active antibody-mediated rejection (cABMR) poses a threat to the long-term survival of kidney allografts. Here, we report a case of FNG in a kidney allograft with cABMR. Case summary A 51-year-old male underwent living-related kidney transplantation in March 2020 for end-stage kidney disease caused by diabetic nephropathy. Three years after kidney transplantation, he presented with 2+ proteinuria, hematuria, and progressive worsening of kidney allograft function, for which an allograft biopsy was performed. Histopathological examination revealed glomerular lobulation, glomerular duplication, peritubular capillaritis, and glomerulitis, which was consistent with cABMR. Immunohistochemistry revealed strong staining for fibronectin in the glomeruli, thus suggesting FNG. The patient was administered rituximab, plasma exchange, and intravenous glucocorticoids. However, these treatments have not yet achieved ideal effects. Conclusion We report a rare case of FGN with cABMR in a kidney allograft that was unresponsive to treatments. This case highlights the need for physicians that perform kidney transplants to familiarize themselves with these rare diseases. Moreover, timely kidney biopsy can help with the diagnosis.

Purpose:Acute kidney injury (AKI) is often associated with kidney ischemia-reperfusion injury (KIRI), which is a key driver of AKI progression. Although cuproptosis has been implicated in multiple pathological processes, its relevance to KIRI remains unclear. This study aimed to identify candidate cuproptosis-related genes associated with KIRI and characterize their potential diagnostic and biological relevance. Methods:Bioinformatic analyses of transcriptome datasets were performed to identify cuproptosis-related differentially expressed genes (CRDEGs) in KIRI. GSE43974 served as the discovery cohort, GSE126805 served as the external validation cohort, and GSE161201 was used for exploratory single-cell analysis. Focusing on these CRDEGs, we constructed a diagnostic model for KIRI using machine learning and validated it with a nomogram. Gene set enrichment analysis (GSEA), immune infiltration analysis, and correlation analyses were used to investigate signaling pathways and immune processes associated with CRDEGs. Unsupervised clustering was conducted to classify KIRI samples and characterize CRDEG-related molecular subtypes. CRDEG expression was further verified in a mouse KIRI model treated with cuproptosis modulators. Transcription factor-mRNA, miRNA-mRNA, and drug-gene interaction networks were constructed to explore potential regulatory and therapeutic associations. Results:Four CRDEGs (PPP1R15A, LIPT1, SERPINE1, and HSPD1) were identified. and associated with immune cell infiltration. Machine-learning analyses suggested the potential of these genes as candidate biomarkers for KIRI, and a nomogram based on these genes showed high diagnostic performance in the discovery cohort. These four CRDEGs showed higher expression in KIRI samples than in control samples. GSEA linked these genes to the immune response, oxidative stress, apoptosis-related signaling, and other injury-associated pathways. Cluster analysis revealed two KIRI subtypes (groups A and B) with differing molecular signatures and pathway activity, especially those related to apoptosis signaling, oxidative stress, and immune responses. Their potential diagnostic relevance was further assessed using external datasets and a KIRI animal model. In addition, 103 transcription factors, 152 microRNAs, and 36 drugs potentially interacting with these CRDEGs were predicted. Conclusion:PPP1R15A, LIPT1, SERPINE1, and HSPD1 may serve as candidate indicators of the involvement of cuproptosis in KIRI, although further mechanistic validation is needed.

Donation-after-brain-death (DBD) serves as a major source of kidney transplant donors, and brain death (BD) induces systemic inflammation and gut barrier disruption, leading to renal injury and compromised organ quality. While Lactobacillus reuteri (L. reuteri) demonstrates anti-inflammatory and immunomodulatory properties that maintain gut microbiota homeostasis. However, its role in protecting organs against BD-associated injury remains unclear. This study investigated BD-induced renal injury mechanisms linked to gut-kidney axis dysregulation and evaluated L. reuteri's protective effects through microbiota-immune interactions. BD triggered intestinal barrier dysfunction, elevating gut permeability and promoting translocation of endotoxin lipopolysaccharide (LPS) to kidneys, which activated the TLR4/MyD88/NF-κB pathway, driving proinflammatory cytokine release, neutrophil infiltration, and renal dysfunction. L. reuteri pretreatment attenuated these effects by remodeling gut microbiota-reducing Proteobacteria while enriching Bacteroidota-and enhancing tight junction integrity, thereby suppressing pro-inflammatory LPS leakage and accumulation to renal tubule. Mechanistically, the increase in Bacteroidota abundance correlated with the downregulation of renal TLR4/NF-κB signaling, a pattern that is hypothesized to be explained by putative competitive inhibition by LPS derived from Bacteroidota. Concurrently, L. reuteri induced the upregulation of CD25⁺ immune cell expression in ileal glands and promoted CXCL2 production in renal and intestinal tissues, which is associated with the establishment of a gut-kidney immune homeostasis network. L. reuteri mitigates BD-induced renal injury through dual mechanisms-structural modulation of microbiota-derived LPS and intestinal immune remodeling-providing a novel microbiota-targeted adjunctive strategy to enhance donor organ viability in transplantation medicine.

BACKGROUND:We report orthotopic combined whole-liver and bilateral-kidney xenotransplantation (xeno-CLKT) from a six-gene-edited pig into a 53-year-old human decedent recipient. METHODS:After simultaneous implantation and reperfusion, graft function was monitored for nearly 5 days using continuous clinical assessments. Host responses were further characterized with single-cell RNA sequencing, proteomics, and metabolomics of blood and graft tissues collected before and after transplantation. FINDINGS:All grafts maintained basic physiological function throughout the observation period, with no evidence of hyperacute rejection. Early post-transplant immune analysis showed expansion of S100A12+ neutrophils, which emerged as central hubs in inferred intercellular communication networks. Systems-level metabolomic profiling indicated that post-transplant metabolic patterns remained positively correlated with the recipient's pre-transplant baseline, with generally higher magnitudes. CONCLUSIONS:This study provides initial evidence for the feasibility of pig-to-human orthotopic whole-liver plus bilateral-kidney transplantation and identifies early immune and metabolic features that may inform perioperative management and future clinical translation. FUNDING:The research was supported by the Guangxi Key Research and Development Program (AB24010059), the Shenzhen Medical Research Fund (SMAF) (B2302008), and the Guangdong Province Guangdong-Shenzhen Joint Key Project (2023B1515120083).

The prognosis for patients diagnosed with hepatocellular carcinoma with bile duct tumor thrombus (HCC-BDTT) remains dismal, and there are presently no universally accepted treatment guidelines to address this complex condition. Long-term outcomes of liver transplantation (LT) for HCC-BDTT patients are unclear, and whether LT is a proper therapeutic option for HCC-BDTT patients remains to be determined. Therefore, we design a clinical trial to evaluate whether LT can improve recurrence-free survival (RFS) and overall survival (OS) in HCC-BDTT patients. This is an open-labeled, single-arm, prospective, multicenter and real-world study aiming to assess the survival outcomes of HCC-BDTT patients in LT. Patients will be enrolled based on histological confirmation of HCC with BDTT. The study is planned to take 4 years, 2 years for enrollment and 2 years for follow-up. We anticipate that LT confers beneficial survival outcomes for HCC-BDTT patients, specifically in terms of the pivotal parameters, such as RFS and quality of life. Upon successful completion of the trial, we will extend our monitoring over a longer follow-up time to accurately estimate important indicators such as OS. We expect that this study provides substantial evidence to refine treatment guidelines through thorough data analysis, ultimately contributing to better patient outcomes and advancing our understanding of the disease.Trial Register: Trial registered at www.clinicaltrials.gov (NCT06928415)

BackgroundHepatic ischemia-reperfusion injury (HIRI) is clinically linked to post-transplant complications, yet the pathogenic role of programmed cell death (PCD) patterns in this process remains poorly delineated. This study aimed to investigate the diversity of programmed cell death (PCD) patterns underlying HIRI, with a focus on mechanistically dissecting macrophage-hepatocyte crosstalk mediated by the THBS1-CD47 axis.MethodsGSE151648, GSE14951, GSE12720 and GSE171539 were retrieved from the Gene Expression Omnibus (GEO) database. Based on bulk transcriptomic data, we identified differentially expressed PCD-related genes (DE-PCDRGs) in HIRI samples and performed functional annotation of these genes. Furthermore, machine learning algorithms were used to select hub DE-PCDRGs closely related to HIRI, and a robust risk assessment prediction model for HIRI was constructed. Additionally, using single-cell transcriptomic data, we further elucidated 19 diverse patterns of PCD in HIRI samples at the single-cell level and validated the hub DE-PCDRGs. Crucially, we mechanistically linked the THBS1-CD47 axis to apoptosis-exacerbated liver injury via in vivo and in vitro experiments.ResultsBulk transcriptomic analysis identified 25 DE-PCDRGs consistently upregulated in HIRI samples. Machine learning algorithms further screened 5 hub DE-PCDRGs (THBS1, MAP1LC3B, PPP1R15A, CXCL8, ZC3H12A), which formed a risk prediction model that effectively classified patients into high-risk and low-risk groups. These hub genes showed elevated expression in high-risk groups, accompanied by pronounced enrichment of 5 PCD patterns (anoikis, immunogenic cell death, NETosis, Netotic cell death, pyroptosis). Single-cell analysis further uncovered 12 distinct PCD patterns within the HIRI sample microenvironment, with spatial validation confirming the 5 hub DE-PCDRGs. The HIRI animal model confirmed the occurrence of apoptosis in liver tissue and upregulation of THBS1 in macrophages. Subsequent in vitro co-culture experiments demonstrated that macrophage-derived THBS1 directly engaged hepatocyte CD47, thereby suppressing the PI3K-AKT-NF-κB signaling pathway and promoting apoptosis.ConclusionsOur study delineated heterogeneous PCD patterns as pathological process of HIRI, demonstrating that the THBS1-CD47 axis drives macrophage-hepatocyte crosstalk to exacerbate apoptosis by inhibiting PI3K-AKT-NF-κB signaling. These results extend the current understanding of HIRI pathogenesis and nominate THBS1-CD47 as a promising candidate target.

Background The optimal use of induction therapy in low-immunological-risk kidney transplant recipients (KTRs) remains uncertain. While Basiliximab (BSX) is widely utilized, its comparative outcomes with no induction therapy require further evaluation.Method This single-center retrospective cohort study included 182 low-immunological-risk KTRs who underwent transplantation between January 2022 and March 2023. Patients were assigned to either no induction (n = 41) or BSX induction (n = 141) groups. Propensity score matching (PSM) minimized selection bias and controlled for confounding factors. Primary outcomes included the incidence of first acute rejection (AR) within 12 months, while secondary outcomes encompassed graft function, infection rates, and adverse events.Result After 12 months, the cumulative AR incidence was comparable between groups (p = 0.46). The no induction group demonstrated superior renal function, with consistently higher estimated glomerular filtration rates (eGFR) at early postoperative intervals. Additionally, this group exhibited reduced infection-related hospitalizations (respiratory infections: 7.32 vs. 29.1%, p = 0.008) and hematological complications (thrombocytopenia: 0.00% vs. 12.8%, p = 0.014). Mortality and graft loss rates were similar between groups.Conclusion In low-immunological-risk KTRs, no induction therapy achieves comparable AR prevention and renal function outcomes to BSX while reducing infection and hematological complications. These findings challenge the necessity of universal induction therapy in this population and support a personalized approach to immunosuppression protocols.

This study aimed to explore thrombin-related prognostic biomarkers for hepatocellular carcinoma (HCC) recurrence after liver transplantation (LT). Bioinformatics analyses were conducted using TCGA-LIHC and GEO datasets. LASSO Cox regression screened thrombin-related genes (TRGs). Differential expression analysis, GSEA, and protein–protein interaction (PPI) network analysis were performed to identify key pathways and hub genes. Clinical validation included immunohistochemistry (IHC) on 78 post-LT HCC tissues. In vitro assays (CCK-8, Transwell, Colony formation) assessed MMP1/SPP1 roles in HCC cell proliferation and migration. Nine TRGs were prognostic in HCC, with MMP1 and SPP1 emerging as core regulators linked to EMT. Both genes were significantly upregulated in recurrent HCC tissues (1-year recurrence group vs. non-recurrence, P < 0.05) and correlated with reduced overall survival (OS) and recurrence-free survival (RFS). GSEA revealed EMT as a key enriched pathway. PPI network analysis highlighted MMP1/SPP1 centrality in ECM remodeling and cell adhesion. Clinical samples confirmed MMP1 association with vascular invasion (P = 0.023) and poor differentiation. In vitro, MMP1/SPP1 overexpression enhanced HCC cell proliferation, migration, and colony formation. Multivariate analysis identified MMP1 expression and tumor differentiation as independent recurrence risk factors. MMP1 and SPP1 are potential biomarkers for predicting post-LT HCC recurrence, likely driving metastasis via EMT activation. Their overexpression correlates with aggressive tumor behavior and adverse outcomes, offering prognostic utility and therapeutic targets to improve transplant outcomes.

To the Editor: Simultaneous pancreas-kidney transplantation(SPKT)is cur-rently the most effective treatment for diabetes complicated by end-stage renal disease.

Objective:Perioperative T-cell-mediated rejection (TCMR) and pneumonia occurrence significantly impair graft function and patient survival following liver transplantation (LT). This article aims to develop a machine learning (ML)-based model to predict perioperative co-occurrence of TCMR and pneumonia. Methods:Recipient-related data were retrospectively collected. Predictive Variables were identified through LASSO regression analysis. Five machine learning algorithms, including support vector machine (SVM), were employed to develop predictive models. Model performance was appraised via the receiver operating characteristic (ROC) curve, and calibration curve. SHapley Additive exPlanations (SHAP) method was employed to visualize model characteristics and individual predictions. Results:This study enrolled 717 LT recipients, including 93 patients with perioperative co-occurrence of TCMR and pneumonia. LASSO regression identified postoperative direct bilirubin, postoperative international normalized ratio, high-density lipoprotein, postoperative alanine aminotransferase, natural killer cell, tacrolimus (FK506) concentration, Na+, operative time, anhepatic phase, induction regimen, and ICU stay as significant predictors. The SVM model demonstrated superior predictive performance, with area under the curve values of 0.881 (95% CI: 0.83-0.93) and 0.786 (95% CI: 0.69-0.88) in the training and test sets, respectively. The calibration curve showed high agreement between the predicted and observed risks. The SVM model demonstrated superior specificity, sensitivity, F1 score, and recall compared to other models. SHAP analysis identified variables that contributed to the model predictions. Conclusions:This study constructed a robust predictive model for the perioperative co-occurrence of TCMR and pneumonia. The SVM model demonstrated superior predictive performance.

ObjectiveTo comparatively evaluate the efficacy and safety of induction therapies in solid organ transplantation (SOT) using a Bayesian network meta-analysis (NMA).MethodsRandomized controlled trials (RCTs) assessing induction therapies were systematically identified across major databases (up to November 20, 2024). The screening, data extraction, and risk of bias (ROB) assessment were independently conducted by two reviewers through standardized tools. Bayesian NMA synthesized outcomes, including rejection, graft/overall survival, and infection rates.ResultsSixty-eight RCTs (9,626 patients) evaluating 12 therapies were included. Surface Under the Cumulative Ranking Area (SUCRA) probabilities identified alemtuzumab as the most effective agent for reducing rejection rates (93.9%), followed by antilymphocyte globulin (ALG, 87.0%) and belimumab (77.0%). For graft survival, OKT3 ranked highest (87.9%), with subsequent superiority for ALG (83.5%) and alemtuzumab (75.6%). Basiliximab demonstrated the highest overall survival benefit (88.0%), outperforming rabbit antithymocyte globulin (rATG, 82.1%) and inolimomab (70.3%). Belimumab showed the greatest infection risk reduction (94.4%), surpassing alemtuzumab (80.0%) and basiliximab (74.5%).ConclusionAlemtuzumab emerged as the optimal therapy for minimizing rejection, while OKT3 and basiliximab were superior for graft and overall survival, respectively. Belimumab exhibited the strongest potential for reducing incidence of infection. These findings highlight therapy-specific advantages for optimizing SOT outcomes.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/myprospero, identifier CRD42025634120.

Intraportal islet transplantation for treating insulin-dependent diabetes mellitus has been clinically validated. However, the hypoxic environment and sinusoidal architecture of the liver are unsuitable for the long-term survival of transplanted islets, leading to the loss of therapeutic effects within a year. The spleen has oxygen levels that meet islet needs, but intense instant blood-mediated inflammatory reactions (IBMIR) and low extracellular matrix (ECM) concentrations hinder islet engraftment and survival. In this study, we developed constructs of islets encapsulated by hepatocytes and fibroblasts. The hepatocytes and fibroblasts create a protective coating that reduces IBMIR due to the low expression of von Willebrand factor (vWF) in hepatocytes and supports normal islet survival through ECM production by fibroblasts. These constructs can be easily injected into the mouse spleen. The hepatocyte-fibroblast encapsulation significantly reduces islet mortality during the post-transplantation stress period, enabling rapid engraftment and vascularization in the spleen. The spleen's high-oxygen environment then supports long-term (over one year) islet survival and sustained glycemic regulation. Additionally, this method significantly lowers the critical islet dose required for transplantation. The live-cell shielding strategy developed in this study represents a novel approach for islet transplantation and functional regeneration, demonstrating promising clinical potential.

MiRNAs, which are integral to the complex regulatory mechanisms governing gene expression, have emerged as critical contributors to the intricate interplay of physiological and pathological processes within the human body. Their roles transcend mere participation, establishing them as pivotal biomarkers for disease diagnosis, potential therapeutic targets, and prognostic indicators, with significant implications. This prominence is particularly evident in the context of renal transplantation, in which IRI poses a significant challenge. The IRI process, characterized by an exacerbated impairment of tissue and organ functionality upon the re-establishment of blood flow following a period of ischemia, causes cellular structural damage and cell death, thereby compromising the functional integrity of the graft. A network of regulatory pathways regulated by miRNAs is central to the pathological development of IRI. These miRNAs modulate various cell death mechanisms and associated processes, such as ferroptosis, apoptosis, autophagy, pyroptosis, and oxidative stress, all of which critically influence the development of renal IRI. This review aims to elucidate the essence of miRNA-regulated cell death mechanisms within the broader context of renal IRI. By elucidating the nuanced roles of miRNAs in regulating these cell death mechanisms, we hope to unveil new therapeutic avenues and prognostic potential. The potential of miRNAs as novel cell death agents highlights their significance in refining treatment strategies, providing new hope for the management and mitigation of renal IRI.

ObjectiveThis study aimed to examine the benefit-finding experiences of liver transplant recipients who undergo perioperative extracorporeal membrane oxygenation (ECMO) treatments in order to provide targeted nursing care and promote mental health among these patients.MethodsThis study employed the phenomenological research approach within the framework of qualitative research. The determination of the sample size was predicated on achieving information saturation. Between June 2023 and March 2024, eight liver transplant recipients who underwent perioperative ECMO treatment at a qualified liver transplantation hospital in Guangxi were purposively selected for semi-structured interviews. In line with the cognitive adaptation theory, this study employed template analysis as the analytical approach, wherein each word in the text content was meticulously examined and categorized into their respective structures based on the theory's three frameworks. Throughout the analysis process, the researchers continuously refined and adjusted abstract content placed within templates while exploring the potential emergence of new themes.ResultsThe study involved a total of eight participants, comprising seven male and one female patient, aged between 43 and 68 years. Among the eight patients, seven had grade 3 or higher coronary artery disease, and one had severe arrhythmia, all of which were attributed to heart conditions necessitating ECMO support during liver transplantation. The ECMO types used were exclusively VA, with auxiliary durations varying between 5 h and 9.5 h. Three overarching themes and seven corresponding sub-themes were extracted: (1) the search for meaning, including a strong desire to survive, recognize the meaning of therapy; (2) gaining a sense of mastery, including a sense of control over one's body and psychological; (3) self-enhancement, including perceiving social support, strengthening self-management, and affirming self-worth.ConclusionsLiver transplant recipients who undergo preoperative ECMO treatment can have benefit-finding experiences. This study indicates that medical professionals should not only focus on timely and accurate treatment but also prioritize addressing patients' psychological needs while caring for critically ill individuals. Clinical medical staff can guide patients in engaging in positive psychological construction, exploring and providing effective social support resources, fostering patients' self-health management, and enhancing the level and patients' ability of benefit-finding by strengthening knowledge, education, and establishing psychological mutual assistance platforms after liver transplantation.

Organ transplantation is the most effective treatment for endu2010stage organ disease. One of the major challenges in organ transplantation is organ shortage. For this reason, more and more extended criteria donor organs, including those from donation after circulatory determination of death (DCDD), are used in clinical practice. However, DCDD organs suffer from additional warm ischemic damage, which seriously affects transplant outcomes and organ utilization. Recent studies at home and abroad have shown that the application of normothermic regional perfusion (NRP) is able to improve the quality of organs and transplantation outcomes. At present, an expert consensus on the clinical application of NRP in DCDD is lacking in China, which limits the standardization and highu2010quality development of DCDD in our country. We summarized the results of clinical studies and conducted inu2010depth discussions based on the principles of evidenceu2010based medicine to form this consensus on the application of NRP in DCDD. This consensus focuses on the executive specification and corresponding research evidence of applying NRP technology in DCDD, aiming to provide reference opinions and guidance for the standardization of NRP in organ transplantation and to promote the rapid development of NRP technology and DCDD organ transplantation in China.

Islet transplantation is a promising therapy for insulin-dependent diabetes. However, immune rejection and insufficient vascularization hinder the survival and function of transplanted islets. Here, we show effective engraftment of vascularized and functional mouse and rat islets transplanted into biomaterial-remodeled spleens of nonimmunosuppressed rodents and human islets transplanted into the remodeled spleens of nonhuman primates (NHPs) on varying degrees of immunosuppression. We found evidence that konjac glucomannan-modified silica nanoparticles (KSiNPs) remodeled the spleen into an extracellular matrix (ECM)-rich, immunosuppressive niche to support the survival of syngeneic or xenogeneic islets. Transplanted islets in the remodeled spleens showed improved engraftment, neovascularization, and functionality and restored normoglycemia in streptozotocin (STZ)-induced type 1 diabetic models in the mice and macaques, with stable insulin and C-peptide secretion in mice for 90 days and macaques for 28 days. KSiNP injection and islet transplantation into macaque spleens under B-ultrasound guidance were preclinically feasible. These findings highlight the safety and effectiveness of spleen tissue remodeling in supporting the survival and function of transplanted islets, providing a promising strategy for treating type 1 diabetes mellitus (T1DM).

BackgroundKidney transplantation (KT) is the preferred treatment for patients with end-stage renal disease (ESRD); however, postoperative hyperamylasemia (HA) remains common and has been associated with acute rejection (AR), infection, and impaired graft function. Early identification of HA risk factors is essential to improve outcomes of kidney transplant recipients (KTR). This study aimed to develop and internally validate a novel nomogram for predicting the risk of HA after KT, thereby supporting personalized monitoring, prevention and intervention strategies.MethodsWe retrospectively analyzed KTR treated at the Transplant Medicine Institution of the Second Affiliated Hospital of Guangxi Medical University from July 2021 to June 2022. Based on admission dates, patients were assigned to a training cohort (n=243, July 2021 to March 2022) and a validation cohort (n=107, April 2022 to June 2022). In the training cohort, risk factors of HA were identified using logistic regression, Lasso regression and clinical consideration. Subsequently, a nomogram was developed to predict HA risk in patients who underwent KT based on the identified variables. Model performance was evaluated using receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis (DCA).ResultsA total of 350 KTR and their corresponding 182 donors were enrolled in this study. The nomogram incorporated six predictive factors: recipient preoperative white blood cell (WBC) count, induction, tacrolimus (FK506) trough concentration, AR, donor age, and donor total bilirubin (TBIL) level according to results of logistic regression, Lasso regression and clinical consideration. The nomogram showed moderate predictive performance, with an area under the ROC curve (AUC) of 0.730 (Youden index = 0.683) in the training cohort and 0.731 (Youden index = 0.767) in the validation cohort. Furthermore, calibration plots indicated close agreement between predicted and actual outcomes, and DCA confirmed net clinical benefit across a range of threshold probabilities.ConclusionsA novel nomogram was established to predict HA after KT, which may support early risk stratification and personalized management of KTR. External multicenter validation is needed before clinical implementation.

BACKGROUND:Glioma is the most common brain tumor. IDH mutations occur frequently in glioma, indicating a more favorable prognosis. We aimed to explore energy metabolism-related genes in glioma to promote the research and treatment. METHODS:Datasets were obtained from TCGA and GEO databases. Candidate genes were screened by differential gene expression analysis, then functional enrichment analysis was conducted on the candidate genes. PPI was also carried out to help determine the target gene. GSEA and DO analysis were conducted in the different expression level groups of the target gene. Survival analysis and immune cell infiltrating analysis were performed as well. RESULTS:We screened 34 candidate genes and selected GLUD1 as the target gene. All candidate genes were significantly enriched in 10 KEGG pathways and 330 GO terms. GLUD1 expression was higher in IDH-mutant samples than IDH-wildtype samples, and higher in normal samples than tumor samples. Low GLUD1 expression was related to poor prognosis according to survival analysis. Most types of immune cells were negatively related to GLUD1 expression, but monocytes and activated mast cells exhibited significantly positive correlation with GLUD1 expression. GLUD1 expression was significantly related to 119 drugs and 6 immune checkpoint genes. GLUD1 was able to serve as an independent prognostic indicator of IDH-mutant glioma. CONCLUSION:In this study, we identified an energy metabolism-related gene GLUD1 potentially contributing to favorable clinical outcomes of IDH-mutant glioma. In glioma, GLUD1 related clinical outcomes and immune landscape were clearer, and more valuable information was provided for immunotherapy.