Donation after circulatory death (DCD) kidneys are discarded because of long donor warm ischemic times (WIT), despite an unclear association between WIT and outcomes. Using Organ Procurement and Transplantation Network data of adult DCD kidney recipients from 2015 to 2022, we examined donor WIT, using total WIT and 6 definitions of functional WIT (agonal, asystolic, and time beyond derangements in blood pressure or oxygen saturation). We fit logistic and Cox regression models for primary nonfunction (PNF) and 1-y death-censored graft failure (DCGF), respectively, treating WIT linearly and with a spline at the 87.5th percentile. Among 13 673 donors and 24 271 recipients, the median total WIT was 26 min and 1474 transplants were performed from donors with >60 min of total WIT. PNF incidence was 2.6%; 1-y DCGF was 3.8 events per 100 patient-years. In both models, asystolic time was associated with increased hazard of 1-y DCGF (adjusted hazard ratio per 5 min with time linear, 1.12; 95% confidence interval [CI], 1.03-1.22; adjusted hazard ratio per 1 min beyond 12 min, 1.07; 95% CI, 1.02-1.13) and increased odds of PNF (adjusted odds ratio per 5 min with time linear, 1.18; 95% CI, 1.07-1.30; adjusted odds ratio per 1 min beyond 12 min, 1.08; 95% CI, 1.02-1.13). Other measures of donor WIT were not associated with DCGF or PNF. Holding other covariates constant, the absolute risk of 1-y DCGF increased by 0.9% when asystolic time increased from 5 to 25 min in the linear model. Donors with prolonged total and functional WITs, apart from asystolic time, show no association with 1-y DCGF and PNF. We advocate using these kidneys to expand the donor pool.

Kidney transplantation outcomes have improved in the short term, but long-term graft survival gains have plateaued. Aging donors and recipients with increasing comorbidities may alter contemporary allograft outcomes. We retrospectively analyzed 2076 consecutive kidney transplants performed at a single Canadian center from 1969 to 2024, representing up to 50 y of complete follow-up. All-cause graft survival (ACGS) and death-censored graft survival were compared across 5 transplant eras using era-stratified Cox regression. The median recipient age increased significantly across the eras from 35 to 54 y (P < 0.01) and the donor age from 28 to 45 y (P < 0.01), paralleled by 3-5-fold increases in pretransplant diabetes and obesity. Death-censored graft survival improved through the early 2000s but has since plateaued, whereas ACGS declined in the modern era (2018-2024) compared with the 1998-2009 peak (P = 0.007). Death with function accounted for >60% of graft losses in recent years, with infectious deaths rising from 21% to 45% (P < 0.01). Increasing donor and recipient age, comorbidities, and delayed graft function independently predicted inferior survival. These findings reveal a reversal in ACGS gains in the contemporary era, highlighting the need for precision immunosuppression strategies tailored to the aging, comorbid transplant population.

Liver transplantation (LT) is the definitive treatment for end-stage liver diseases such as hepatocellular carcinoma (HCC) or cirrhosis, in a clinical context increasingly influenced by the high prevalence of Metabolic Dysfunction-Associated Steatotic Liver Disease. Organ shortages have expanded the use of extended-criteria donor grafts, including steatotic livers from donors after brain death or cardiocirculatory death. However, graft steatosis remains a major risk factor for ischemia/reperfusion (I/R) injury, early allograft dysfunction, and posttransplant outcomes, and current protective strategies are insufficient to fully overcome these challenges. Visceral adipose tissue (VAT) is an active endocrine and immunometabolic organ that can shape systemic inflammation and immune tone. Clinical studies report an association between increased VAT and I/R injury, graft dysfunction, rejection, frailty, and HCC recurrence after LT, particularly in recipients with obesity and in recipients transplanted for cirrhosis and/or HCC. Under stress conditions, dysfunctional VAT shifts toward a proinflammatory phenotype characterized by altered secretion of cytokines, adipokines, chemokines, and lipid mediators. This review analyzes the role of the adipose tissue-liver axis in LT, with emphasis on how adipose-related mediators may modulate I/R injury and alloimmune responses in clinically relevant settings. We synthesize evidence from human cohorts and preclinical LT and warm I/R models, highlight major knowledge gaps related to tissue-source attribution and context-dependent mechanisms, and discuss emerging therapeutic strategies to modulate adipose tissue inflammation and immunometabolic signaling. Integrating adipose biology into LT research may help refine risk stratification and identify new avenues to improve graft utilization and long-term outcomes.

Observational studies have shown that kidney transplant (KT) recipients who are cytomegalovirus (CMV)-seropositive (R+) but lack effective CMV-specific cell-mediated immunity (CMV-CMI) are at increased risk of CMV infection. In this quasi-experimental study, an immune-guided prevention strategy based on early CMV-CMI assessment (1-2 posttransplant weeks) was evaluated in intermediate-risk KT recipients (R+ without lymphocyte-depleting induction). CMV-CMI was measured using the QuantiFERON assay (QTF-CMV). Recipients with nonreactive QTF-CMV received antiviral prophylaxis until either CMV-CMI reconstitution or month 6, while those with reactive QTF-CMV were managed with preemptive therapy. The primary outcome was the proportion of patients who developed CMV infection during the first posttransplant year. Secondary outcomes included CMV disease, CMV DNAemia requiring preemptive therapy, rejection, vascular events, and all-cause mortality. Outcomes were compared with a prospective preintervention cohort managed by standard-of-care preemptive therapy. We included 91 and 100 patients in the preintervention and intervention groups, with similar baseline characteristics. One-year incidence of CMV infection was similar between both groups (48.4% versus 50.0%; odds ratio [OR], 1.07; 95% confidence interval [CI], 0.61-1.89; P = 0.820). One-year incidence of CMV disease (secondary outcome) was lower in the intervention group (9.9% versus 3.0%; OR, 0.28; 95% CI, 0.07-1.08; P = 0.064), as confirmed in the per-protocol analysis (9.9% versus 2.2%; OR, 0.20; 95% CI, 0.04-0.97; P = 0.028). Although the tested QTF-CMV-based immune-guided strategy did not result in a reduction in the overall occurrence of CMV infection in intermediate-risk KT recipients, the lower incidence of CMV disease observed merits further research.