Transplant Surgery

Emergency general surgery outcomes in SOT recipients are better at transplant centers

This population-based Ontario cohort included 2,679 emergency general surgery hospitalizations in solid-organ transplant recipients over nearly two decades. Thirty-day mortality was 4%, and 31% had complications or death within 30 days. For kidney recipients, academic non-transplant centers had higher 30-day mortality than transplant centers (adjusted OR 3.52, 95% CI 1.43–8.65). Across all organ types, composite 30-day complications or mortality were significantly higher at most non-transplant center types than at transplant centers. 1

Dynamic non-HLA antibody profiles track kidney graft outcomes beyond DSA status

This longitudinal study followed 167 deceased-donor kidney recipients with paired pre- and posttransplant sera tested against 88 non-HLA antigens. Among recipients with functioning grafts, global non-HLA panel reactive antibody (PRA) declined from 9% to 6% posttransplant, suggesting dampened non-HLA reactivity. Higher pretransplant non-HLA PRA associated with prior sensitization, IgA nephropathy, and African American ancestry, independent of HLA cPRA. Antibody-mediated rejection clustered in patients with both preformed and de novo HLA-DSA, while DSA-negative recipients had no rejection events. 2

Pretransplant cancer history strongly shapes posttransplant malignancy risk patterns

This registry-based cohort analyzed 520,424 US solid-organ transplant recipients from 1995 to 2019 using linked transplant and cancer registries. Seven pretransplant cancers significantly increased risk of the same cancer posttransplant: breast, melanoma, lung, kidney, bladder, liver, and colorectal. Incidence rate ratios were especially high for melanoma (10.4; 95% CI, 7.43–14.1), with notable elevations for several other cancers. Other significant patterns included liver cancer preceding lung or prostate cancer, bladder cancer preceding lung cancer, and kidney cancer preceding thyroid cancer. 3

Single-cell profiling links BK viremia to early tubular injury and persistent intrarenal immunity

Single-cell RNA sequencing of kidney allograft biopsies compared uninfected controls with peaking and resolving BK polyomavirus infection. BK viral nephropathy biopsies upregulated polyomavirus hallmarks, including ribosome biogenesis, translation, and energy restructuring pathways, plus wound-healing and immune signaling programs. Even during peaking viremia without histologic nephropathy, tubular cells showed wound-healing, stress, and matrix-remodeling signatures, indicating early epithelial injury. In vivo tubular cells shifted toward fatty acid oxidation and proinflammatory responses not seen in culture models lacking immune components. 4