ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2020
Targeted donor complement blockade after brain death prevents delayed graft function in a nonhuman primate model of kidney transplantation.
Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 30 citations in OpenAlex.
- Therapeutic Potential of C1-Inhibitor in Vascular Diseases and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Ischemia-Reperfusion Injury in Kidney Transplantation: Mechanisms and Potential Therapeutic Targets.International journal of molecular sciences · 2024Review
- The Complement System in Kidney Transplantation.Cells · 2023Review
- Sterile Pancreas Inflammation during Preservation and after Transplantation.International journal of molecular sciences · 2023Review
- How to Best Protect Kidneys for Transplantation-Mechanistic Target.Journal of clinical medicine · 2023Review
- Innate immune modulation in transplantation: mechanisms, challenges, and opportunities.Frontiers in transplantation · 2023Review
- Complement-targeting therapeutics for ischemia-reperfusion injury in transplantation and the potential forFrontiers in immunology · 2022Review
- Role of Complement System in Kidney Transplantation: Stepping From Animal Models to Clinical Application.Frontiers in immunology · 2022Review
- Balancing the View of C1q in Transplantation: Consideration of the Beneficial and Detrimental Aspects.Frontiers in immunology · 2022Article
- Complement Is Activated During Normothermic Machine Perfusion of Porcine and Human Discarded Kidneys.Frontiers in immunology · 2022Article
- C1q as a potential tolerogenic therapeutic in transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021Article
- Multiplex gene analysis reveals T-cell and antibody-mediated rejection-specific upregulation of complement in renal transplants.Scientific reports · 2021Article
- Renal diseases and the role of complement: Linking complement to immune effector pathways and therapeutics.Advances in immunology · 2021Review
- Functional and Structural Characterization of a Potent C1q Inhibitor Targeting the Classical Pathway of the Complement System.Frontiers in immunology · 2020Article
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22 authors at 4 institutions in 2 countries.
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Abstract
Delayed graft function (DGF) in renal transplant is associated with reduced graft survival and increased immunogenicity. The complement-driven inflammatory response after brain death (BD) and posttransplant reperfusion injury play significant roles in the pathogenesis of DGF. In a nonhuman primate model, we tested complement-blockade in BD donors to prevent DGF and improve graft survival. BD donors were maintained for 20 hours; kidneys were procured and stored at 4°C for 43-48 hours prior to implantation into ABO-compatible, nonsensitized, MHC-mismatched recipients. Animals were divided into 3 donor-treatment groups: G1 - vehicle, G2 - rhC1INH+heparin, and G3 - heparin. G2 donors showed significant reduction in classical complement pathway activation and decreased levels of tumor necrosis factor α and monocyte chemoattractant protein 1. DGF was diagnosed in 4/6 (67%) G1 recipients, 3/3 (100%) G3 recipients, and 0/6 (0%) G2 recipients (P = .008). In addition, G2 recipients showed superior renal function, reduced sC5b-9, and reduced urinary neutrophil gelatinase-associated lipocalin in the first week posttransplant. We observed no differences in incidence or severity of graft rejection between groups. Collectively, the data indicate that donor-management targeting complement activation prevents the development of DGF. Our results suggest a pivotal role for complement activation in BD-induced renal injury and postulate complement blockade as a promising strategy for the prevention of DGF after transplantation.
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