ReviewTransplantation reviews (Orlando, Fla.)2018
Innate networking: Thrombotic microangiopathy, the activation of coagulation and complement in the sensitized kidney transplant recipient.
Review in Transplantation reviews (Orlando, Fla.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Increased thrombin generation in kidney transplant recipients with donor-specific antibodies directed against human leukocyte antigens.Frontiers in immunology · 2024Observational
- Immunological risk and complement genetic evaluations in early onset de novo thrombotic microangiopathy after living donor kidney transplantation: A Japanese multicenter registry.Clinical and experimental nephrology · 2023Article
- Innate immune modulation in transplantation: mechanisms, challenges, and opportunities.Frontiers in transplantation · 2023Review
- Complement-targeted therapies in kidney transplantation-insights from preclinical studies.Frontiers in immunology · 2022Review
- Sensitization and Desensitization in Vascularized Composite Allotransplantation.Frontiers in immunology · 2021Review
- Emerging evidence of a COVID-19 thrombotic syndrome has treatment implications.Nature reviews. Rheumatology · 2020Review
- Coagulation and Fibrinolysis in Kidney Graft Rejection.Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Thrombotic microangiopathy (TMA) is a histological feature of antibody-mediated rejection and has the potential to cause problematic graft dysfunction, particularly for highly sensitized cross-match positive kidney transplant recipients. Prompt recognition of pertinent histopathological and systemic features of TMA in kidney transplantation is necessary. Underlying mechanisms of this process involve the activation of both complement and coagulation systems as a response to HLA antibody. As serine proteases, coagulation and complement cascades exhibit similar characteristics with respect to homeostatic function. Increasing evidence now exists for the interaction between these innate defenses in both activation and regulation, lending scope for intervention. Understanding the complexities of these interactions remains a challenge. This review provides an overview of the current understanding, particularly with respect to the activation of coagulation and complement by HLA antibody in the setting of highly sensitized kidney transplantation.
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Registered trials
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