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Войти в исследования Microvascular Inflammation of Kidney Allografts and Clinical Outcomes.
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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Sablik Marta, Sannier Aurélie, Raynaud Marc, Goutaudier Valentin, Divard Gillian, Astor Brad C, Weng Patricia, Smith Jodi, Garro Rouba, Warady Bradley A, Zahr Rima S, Twombley Katherine, Dharnidharka Vikas R, Dandamudi Raja S, Fila Marc, Huang Edmund, Sellier-Leclerc Anne-Laure, Tönshoff Burkhard, Rabant Marion, Verine Jérôme, Del Bello Arnaud, Berney Thierry, Boyer Olivia, Catar Rusan Ali, Danger Richard, Giral Magali, Yoo Daniel, Girardin François R, Alsadi Alaa, Gourraud Pierre-Antoine, Morelon Emmanuel, Le Quintrec Moglie, Try Mélanie, Villard Jean, Zhong Weixiong, Bestard Oriol, Budde Klemens, Chauveau Bertrand, Couzi Lionel, Brouard Sophie, Hogan Julien, Legendre Christophe, Anglicheau Dany, Aubert Olivier, Kamar Nassim, Lefaucheur Carmen, Loupy Alexandre
Аннотация
METHODS: We conducted a cohort study that included kidney-transplant recipients from more than 30 transplantation centers in Europe and North America who had undergone allograft biopsy between 2004 and 2023. We integrated clinical and pathological data to classify biopsy specimens according to the 2022 Banff Classification of Renal Allograft Pathology, which includes two new diagnostic categories: probable antibody-mediated rejection and microvascular inflammation without evidence of an antibody-mediated response. We then assessed the association between the newly recognized microvascular inflammation phenotypes and allograft survival and disease progression.
RESULTS: A total of 16,293 kidney-transplant biopsy specimens from 6798 patients were assessed. We identified the newly recognized microvascular inflammation phenotypes in 788 specimens, of which 641 were previously categorized as specimens with no evidence of rejection. As compared with patients without rejection, the hazard ratio for graft loss was 2.1 (95% confidence interval [CI], 1.5 to 3.1) among patients with microvascular inflammation without evidence of an antibody-mediated response and 2.7 (95% CI, 2.2 to 3.3) among patients with antibody-mediated rejection. Patients with a diagnosis of probable antibody-mediated rejection had a higher risk of graft failure beyond year 5 after biopsy than those without rejection (hazard ratio, 1.7; 95% CI, 0.8 to 3.5). Patients with a diagnosis of either newly recognized microvascular inflammation phenotype had a higher risk of progression of transplant glomerulopathy during follow-up than patients without microvascular inflammation.
CONCLUSIONS: Microvascular inflammation in kidney allografts includes distinct phenotypes, with various disease progression and allograft outcomes. Our findings support the clinical use of additional rejection phenotypes to standardize diagnostics for kidney allografts. (Funded by OrganX. ClinicalTrials.gov number, NCT06496269.).