AI Article Synopsis

  • Chronic-active antibody-mediated rejection (c-aABMR) involves chronic endothelial injury and the presence of donor-specific antibodies (DSA) for diagnosis, with complications like transplant glomerulopathy.
  • A study of 41 patients showed no significant differences in renal histology, allograft function, or survival between DSA positive and negative cases, suggesting that both groups exhibit similar chronic damage.
  • The findings contribute to the discussion on whether DSA are essential for diagnosing c-aABMR, as outcomes appeared similar regardless of DSA presence.

Article Abstract

Chronic-active antibody-mediated rejection (c-aABMR) is defined as histological evidence of chronic endothelial injury (cg), also known as transplant glomerulopathy, and either microvascular inflammation (MVI) or positivity for C4d. Importantly, the presence of donor-specific antibodies (DSA) is currently still mandatory for the diagnosis of c-aABMR. This retrospective study of 41 c-aABMR patients investigates whether cases suspicious for c-aABMR (DSA negative, n = 24) differ from cases of c-aABMR (DSA positive, n = 17) with respect to renal histology, allograft function and long-term graft survival. All included patients had progressive loss of allograft function and were diagnosed by for cause biopsy and scored according to the Banff '15 criteria. In all DSApos cases, DSA were de novo and the majority was directed against HLA-II being mostly anti-HLA-DQ antibodies. There were no statistically significant differences in clinical characteristics, decline in allograft function and renal allograft survival in cases with or without DSAs. All cases showed chronic histomorphological damage and inflammation, irrespective of the presence of DSA. Renal histology and clinical outcome of patients suspicious for c-aABMR (DSAneg) do not significantly differ from patients with a diagnosis of c-aABMR (DSApos). We believe that our study adds to the ongoing debate regarding the need for DSAs to be present for the diagnosis of c-aABMR.

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http://dx.doi.org/10.1111/tri.13154DOI Listing

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