Better understanding of transplant glomerulopathy secondary to chronic antibody-mediated rejection

Adam Remport, Bela Ivanyi, Zoltan Mathe, Kathryn Tinckam, Istvan Mucsi, Miklos Z. Molnar

Research output: Contribution to journalReview article

28 Citations (Scopus)


Transplant glomerulopathy (TG) is generally accepted to result from repeated episodes of endothelial activation, injury and repair, leading to pathological abnormalities of double contouring or multi-layering of the glomerular basement membrane. TG is a major sequel of chronic active antibody-mediated rejection (cABMR), from pre-existing or de novo anti-HLA antibodies. Hepatitis C infection, thrombotic microangiopathy or other factors may also contribute to TG development. TG prevalence is 5-20% in most series, reaching 55%, in some high-risk cohorts, and is associated with worse allograft outcomes. Despite its prevalence and clinical significance, few well-studied treatment options have been proposed. Similar to desensitization protocols, plasmapheresis with or without immunoabsorption, high-dose intravenous immunoglobulin, rituximab, bortezomib and eculizumab have been proposed in the treatment of TG due to cABMR individually or in various combinations. Robust clinical trials are urgently needed to address this major cause of allograft loss. This review summarizes the current knowledge of the epidemiology, etiology, pathology, and the preventive and treatment options for TG secondary to cABMR.

Original languageEnglish
Pages (from-to)1825-1833
Number of pages9
JournalNephrology Dialysis Transplantation
Issue number11
Publication statusPublished - 2015


  • Chronic active antibody-mediated rejection
  • Kidney transplantation
  • Pathology
  • Transplant glomerulopathy
  • Treatment

ASJC Scopus subject areas

  • Nephrology
  • Transplantation

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