TY - JOUR
T1 - Re-Evaluating the Transplant Glomerulopathy Lesion—Beyond Donor-Specific Antibodies
AU - Chutani, Arun
AU - Guevara-Pineda, Daniel
AU - Lerner, Gabriel B.
AU - Menon, Madhav C.
N1 - Publisher Copyright:
Copyright © 2024 Chutani, Guevara-Pineda, Lerner and Menon.
PY - 2024
Y1 - 2024
N2 - There have been significant advances in short-term outcomes in renal transplantation. However, longer-term graft survival has improved only minimally. After the first post-transplant year, it has been estimated that chronic allograft damage is responsible for 5% of graft loss per year. Transplant glomerulopathy (TG), a unique morphologic lesion, is reported to accompany progressive chronic allograft dysfunction in many cases. While not constituting a specific etiologic diagnosis, TG is primarily considered as a histologic manifestation of ongoing allo-immune damage from donor-specific anti-HLA alloantibodies (DSA). In this review article, we re-evaluate the existing literature on TG, with particular emphasis on the role of non-HLA-antibodies and complement-mediated injury, cell-mediated immune mechanisms, and early podocyte stress in the pathogenesis of Transplant Glomerulopathy.
AB - There have been significant advances in short-term outcomes in renal transplantation. However, longer-term graft survival has improved only minimally. After the first post-transplant year, it has been estimated that chronic allograft damage is responsible for 5% of graft loss per year. Transplant glomerulopathy (TG), a unique morphologic lesion, is reported to accompany progressive chronic allograft dysfunction in many cases. While not constituting a specific etiologic diagnosis, TG is primarily considered as a histologic manifestation of ongoing allo-immune damage from donor-specific anti-HLA alloantibodies (DSA). In this review article, we re-evaluate the existing literature on TG, with particular emphasis on the role of non-HLA-antibodies and complement-mediated injury, cell-mediated immune mechanisms, and early podocyte stress in the pathogenesis of Transplant Glomerulopathy.
KW - anti HLA antibodies
KW - banff criteria
KW - C4d
KW - podocyte
KW - transplant glomerulopathy (TG)
UR - http://www.scopus.com/inward/record.url?scp=85210930622&partnerID=8YFLogxK
U2 - 10.3389/ti.2024.13365
DO - 10.3389/ti.2024.13365
M3 - Review article
AN - SCOPUS:85210930622
SN - 0934-0874
VL - 37
JO - Transplant International
JF - Transplant International
M1 - 13365
ER -