title: New insights regarding chronic antibody-mediated rejection and its progression to transplant glomerulopathy.
abstract: OBJECTIVE
  To discuss new insights regarding chronic antibody-mediated rejection (CAMR) and its progression to transplant glomerulopathy. We will describe the progression to transplant glomerulopathy from a histologic perspective and provide updates on what is known about its pathophysiology, prognosis, and potential therapy.
  
  
  RESULTS
  Transplant glomerulopathy is a major contributor to long-term renal allograft loss and is most often associated with CAMR. On the basis of protocol biopsies, we have found that 3.5% of conventional transplants and 27.5% of positive crossmatch kidney transplants have transplant glomerulopathy at 1 year. The pathophysiology of the process is largely unknown, but complement activation was previously thought to be essential. However, CAMR appears to develop despite terminal complement blockade and many C4d negative cases of CAMR have been identified. Thus, complement independent mechanisms, such as direct endothelial cell activation and the infiltration of natural killer cells and monocytes, are likely key to the development of transplant glomerulopathy.
  
  
  CONCLUSIONS
  Transplant glomerulopathy is often the result of CAMR and leads to allograft loss. It is characterized by distinctive histologic changes, and its pathophysiology is a multifaceted process involving both innate and adaptive immunity. Despite advances in the understanding of this condition, no effective therapy exists.
authors.affiliation: William J. von Liebig Transplant Center, Mayo Clinic, Rochester, Minnesota, USA.
authors.forename: Carrie A
authors.initials: CA
authors.lastname: Schinstock
authors.forename: Mark
authors.initials: M
authors.lastname: Stegall
authors.forename: Fernando
authors.initials: F
authors.lastname: Cosio
mesh_terms: D000818:Animals; D002908:Chronic Disease; D018450:Disease Progression; D005921:Glomerulonephritis / Q000175:diagnosis / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy; D006084:Graft Rejection / Q000175:diagnosis / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy; D006085:Graft Survival; D006648:Histocompatibility; D006801:Humans; D007518:Isoantibodies / Q000276:immunology*; D007668:Kidney / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D016030:Kidney Transplantation / Q000009:adverse effects*; D016896:Treatment Outcome
chemical_list: D007518:Isoantibodies