title: Early and late humoral rejection: a clinicopathologic entity in two times.
abstract: Humoral rejection is an important cause of early and late graft loss. The late variant is difficult to diagnose and treat. There is a close correlation between sclerosing nephropathy and anti-HLA antibodies. We analyzed 113 renal allograft recipients between August 2004 and April 2007. Acute humoral rejection was defined as acute graft dysfunction in presence of donor-specific antibodies (DSA) detected by flow panel reactive antibodies (PRA) and/or C4d positive pericapilary tubules (PTC) detected histopathologically by immunofluorescent or immunoperoxidase at less than 3 months postransplantation. Late humoral rejection was defined as dysfunction occurring after 3 months postransplantation with histopathologic glomerulopathy or vasculopathy and positive C4d PTC. We included all patients who were diagnosed with early or late graft dysfunction and underwent biopsy, all of which were examined for C4d. Four patients had acute humoral rejection treated with IVIG or plasmapheresis. The patient and graft survivals were 100% and serum creatinine averaged 1.7 mg/dL. Three recipients experienced late humoral rejection at 3 to 10 years posttransplantation All received high-dose IVIG; one also was treated with thymoglobulin. Immunosuppression was switched to tacrolimus, mycophenolate mofetil, and steroids. Only one patient recovered renal function; the others returned to dialysis. Among seven patients only one had an actual PRA (>20%) and three showed 10% to 20%. However, six had a positive historical PRA of 10% to 50%. In conclusion, Recognition of acute humoral rejection has contributed to graft rescue by controlling alloantibody production through new specific immunosuppressive therapies in contrast with the clinical response to acute therapy, treatment of a chronic entity has shown poor outcomes, probably because antibody mediated chronic graft damage is already present when the late diagnosis is established by biopsy.
authors.affiliation: Hospital Barros Luco Trudeau, Santiago, Chile.
authors.forename: J
authors.initials: J
authors.lastname: Péfaur
authors.forename: P
authors.initials: P
authors.lastname: Díaz
authors.forename: R
authors.initials: R
authors.lastname: Panace
authors.forename: P
authors.initials: P
authors.lastname: Salinas
authors.forename: A
authors.initials: A
authors.lastname: Fiabane
authors.forename: N
authors.initials: N
authors.lastname: Quinteros
authors.forename: R
authors.initials: R
authors.lastname: Chea
authors.forename: E
authors.initials: E
authors.lastname: Naranjo
authors.forename: A
authors.initials: A
authors.lastname: Wurgaft
authors.forename: E
authors.initials: E
authors.lastname: Beltran
authors.forename: S
authors.initials: S
authors.lastname: Elgueta
authors.forename: M E
authors.initials: ME
authors.lastname: Wegmann
authors.forename: J G
authors.initials: JG
authors.lastname: Gajardo
authors.forename: L
authors.initials: L
authors.lastname: Contreras
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology / Q000627:therapeutic use; D000917:Antibody Formation; D015703:Antigens, CD / Q000276:immunology; D018951:Antigens, CD20 / Q000276:immunology; D000961:Antilymphocyte Serum; D001706:Biopsy; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D003404:Creatinine / Q000097:blood; D005500:Follow-Up Studies; D006084:Graft Rejection / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016030:Kidney Transplantation / Q000276:immunology* / Q000473:pathology*; D010956:Plasmapheresis; D013997:Time Factors; D014184:Transplantation, Homologous / Q000276:immunology / Q000473:pathology
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D018951:Antigens, CD20; D000961:Antilymphocyte Serum; D016756:Immunoglobulins, Intravenous; D007166:Immunosuppressive Agents; D003404:Creatinine; C512542:thymoglobulin