title: De novo thrombotic microangiopathy in renal allograft biopsies-role of antibody-mediated rejection.
abstract: The most common cause of thrombotic microangiopathy (TMA) in renal allografts is thought to be calcineurin inhibitor toxicity. Antibody-mediated rejection (AMR) can also cause TMA, but its true impact on de novo TMA is unknown. In a retrospective review of renal allograft biopsies from January 2003 to December 2008 at our institution, we determined the prevalence of TMA in patients with C4d positive (n = 243) and C4d negative (n = 715) biopsies. Over 90% of patients received cyclosporine in both groups. De novo TMA was seen in 59 (6.1%) patients; most of them (55%) with C4d positive biopsy. Among patients with C4d positive biopsies, 13.6% had TMA, as compared to only 3.6% patients with C4d negative biopsies (p < 0.0001). Incidence of graft loss between C4d positive and C4d negative TMA groups was not significantly different, but 70% of patients with C4d positive TMA who received plasmapheresis had slightly lower graft loss rate. In biopsies with AMR-associated TMA, glomerulitis and peritubular capillaritis were significantly more prominent. AMR is the most common cause of TMA in renal allografts in our patient population. It is important to recognize AMR-related TMA because plasmapheresis treatment may be beneficial.
authors.affiliation: Department of Pathology, Ohio State University, Columbus, OH, USA. anjali.satoskar@osumc.edu
authors.forename: A A
authors.initials: AA
authors.lastname: Satoskar
authors.forename: R
authors.initials: R
authors.lastname: Pelletier
authors.forename: P
authors.initials: P
authors.lastname: Adams
authors.forename: G M
authors.initials: GM
authors.lastname: Nadasdy
authors.forename: S
authors.initials: S
authors.lastname: Brodsky
authors.forename: T
authors.initials: T
authors.lastname: Pesavento
authors.forename: M
authors.initials: M
authors.lastname: Henry
authors.forename: T
authors.initials: T
authors.lastname: Nadasdy
mesh_terms: D001706:Biopsy; D015935:Complement C4b / Q000032:analysis; D016572:Cyclosporine / Q000009:adverse effects; D006084:Graft Rejection / Q000473:pathology; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007668:Kidney / Q000473:pathology; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000473:pathology; D009820:Ohio / Q000453:epidemiology; D010446:Peptide Fragments / Q000032:analysis; D010956:Plasmapheresis; D015995:Prevalence; D012189:Retrospective Studies; D057049:Thrombotic Microangiopathies / Q000453:epidemiology* / Q000209:etiology / Q000628:therapy
chemical_list: D016756:Immunoglobulins, Intravenous; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d; D016572:Cyclosporine