title: Acute transplant glomerulopathy is associated with antibody-mediated rejection and poor graft outcome.
abstract: Transplant glomerulopathy (TG) is traditionally considered to be a chronic entity. However, in our practice we observed patients who presented with features of TG as early as 14 days posttransplantation. We investigated the clinicopathological features of these cases. During a 4-year period, all patients with acute rejection were identified. Charts were reviewed to identify patients with antibody-mediated rejection and biopsy features of TG within 6 months posttransplantation. Three patients met the above-mentioned criteria. All of them had diffuse margination of inflammatory cells in peritubular capillaries in the setting of acute renal failure or delayed graft function. Monocyte (CD68-positive) margination in peritubular capillaries was a common feature. All 3 patients had donor-specific antibodies and features suggestive of antibody-mediated rejection. C4d stain in peritubular capillaries was focal and mild or absent in serial biopsies. Occlusive endothelial swelling of glomerular capillary loops (endotheliosis) preceded TG. None of the patients had evidence for other causes of similar glomerular changes in a transplant, such as calcineurin inhibitor toxicity, ischemia, hepatitis C, or immune complex glomerulonephritis. They did not have other biopsy features of chronicity when TG appeared and as it progressed. TG can occur as an acute phenomenon. We propose that endotheliosis is a more accurate and specific precursor of TG than mere glomerulitis. These cases of acute TG may represent a form of antibody-mediated rejection associated with proteinuria and poor response to treatment.
authors.affiliation: Department of Pathology, University of Iowa Hospitals and Clinics, 200 Hawkins, Dr., 5243 RCP, Iowa City, IA 52242, USA. ramesh-nair@uiowa.edu
authors.forename: R
authors.initials: R
authors.lastname: Nair
authors.forename: M
authors.initials: M
authors.lastname: Fraer
authors.forename: N
authors.initials: N
authors.lastname: Agrawal
authors.forename: M
authors.initials: M
authors.lastname: Suneja
mesh_terms: D000208:Acute Disease; D058186:Acute Kidney Injury / Q000276:immunology; D000368:Aged; D015703:Antigens, CD / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology; D001706:Biopsy; D002196:Capillaries / Q000276:immunology; D015935:Complement C4b / Q000032:analysis; D051799:Delayed Graft Function / Q000276:immunology; D006084:Graft Rejection / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D006801:Humans; D056724:Immunity, Humoral; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007484:Iowa; D007668:Kidney / Q000098:blood supply / Q000276:immunology* / Q000473:pathology; D007674:Kidney Diseases / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D016030:Kidney Transplantation / Q000009:adverse effects*; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis; D011507:Proteinuria / Q000276:immunology; D013997:Time Factors; D016896:Treatment Outcome; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015935:Complement C4b; D007166:Immunosuppressive Agents; D010446:Peptide Fragments; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C032261:complement C4d