title: Late acute kidney transplant rejection: clinicopathological correlates and response to corticosteroid therapy.
abstract: Acute rejection is a major cause of kidney allograft dysfunction. It is important to distinguish between cellular and antibody-mediated rejection to guide the treatment strategy. The management of acute antibody-mediated rejection includes aggressive therapy with plasmapheresis and intravenous immunoglobulin. C4d staining of peritubular capillaries has emerged as a valuable tool in identifying antibody-mediated rejection. Late acute rejection has a worse prognosis than early acute rejection. The clinical and pathological features of late acute kidney allograft rejection are not fully understood. We studied the clinicopathological correlates of late acute rejection in our patient population. During an 8-year period, all patients who had late acute rejection (6 months posttransplant) were identified. Patients with severe chronic changes and transplant glomerulopathy were excluded. Patients were divided into C4d+ and C4d- groups [corrected]. Histopathological features and treatment response were evaluated. Nine patients met inclusion criteria (4 C4d+, 5 C4d-). Maintenance therapy consisted of mycophenolate mofetil, calcineurin inhibitors, and low-dose prednisone. All patients received intravenous methlyprednisolone or high-dose oral prednisone as antirejection therapy. Seventy-five percent of patients in the C4d+ group and 80% of patients in the C4d- group had a clinical response to antirejection therapy. The majority of C4d+ patients with late acute rejection who were treated with corticosteroids alone responded to treatment. The study raises the possibility that a subset of C4d+ patients with acute rejection who do not have severe chronic changes might respond to corticosteroid therapy alone.
authors.affiliation: Department of Pathology, University of Iowa Hospitals and Clinics and Veterans Administration Medical Center, 200 Hawkins Drive 5243 RCP, Iowa City, Iowa 52242, USA. ramesh-nair@uiowa.edu
authors.forename: R
authors.initials: R
authors.lastname: Nair
authors.forename: N
authors.initials: N
authors.lastname: Agrawal
authors.forename: M
authors.initials: M
authors.lastname: Lebaeau
authors.forename: S
authors.initials: S
authors.lastname: Tuteja
authors.forename: P K G
authors.initials: PK
authors.lastname: Chandran
authors.forename: M
authors.initials: M
authors.lastname: Suneja
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D001706:Biopsy; D002102:Cadaver; D002196:Capillaries / Q000276:immunology; D004396:Coloring Agents; D015935:Complement C4b; D006084:Graft Rejection / Q000188:drug therapy / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D016030:Kidney Transplantation / Q000276:immunology* / Q000473:pathology; D019520:Living Donors; D010446:Peptide Fragments / Q000097:blood; D012079:Renal Circulation; D012189:Retrospective Studies; D014019:Tissue Donors
chemical_list: D000305:Adrenal Cortex Hormones; D004396:Coloring Agents; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d