PLASMA CELL-RICH ACUTE RENAL ALLOGRAFT REJECTION1

医学 急性肾小管坏死 慢性移植物肾病 肾病 活检 移植 等离子体电池 免疫学 内科学 胃肠病学 病理 肾移植 抗体 内分泌学 糖尿病
作者
Douglas Charney,Tibor Nádasdy,Andy Wing-Hong Lo,Lorraine C. Racusen
出处
期刊:Transplantation [Ovid Technologies (Wolters Kluwer)]
卷期号:68 (6): 791-797 被引量:96
标识
DOI:10.1097/00007890-199909270-00011
摘要

Background. Acute renal allograft rejection is usually seen within the first 3 months posttransplant, and is characterized by an intense infiltrate of T cells. Some acute rejections, however, contain many plasma cells and/or appear late posttransplant. Methods. We have investigated 27 cases of intensely plasma cell-rich acute rejections (PCAR) from 1987 to 1997 and have compared them to 21 control cases (CAR) of typical acute rejection. Each group was divided into early (<6 months) and late (>6 months) subgroups. PCAR and CAR cases were matched for histological features of chronic allograft nephropathy. In all four groups, most cases had Banff'97 type IB and IIA acute rejection. Results. A significantly greater number of PCAR cases experienced graft failure due to chronic allograft nephropathy or complications of acute rejection (P<0.05). There was no significant difference between PCAR and CAR in HLA matching, occurrence of posttransplant acute tubular necrosis, presence versus absence of previous allografts, number of previous or subsequent acute rejection episodes, Banff '97 sum scores for acute rejection, cyclosporine A or FK506 levels, or percent change from baseline creatinine at time of biopsy. Plasma cells in PCAR cases showed IgG predominance whereas those in CAR had comparable staining for IgG and IgA. Kappa and lambda light chain immunostaining of all PCAR cases revealed polyclonality. Three of 18 PCAR cases studied for the presence of Epstein-Barr virus RNA showed scattered positivity in 2-7% of lymphoid cells, although the remainder was negative. None of the PCAR cases developed posttransplant lymphoproliferative disorder. Conclusions. We conclude that PCAR can occur from 1 month to many years posttransplant, is associated with poor graft survival, and is not a manifestation of concomitant chronic allograft nephropathy or viral infection, including posttransplant lymphoproliferative disorder.

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