Department of Pediatric Nephrology, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.
Clin Transplant. 2012 Jul;26 Suppl 24:54-7. doi: 10.1111/j.1399-0012.2012.01638.x.
We report here the case of a girl who developed plasma cell-rich acute rejection (PCAR), a condition characterized by the presence of mature plasma cells infiltrating a renal allograft. The patient's creatinine level increased sharply to 4.3 mg/dL from 0.9 mg/dL at 19 months post-renal transplantation. She showed no response to methylprednisolone pulse therapy at a dose of 500 mg for three d but did show an immediate clinical and histopathological response to muromonab-CD3 (OKT3) administration. She had two episodes of PCAR recurrence and subsequently lost her graft. She had no evidences of antibody-mediated rejection including C4d deposition in peritubular capillaries and donor-specific antibodies during the entire follow-up period. To elucidate the pathogenesis of PCAR, immunohistological examination of infiltrating cells was performed. CD3-positive cells infiltration seemed to be associated with the CD138-positive cells infiltration, and the number of CD3-positive cells was increased preceding PCAR recurrence. Additionally, a rapid decrease in the number of CD138-positive cells and CD3-positive cells following the OKT3 administration was observed. This case suggests that T-cell mediated immune mechanisms might play a role in the development of PCAR.
我们在此报告一例发生浆细胞丰富性急性排斥反应(PCAR)的患者,其特征为成熟浆细胞浸润移植肾。患者在肾移植后 19 个月时,血肌酐水平从 0.9mg/dL 急剧升高至 4.3mg/dL。她对 500mg 甲基泼尼松龙脉冲治疗 3 天没有反应,但对 muromonab-CD3(OKT3)的给药立即有临床和组织病理学反应。她发生了 2 次 PCAR 复发,随后失去了移植物。在整个随访期间,她没有证据表明存在抗体介导的排斥反应,包括管周毛细血管中的 C4d 沉积和供体特异性抗体。为了阐明 PCAR 的发病机制,对浸润细胞进行了免疫组织化学检查。CD3 阳性细胞浸润似乎与 CD138 阳性细胞浸润有关,并且在 PCAR 复发之前 CD3 阳性细胞的数量增加。此外,在 OKT3 给药后,CD138 阳性细胞和 CD3 阳性细胞的数量迅速减少。该病例提示 T 细胞介导的免疫机制可能在 PCAR 的发生中起作用。