1 Department of Surgery, Division of Transplantation, Medical University of Vienna, Vienna, Austria. 2 Section of Transplantation Immunology, Department of Surgery, Medical University of Vienna, Vienna, Austria. 3 St. Anna Children's Hospital, Medical University of Vienna, Vienna, Austria. 4 Department of Internal Medicine III/Division of Nephrology and Dialysis, Medical University of Vienna, Vienna, Austria. 5 Department of Blood Group Serology and Transfusion Medicine, Medical University of Vienna, Vienna, Austria. 6 Department of Internal Medicine I, Division of Bone Marrow Transplantation, Medical University of Vienna, Vienna, Austria. 7 Division of Hematology, Medical University of Graz, Graz, Austria. 8 Department of Clinical Pathology, Medical University of Vienna, Vienna, Austria.
Transplantation. 2016 Oct;100(10):2219-21. doi: 10.1097/TP.0000000000001213.
Allogeneic hematopoietic stem cell transplantation (HSCT) can lead to donor-specific tolerance. Patients reported in the literature that underwent kidney transplantation (KT) after a previous HSCT from the same haploidentical donor typically received short-term immunosuppression, mainly for safety reasons and concerns of triggering graft-versus-host disease.
We describe the case of a 22-year-old patient who developed chronic kidney failure after receiving haploidentical HSCT from his father for the treatment of metastatic rhabdomyosarcoma. Five years after HSCT, he received a preemptive kidney transplant from his father. Steroid treatment, which had been prescribed for the underlying kidney disease, was withdrawn within 2 months posttransplant, and no de novo immunosuppression was given. Donor-specific tolerance was assessed with mixed lymphocyte reaction and INF-γ ELISPOT before (D0) and after KT (D9). Furthermore, the exact level of donor-derived T cells was measured with real-time polymerase chain reaction before and 1 year after KT.
In vitro assays (mixed lymphocyte reaction and ELISPOT) revealed donor-specific tolerance before and after transplantation, respectively. The number of recipient-derived T cells was low before KT and virtually did not change over time (0.0139% ± 0.0039 and 0.0120% ± 0.0067; P = NS). Graft function was excellent throughout the follow-up (36 months post KT: serum creatinine, 1.18 mg/dL). Protocol biopsies performed 1 and 12 months after transplantation confirmed the absence of rejection.
This is one of the first cases of kidney transplantation from the same donor after previous haploidentical HSCT with a corticosteroid taper alone. Our results suggest that immunosuppression can be avoided in such cases.
异基因造血干细胞移植（HSCT）可导致供者特异性耐受。文献报道，先前接受来自同一单倍体相合供者的 HSCT 后行肾移植（KT）的患者通常接受短期免疫抑制治疗，主要是出于安全性考虑和担心触发移植物抗宿主病。
我们描述了 1 例 22 岁患者，他因转移性横纹肌肉瘤接受来自其父亲的单倍体相合 HSCT 后发生慢性肾衰竭。HSCT 后 5 年，他从父亲那里接受了抢先性肾移植。移植后 2 个月内停用了用于治疗基础肾脏病的类固醇治疗，并且没有给予新的免疫抑制治疗。在移植前（D0）和移植后（D9）进行混合淋巴细胞反应和 IFN-γ ELISPOT 评估供者特异性耐受。此外，在移植前和移植后 1 年，通过实时聚合酶链反应测量确切的供者衍生 T 细胞水平。
体外检测（混合淋巴细胞反应和 ELISPOT）分别在移植前和移植后显示供者特异性耐受。移植前患者的受体衍生 T 细胞数量较低，并且随时间几乎没有变化（0.0139%±0.0039 和 0.0120%±0.0067；P=NS）。整个随访期间（移植后 36 个月）移植物功能均良好（血清肌酐 1.18mg/dL）。移植后 1 个月和 12 个月进行的方案活检证实无排斥反应。
这是先前接受来自同一单倍体相合供者的 HSCT 后，单独使用皮质类固醇减量行肾移植的首批病例之一。我们的结果表明，在这种情况下可以避免免疫抑制。
