Boratyńska M, Banasik M, Hałoń A, Patrzałek D, Klinger M
Department of Nephrology and Transplantation Medicine, Wroclaw Medical University, Wroclaw, Poland.
Transplant Proc. 2007 Nov;39(9):2711-4. doi: 10.1016/j.transproceed.2007.08.053.
Three patients with negative Lewis phenotypes who displayed anti-Lewis antibodies suffered severe kidney allograft dysfunction. One woman and two men (22-44 years) received ABO compatible kidney transplants with negative donor-recipient cross-match tests. Two patients had the phenotype Le(a-b-) with anti-Le(a) and anti-Le(b) complement binding antibodies. The third patient of phenotype Le(a+b-) developed anti-Lewis(b) antibody a few months after transplantation. One patient presented recurrence of worsened graft function from the day 6 to 4 months after transplantation; despite treatment there was not full recovery. The second patient had recurrences of acute graft dysfunction at 4 and 6 months after transplantation with nephrotic range proteinuria. The third patient showed progressive graft dysfunction at 7 months after transplantation. Biopsy specimens showed histological changes of antibody-mediated rejection. In the third patient, we observed fibrinoid necrosis and thrombosis of arterioles and glomerular capillaries. Immunofluorescence studies showed immunoglobulin IgG and IgM in glomerular capillaries and C4d and C3 on endothelial cells of peritubular capillaries. Posttransplantation cross-match tests with donor lymphocytes were negative. Anti-Lewis antibodies were observed during follow-up. All patients were treated with methylprednisolone boluses. In addition, one subject received antithymocyte globulin (ATG) and 1 received plasmapheresis. Two patients had moderate renal dysfunction (creatinine levels 1.8 and 1.9 mg/dL) after 8-17 months follow-up. The third patient lost her graft at 11 months after transplantation. Lewis antibodies may injure a renal allograft. C4d deposition and failure to show donor-specific anti-HLA antibodies suggested the participation of other antibodies.
三名Lewis血型表型为阴性但出现抗Lewis抗体的患者发生了严重的肾移植功能障碍。一名女性和两名男性（22 - 44岁）接受了ABO血型相容的肾移植，供受者交叉配型试验为阴性。两名患者的表型为Le(a - b -)，具有抗Le(a)和抗Le(b)补体结合抗体。第三名表型为Le(a + b -)的患者在移植后几个月出现了抗Lewis(b)抗体。一名患者在移植后第6天至4个月出现移植肾功能恶化复发；尽管进行了治疗，但未完全恢复。第二名患者在移植后4个月和6个月出现急性移植功能障碍复发，并伴有肾病范围的蛋白尿。第三名患者在移植后7个月出现进行性移植功能障碍。活检标本显示有抗体介导排斥反应的组织学改变。在第三名患者中，我们观察到小动脉和肾小球毛细血管的纤维蛋白样坏死和血栓形成。免疫荧光研究显示肾小球毛细血管中有免疫球蛋白IgG和IgM，肾小管周围毛细血管内皮细胞上有C4d和C3。移植后与供者淋巴细胞进行的交叉配型试验为阴性。随访期间观察到抗Lewis抗体。所有患者均接受了甲泼尼龙冲击治疗。此外，一名患者接受了抗胸腺细胞球蛋白（ATG），一名患者接受了血浆置换。经过8 - 17个月的随访，两名患者出现中度肾功能不全（肌酐水平分别为1.8和1.9 mg/dL）。第三名患者在移植后11个月失去了移植肾。Lewis抗体可能会损伤肾移植。C4d沉积以及未检测到供者特异性抗HLA抗体提示有其他抗体参与。
