THE SIGNIFICANCE OF THE ANTI-CLASS-I ANTIBODY-RESPONSE .1. CLINICAL AND PATHOLOGICAL FEATURES OF ANTI-CLASS I-MEDIATED REJECTION
THE SIGNIFICANCE OF THE ANTI-CLASS-I ANTIBODY-RESPONSE .1. CLINICAL AND PATHOLOGICAL FEATURES OF ANTI-CLASS I-MEDIATED REJECTION
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DOI：
10.1097/00007890-199001000-00019
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发表时间：
1990-01-01
期刊：
影响因子：
6.2
通讯作者：
SRINIVASA, NS
中科院分区：
文献类型：
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作者：
HALLORAN, PF;WADGYMAR, A;SRINIVASA, NS
在肾移植中，针对供体HLA I类抗原的预先形成的细胞毒性抗体引起同种异体肾移植物的超急性排斥反应，但其在移植后时期发展时的致病意义尚不清楚。在目前的研究中，我们描述了与抗I类抗体相关的排斥反应患者的临床和病理特征。在400例连续尸体肾移植的过程中，7例患者被确定谁有抗体对供体I类HLA抗原与非典型，但独特的排斥反应模式。所有7个都是预先准备好的。在3例患者中，无意中进行了移植，供体特异性T细胞交叉配型阳性。在其余4例患者中，T细胞交叉配型在当前血清中为阴性，但在移植后变为阳性。临床表现为移植肾功能恶化，并迅速出现少尿，这显然是由于急性肾小管坏死，但放射性同位素扫描研究可证实血流持续存在。肾组织学显示，细胞介导的排斥反应中观察到的典型病变，如小管炎和间质浸润，是不存在的。颗粒补体沉积（6）、多形性浸润（6）和微血管内皮损伤（6）很常见，单核细胞浸润不存在（2）或不明显（4）。3例患者的肾小球变化类似于溶血性尿毒综合征的情况，伴有毛细血管纤维蛋白血栓和内皮下间隙增宽。IgG染色为阴性。病理学特征提示，移植后早期出现或持续存在的抗I类抗体损伤微血管内皮，其临床表现与超急性排斥反应不同。特别是在致敏患者中，功能快速恶化，导致急性肾小管坏死，微循环中内皮损伤的病理特征，应建议诊断为抗I类介导的排斥反应。
In renal transplantation, preformed cytotoxic antibody against donor HLA class I antigens caused hyperacute rejection of renal allografts, but its pathogenic significance when it develops in the posttransplant period is unknown. In the present studies we describe the clinical and pathologic features of patients with rejection associated with anti-class I. In the course of 400 consecutive cadaveric renal transplants, 7 patients were identified who had antibody against donor class I HLA antigens in association with atypical but distinctive patterns of rejection. All 7 were presensitized. In 3 patients, the transplant had been inadvertently performed with a positive donor-specific T cell crossmatch. In the remaining 4, the T cell crossmatch on current sera was negative but became positive posttransplant. The clinical picture was deterioration of graft function with rapid onset of oliguria, apparently due to acute tubular necrosis, but with persistance of blood flow demonstrable by radioisotope scan studies. Renal histology showed that the typical lesions observed in cell-mediated rejection, such as tubulitis and interstitial infiltration, were absent. Granular complement deposition (6), polymorphonuclear infiltration (6), and endothelial injury in the microvasculature (6) were common, and mononuclear infiltrates were absent (2) or not prominent (4). In 3 patients the glomerular changes resembled a picture of hemolytic uremic syndrome, with capillary fibrin thrombi and widening of the subendothelial space. IgG staining was negative. The pathologic features suggest that anti-class I antibody appearing or persisting in the early posttransplant period injures the endothelium of the microvasculature, with the clinical presentation different from that of hyperacute rejection. Particularly in sensitized patients, rapid deterioration in function, leading to a picture of acute tubular necrosis, with pathologic features of endothelial injury in the microcirculation, should suggest the diagnosis of anti-class I-mediated rejection.