通常我们认为蛋白尿及肾功能下降相关的迟发慢性组织学异常与移植肾小球病（TG）相互影响。当前的研究我们采用计划性活检及临床指示性活检来明确临床和亚临床的TG、其进程及其与同种异体抗体的联系。我们回顾性研究了582名移植前T细胞补体依赖淋巴毒试验阴性的肾移植患者中有55名患者被诊断为TG，其中27名患者（49％）为肾功能良好的患者通过计划性活检证实。TG的累计发生率在5年时为20％。亚临床TG的预后和通过移植物功能减退诊断的TG预后均较差，组织学和肾功能改变均渐进性恶化。虽然TG与急慢性组织学改变相关，但是14.5%的TG活检并未提示间质纤维化及肾小管的萎缩，58％（7/12）严重TG活检标本提示仅为极微小的异常。TG和急性排斥反应、移植前丙肝抗体阳性及供者特异性抗HLA抗体（尤其是II类抗体）升高相关。我们认为亚临床TG是一种未被认识的抗体介导的移植肾慢性损伤的诱因，其可以独立于其他导致肾小球病的因素之外。

Transplant glomerulopathy (TG) usually has been described as part of a constellation of late chronic histologic abnormalities associated with proteinuria and declining function. The current study used both protocol and clinically-indicated biopsies to investigate clinical and subclinical TG, their prognosis and possible association with alloantibody. We retrospectively studied 582 renal transplants with a negative pre-transplant T-cell complement dependent cytotoxicity crossmatch. TG was diagnosed in 55 patients, 27 (49%) based on protocol biopsy in well-functioning grafts. The cumulative incidence of TG increased over time to 20% at 5 years. The prognosis of subclinical TG was equally as poor as TG diagnosed with graft dysfunction, with progressive worsening of histopathologic changes and function. Although TG was associated with both acute and chronic histologic abnormalities, 14.5% of TG biopsies showed no interstitial fibrosis or tubular atrophy, while 58% (7/12) of biopsies with severe TG showed only minimal abnormalities. TG was associated with acute rejection, pretransplant hepatitis C antibody positivity and anti-HLA antibodies (especially anti-Class II), with the risk increasing if the antibodies were donor specific. We suggest that subclinical TG is an under-recognized cause of antibody-mediated, chronic renal allograft injury which may be mechanistically distinct from other causes of nephropathy.

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