肾移植中新生膜性肾病是否提示同种异体免疫?一份病例报告。

Prakash I Darji, Himanshu A Patel, Bhavya P Darji, Ajay Sharma, Ahmed Halawa
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引用次数: 2

摘要

背景:如果蛋白尿持续存在,同种异体肾移植后肾病综合征(PTNS)在5年内移植失败的风险为48%至77%。PTNS可由原生肾脏疾病复发或新生肾小球疾病引起。其预后取决于潜在的病理生理。我们报告一例肾移植后膜性肾病(MN)在肾移植后3个月发生。对患者病理生理进行了适当的评估,这有助于对病例的处理。病例总结:22岁的慢性肾盂肾炎患者。他接受了活体供体肾脏,人类白细胞抗原- dr (HLA-DR)错配为零。移植后3个月随访发现PTNS。移植物组织病理学提示MN。在过去,由于缺乏准确诊断的技术,抗体介导的排斥反应(ABMR)可能被误解为新生MN。一些研究人员观察到HLA-DR存在于足细胞上,引起抗dr抗体沉积和新生MN的发展。他们也报告了预后不良。在这里,我们排除了MN的次要原因。免疫组织化学提示IgG1沉积有利于诊断新发MN。患者对他克莫司和血管紧张素转换酶抑制剂剂量的增加反应良好。结论:暴露在异体移植足细胞上的隐藏抗原可能导致上皮下抗体沉积,引起新生MN。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Is <i>de novo</i> membranous nephropathy suggestive of alloimmunity in renal transplantation? A case report.

Is <i>de novo</i> membranous nephropathy suggestive of alloimmunity in renal transplantation? A case report.

Is <i>de novo</i> membranous nephropathy suggestive of alloimmunity in renal transplantation? A case report.

Is de novo membranous nephropathy suggestive of alloimmunity in renal transplantation? A case report.

Background: Post-transplant nephrotic syndrome (PTNS) in a renal allograft carries a 48% to 77% risk of graft failure at 5 years if proteinuria persists. PTNS can be due to either recurrence of native renal disease or de novo glomerular disease. Its prognosis depends upon the underlying pathophysiology. We describe a case of post-transplant membranous nephropathy (MN) that developed 3 mo after kidney transplant. The patient was properly evaluated for pathophysiology, which helped in the management of the case.

Case summary: This 22-year-old patient had chronic pyelonephritis. He received a living donor kidney, and human leukocyte antigen-DR (HLA-DR) mismatching was zero. PTNS was discovered at the follow-up visit 3 mo after the transplant. Graft histopathology was suggestive of MN. In the past antibody-mediated rejection (ABMR) might have been misinterpreted as de novo MN due to the lack of technologies available to make an accurate diagnosis. Some researchers have observed that HLA-DR is present on podocytes causing an anti-DR antibody deposition and development of de novo MN. They also reported poor prognosis in their series. Here, we excluded the secondary causes of MN. Immunohistochemistry was suggestive of IgG1 deposits that favoured the diagnosis of de novo MN. The patient responded well to an increase in the dose of tacrolimus and angiotensin converting enzyme inhibitor.

Conclusion: Exposure of hidden antigens on the podocytes in allografts may have led to subepithelial antibody deposition causing de novo MN.

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