Pauci-immune and immune glomerular lesions in kidney transplants for systemic lupus erythematosus
Pauci-immune and immune glomerular lesions in kidney transplants for systemic lupus erythematosus
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DOI：
10.2215/cjn.00790208
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发表时间：
2008-09-01
影响因子：
9.8
通讯作者：
Javaid, Basit
中科院分区：
文献类型：
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作者：
Meehan, Shane M.;Chang, Anthony;Javaid, Basit
背景和目的：对系统性红斑狼疮（SLE）引起的终末期肾炎患者的同种异体移植肾小球病变进行检查，以确定复发性肾小球肾炎（GN）的肾小球病理谱。设计、设置、参与者和测量：共有156个活检样本，来自43例终末期狼疮肾炎受者的49个连续同种异体移植，通过光镜检查，并在选定的病例中通过免疫荧光和电子显微镜检查。将这些与对照同种异体移植物进行比较（n = 35）。结果：狼疮患者49例异体移植物中有19例（38.8%）出现复发性狼疮肾炎引起的肾小球病变。肾小球病变分为三类：1)免疫复合物肾小球病变，包括系膜性肾小球病变（28%）和膜性肾小球病变（4%）；2)非典型肾小球病变，包括急性增生性肾小球n（32%）和局灶节段性肾小球硬化（12%），肾小球毛细血管中免疫沉积不足，内皮管网状包涵体频发，血栓性微血管病变；3)移植相关肾小球病变（24%）。结论：来自SLE患者的同种异体移植物具有典型的免疫复合物介导的GN和非典型的少免疫、增殖性GN和节段性肾小球硬化。这些非典型肾小球病变提示非免疫复合物介导的肾小球损伤在复发性狼疮GN中的作用。
Background and objectives: Glomerular lesions in allografts in recipients with end-stage nephritis resulting from systemic lupus erythematosus (SLE) were examined to determine the spectrum of glomerular pathology in recurrent glomerulonephritis (GN).Design, setting, participants, & measurements: A total of 156 biopsy samples, from 49 serial allografts in 43 recipients with end-stage lupus nephritis, were examined by light microscopy, and by immunofluorescence and electron microscopy in selected cases. These were compared with control allografts (n = 35).Results: Glomerular lesions best explained by recurrent lupus nephritis were observed in 19 of 49 allografts (38.8%) in lupus recipients. Three categories of glomerulopathies were identified: 1) immune complex glomerulopathies, including mesangial GN (28%) and membranous GN (4%); 2) atypical glomerulopathies, including acute proliferative GN (32%) and focal segmental glomerulosclerosis (12%), with scant immune deposits in glomerular capillaries, frequent endothelial tubuloreticular inclusions, and thrombotic microangiopathy; and 3) transplant-associated glomerulopathies (24%).Conclusions: Allografts from recipients with SLE had typical immune complex-mediated GN and atypical pauci-immune, proliferative GN and segmental glomerular sclerosis. Atypical glomerulopathies like these suggest a role for nonimmune complex-mediated glomerular injury in recurrent lupus GN.