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目的：观察移植肾动脉病的超微结构形态，探讨移植肾动脉病的发生机制。方法：应用ＬｏｗｉｃｒｙｌＫ４Ｍ（Ｋ４Ｍ）低温包埋、免疫金标记的透射电镜技术观察了５例发生移植肾动脉病的肾动脉内膜形态改变，５例正常供肾肾动脉作为对照。结果：①内膜内皮细胞和平滑肌细胞异常表达Ⅱ类主要组织相容性抗原（ＨＬＡ－Ｄ）。５例正常供肾肾动脉内膜内皮细胞和平滑肌细胞则呈阴性。②病变内膜中的主要成分为“合成型”平滑肌细胞及其细胞外基质。平滑肌细胞胞浆中除含有密斑、密体样结构外，还可见到丰富的粗面内质网，并表达核增殖基因ｃ－ｍｙｃ蛋白。③内膜病变中Ｔ淋巴细胞与单核吞噬细胞各占６５％与３５％。④ＣＤ４阳性Ｔ与ＣＤ８阳性Ｔ淋巴细胞的数量基本相等，它们的超微结构形态十分相似，难以区分。⑤病变中未能发现ＣＤ２０阳性的Ｂ淋巴细胞。结论：移植肾动脉病是内皮损伤后单核吞噬细胞、Ｔ淋巴细胞、平滑肌细胞之间通过ＨＬＡ－Ｄ相互作用，从而形成了一种以平滑肌细胞增殖为主的动脉内膜炎
OBJECTIVE: To observe the ultrastructure of renal artery graft disease and to explore the mechanism of renal artery disease. Methods: The morphological changes of renal artery in 5 patients with renal artery graft were observed by transmission electron microscopy with LowicrylK4M (K4M) cryogenic embedding and immunogold labeling. Five normal renal arteries served as control. Results: ① Intimal endothelial cells and smooth muscle cells abnormally expressed class Ⅱ major histocompatibility antigen (HLA-D). 5 cases of normal renal artery endothelium cells and smooth muscle cells were negative. The main component of the lesion intima “synthetic” smooth muscle cells and extracellular matrix. Smooth muscle cell cytoplasm in addition to containing dense, dense body-like structure, but also to see a rich rough endoplasmic reticulum and express the nuclear proliferation gene c-myc protein. ③ endometrial lesions in T lymphocytes and mononuclear phagocytes accounted for 65% and 35%. ④CD4-positive T and CD8-positive T lymphocytes in the same number, their ultrastructure morphology is very similar, it is difficult to distinguish. ⑤ lesions found in CD20-positive B lymphocytes. CONCLUSION: Renal artery disease is the result of HLA-D interaction between mononuclear phagocytes, T lymphocytes and smooth muscle cells after endothelial cell injury, thus forming an endarteritoneum with smooth muscle cell proliferation