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应用透射电镜观察了５倒危重型肾综合征出血热（ＨＦＲＳ）死亡病人的肾组织超微形态。结果表明：５例病人的肾小球超微形态结构均出现明显的病理改变，其中１例的肾小球基膜足突侧可见免疫复合物沉积且与病程有明显关系，肾小管上皮细胞增生和肥大。结果提示：肾小球的超微结构改变是ＨＦＨＳ进入肾衰少尿或无尿的主要原因之一，是参与形成ＨＦＲＳ肾衰的重要细胞学基础，肾小管的组织学改变使肾小管重吸收功能受到破坏，因而加剧了肾功能恶化导致肾衰，免疫复合物的沉积可能在介导ＨＦＲＳ的初期病变中具有一定作用。
Transmission electron microscopy was used to observe the ultrastructures of renal tissue in 5 dead patients with critically ill hemorrhagic fever with renal syndrome (HFRS). The results showed that all of the 5 patients showed obvious pathological changes in glomerular ultrastructure, of which 1 showed glomerular basement membrane foot process side of the immune complex deposition and a clear relationship with the course of disease, tubular epithelial cell proliferation And hypertrophy. The results suggest that the ultrastructural changes of glomeruli are one of the main reasons for HFHS to enter oliguria or anuria of renal failure. It is an important cytological basis involved in the formation of renal failure in HFRS. Renal tubular reorganization changes renal tubular reabsorption Function is damaged, thus exacerbating the deterioration of renal function leading to renal failure, the deposition of immune complexes may play an important role in mediating the initial lesion of HFRS.