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伯氏疟原虫感染引起的小鼠肾脏超微结构病理变化。

Ultrastructural pathological changes in mice kidney caused by Plasmodium berghei infection.

作者信息

Pulido-Méndez M, Finol H J, Girón M E, Aguilar I

机构信息

Institute of Experimental Medicine, Faculty of Medicine, Central University of Venezuela, Caracas, Venezuela.

出版信息

J Submicrosc Cytol Pathol. 2006 Jun-Sep;38(2-3):143-8.

PMID:17784642
Abstract

Malaria, a common health problem in certain parts of the world, has a considerable morbidity and mortality. This work reports under electron microscopy studies serious ultrastructural kidney damage such as extensive cytoplasmic vacuolation, vesiculation and autophagic vacuoles in proximal tubular cells. A thickened endothelial wall on peritubular capillary, interdigitation disorganization and significant decrease of their number in some areas were detected. Swollen rough endoplasmic reticulum, swollen mitochondria, and parasitized erythrocytes were observed. Many epithelial cells exhibited cytoplasmic areas of autophagia and a myelin-like form. A tubular cell presented severe cytoarchitecture alterations. Abundant lipid droplets were noticed. Almost total loss of interdigitations, rough endoplasmic reticulum vesiculation, peritubular capillaries with endothelial cells thickened cytoplasm, papillary processes projected to the lumen, and an inflammatory infiltrate of macrophages were also observed. These ultrastructural kidney changes could cause, on the basis of their clinical and pathologic expressions, a fat accumulation, an acute temporary reversible glomerulonephritis, a chronic progressive irreversible glomerulonephritis, and an acute renal failure (ARF).

摘要

疟疾是世界某些地区常见的健康问题,具有相当高的发病率和死亡率。这项研究报告了在电子显微镜下观察到的严重肾脏超微结构损伤,如近端肾小管细胞中广泛的细胞质空泡化、小泡形成和自噬空泡。检测到肾小管周围毛细血管的内皮壁增厚、指状交叉紊乱以及某些区域其数量显著减少。观察到粗面内质网肿胀、线粒体肿胀和被寄生的红细胞。许多上皮细胞呈现出自噬的细胞质区域和髓鞘样形态。一个肾小管细胞呈现出严重的细胞结构改变。发现大量脂滴。还观察到指状交叉几乎完全消失、粗面内质网小泡化、肾小管周围毛细血管内皮细胞胞质增厚、乳头突向管腔以及巨噬细胞炎性浸润。基于这些临床和病理表现,这些肾脏超微结构改变可能导致脂肪堆积、急性暂时性可逆性肾小球肾炎、慢性进行性不可逆性肾小球肾炎和急性肾衰竭(ARF)。

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