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[慢性肾小球肾炎发生发展的可能机制之一]

[One of the possible mechanisms of development and progression of chronic glomerulonephritis].

作者信息

Plotkin V Ia

出版信息

Ter Arkh. 1988;60(6):19-24.

PMID:3206361
Abstract

Proceeding from clinical examination of 430 patients with chronic glomerulonephritis (GN) and morphological, histochemical and biochemical studies on kidney biopsy specimens the author has proposed and substantiated a hypothesis, according to which prolonged raised protein reabsorption in cells of the proximal tubules (PT) of the kidney can cause breakage and distortion of the activity of transport systems responsible for the absorption and catabolism of macromolecules. These changes can result in PT cell breakage, escape of lysosomal enzymes into the lumen and basal membrane of PT cells and pericanalicular interstice with further development of cortical interstitial sclerosis. The combination of the above mentioned disturbances would lead to GN progression and development of renal insufficiency.

摘要

基于对430例慢性肾小球肾炎(GN)患者的临床检查以及对肾活检标本的形态学、组织化学和生物化学研究,作者提出并证实了一种假说,即肾脏近端小管(PT)细胞中蛋白质重吸收长期增加可导致负责大分子吸收和分解代谢的转运系统活性的破坏和扭曲。这些变化可导致PT细胞破裂,溶酶体酶逸入PT细胞的管腔和基底膜以及小管周围间隙,进而发展为皮质间质硬化。上述紊乱的综合作用将导致GN进展和肾功能不全的发生。

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1
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Ter Arkh. 1988;60(6):19-24.
2
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