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顶端肾小管补体激活与蛋白尿性肾脏疾病中的肾功能丧失

Apical tubular complement activation and the loss of kidney function in proteinuric kidney diseases.

作者信息

Alkaff Firas F, Lammerts Rosa G M, Daha Mohamed R, Berger Stefan P, van den Born Jacob

机构信息

Division of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Division of Pharmacology and Therapy, Department of Anatomy, Histology, and Pharmacology, Faculty of Medicine Universitas Airlangga, Surabaya, Indonesia.

出版信息

Clin Kidney J. 2024 Jul 10;17(8):sfae215. doi: 10.1093/ckj/sfae215. eCollection 2024 Aug.

DOI:10.1093/ckj/sfae215
PMID:39135935
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11318052/
Abstract

Many kidney diseases are associated with proteinuria. Since proteinuria is independently associated with kidney function loss, anti-proteinuric medication, often in combination with dietary salt restriction, comprises a major cornerstone in the prevention of progressive kidney failure. Nevertheless, complete remission of proteinuria is very difficult to achieve, and most patients with persistent proteinuria slowly progress toward kidney failure. It is well-recognized that proteinuria leads to kidney inflammation and fibrosis via various mechanisms. Among others, complement activation at the apical side of the proximal tubular epithelial cells is suggested to play a crucial role as a cause of progressive loss of kidney function. However, hitherto limited attention is given to the pathophysiological role of tubular complement activation relative to glomerular complement activation. This review aims to summarize the evidence for tubular epithelial complement activation in proteinuric kidney diseases in relation to loss of kidney function.

摘要

许多肾脏疾病都与蛋白尿有关。由于蛋白尿与肾功能丧失独立相关,抗蛋白尿药物通常与饮食限盐联合使用,是预防进行性肾衰竭的主要基石。然而,蛋白尿的完全缓解很难实现,大多数持续性蛋白尿患者会慢慢发展为肾衰竭。众所周知,蛋白尿通过多种机制导致肾脏炎症和纤维化。其中,近端肾小管上皮细胞顶端的补体激活被认为是导致肾功能逐渐丧失的关键原因。然而,迄今为止,相对于肾小球补体激活,肾小管补体激活的病理生理作用受到的关注有限。这篇综述旨在总结蛋白尿性肾脏疾病中肾小管上皮补体激活与肾功能丧失相关的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c36/11318052/ab6b2866cc98/sfae215fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c36/11318052/ba9dafca4eb2/sfae215fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c36/11318052/ec3d9dd24aeb/sfae215fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c36/11318052/ab6b2866cc98/sfae215fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c36/11318052/ba9dafca4eb2/sfae215fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c36/11318052/ec3d9dd24aeb/sfae215fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c36/11318052/ab6b2866cc98/sfae215fig3.jpg

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Front Endocrinol (Lausanne). 2024 Jan 8;14:1256375. doi: 10.3389/fendo.2023.1256375. eCollection 2023.
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