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The role of soluble urokinase-type Plasminogen Activator Receptor (suPAR) in Chronic Kidney Disease
Author(s) -
Ade Yonata,
Ian Effendi,
Zulkhair Ali,
Novadian Suhaimi,
Siti Suprapti
Publication year - 2018
Publication title -
indonesian journal of kidney and hypertension
Language(s) - English
Resource type - Journals
ISSN - 2654-4253
DOI - 10.32867/inakidney.v1i1.5
Subject(s) - podocyte , supar , focal segmental glomerulosclerosis , urokinase receptor , diabetic nephropathy , nephrotic syndrome , medicine , membranous nephropathy , kidney , glomerulosclerosis , kidney disease , pathogenesis , glomerular basement membrane , plasminogen activator , proteinuria , endocrinology , immunology
Kidney disease affects 800 million children and adults worldwide, and the numbers keep increasing. A better understanding of the pathogenesis in kidney diseases, especially on a biomolecular level, is much needed to identify novel biomarkers and therapeutic targets for kidney diseases. The glomerular filtration barrier comprises endothelial cells, the glomerular basement membrane, and podocytes. The podocyte has a central role in part of the glomerular filtration barrier. The nor­mal functioning of podocytes is particularly important in preventing the heavy proteinuria seen in nephrotic syndrome or diabetic nephropathy, or in the disease process of focal segmental glomerulosclerosis. The podocyte is injured by circulating factors, which final­ly results in deranged podocyte motility. Soluble uro­kinase-type plasminogen activator receptor (suPAR) is a circulating form of glycosyl-phosphatidylinositol uPAR domain membrane protein and is known to play a role in the pathogenesis in kidney diseases, specifi­cally focal segmental glomerulosclerosis and diabetic nephropathy. suPAR binds to αvβ3 integrin on podo­cyte foot processes and causes podocyte structure dis­organization leading to glomerular filtration disruption and hence proteinuria. suPAR is also a potential bio­marker to predict the incidence of CKD.

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