Glomerular C4d deposition can precede the development of focal segmental glomerulosclerosis

Lest, Nina A. van de; Zandbergen, Malu; Wolterbeek, Ron; Kreutz, Reinhold; Trouw, Leendert A.; Dorresteijn, Eiske M.; Bruijn, Jan A.; Bajema, Ingeborg M.; Scharpfenecker, Marion; Chua, Jamie S.

doi:10.1016/j.kint.2019.04.028

Cited by 22 publications

(16 citation statements)

References 67 publications

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“…Different techniques of B cell depletion in adriamycin-induced glomerulosclerosis led to decreased IgM deposition and an attenuation of albuminuria (Strassheim et al 2013 ). Similar results were reported on complement subfragments C4d and C1q potentially even preceding the development of sclerotic lesions (Lest et al 2019 ). The precise role of mesangial cells in FSGS and the trigger, which promotes mesangial cell proliferation and extracellular matrix deposition, are not delineated yet and need further examination in order to understand the complete process contributing to FSGS pathogenesis.…”

Section: Mesangial Cellssupporting

confidence: 88%

Immune-mediated entities of (primary) focal segmental glomerulosclerosis

et al. 2021

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Focal segmental glomerulosclerosis (FSGS) represents a glomerular scar formation downstream of various different mechanisms leading to podocytopathy and podocyte loss. Recently, significant advances were made in understanding genetic factors, podocyte intrinsic mechanisms, and adaptive mechanisms causing FSGS. However, while most cases of nephrotic FSGS are being treated with immunosuppressants, the underlying immune dysregulation, involved immune cells, and soluble factors are only incompletely understood. Thus, we here summarize the current knowledge of proposed immune effector cells, secreted soluble factors, and podocyte response in immune-mediated (primary) FSGS.

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Section: Mesangial Cellssupporting

confidence: 88%

Immune-mediated entities of (primary) focal segmental glomerulosclerosis

et al. 2021

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“…28 In addition, we recently published a paper illustrating a role for complement activation in patients with FSGS. 29 Complement activation is commonly seen in kidney diseases characterized by endothelial damage and could thus be an indicator of endothelial injury. However, despite these studies supporting a role for the glomerular endothelium in FSGS, altered endothelial-podocyte crosstalk has not been comprehensively investigated in patients with FSGS.…”

Section: J O U R N a L P R E -P R O O F Discussionmentioning

confidence: 99%

Endothelial Endothelin Receptor A Expression Is Associated With Podocyte Injury and Oxidative Stress in Patients With Focal Segmental Glomerulosclerosis

Lest

Bakker

Dijkstra

et al. 2021

Kidney International Reports

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Complement activation contributes to glomerular injury in autoimmune GN, including MN, 1 , 2 , 3 , 4 , 5 , 6 , 7 IgAN, 10 , 11 , 12 , 13 , 14 , 15 , 8 , 9 LN, 3 , 16 , 17 , 18 , 19 , 20 AAV, 20 , 21 , 22 , 23 and FSGS. 3 , 5 , 24 , 25 , 26 , 27 …”

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confidence: 99%