Very Late Activation-3 Integrin Is the Dominant β1-Integrin on the Glomerular Capillary Wall: An Immunofluorescence Study in Nephrotic Syndrome

Nephron ◽  
1992 ◽  
Vol 62 (4) ◽  
pp. 382-388 ◽  
Author(s):  
Alberto Baraldi ◽  
Luciana Furci ◽  
Giovanna Zambruno ◽  
Elisabetta Rubbiani ◽  
Giorgio Annessi ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Capillary Wall ◽  
Immunofluorescence Study ◽  
Glomerular Capillary Wall ◽  
Glomerular Capillary

scholarly journals Treatment-resistant nephrotic syndrome in dense deposit disease: complement-mediated glomerular capillary wall injury?

2020 ◽  
Vol 35 (9) ◽  
pp. 1791-1795
Author(s):  
Caroline Duineveld ◽  
Eric J. Steenbergen ◽  
Andrew S. Bomback ◽  
Nicole C. A. J. van de Kar ◽  
Jack F. M. Wetzels
Keyword(s):  
Nephrotic Syndrome ◽  
Capillary Wall ◽  
Dense Deposit Disease ◽  
Treatment Resistant ◽  
Glomerular Capillary Wall ◽  
Glomerular Capillary ◽  
Dense Deposit ◽  
Wall Injury

Membranous Nephropathy with Lambda Light Chain Restriction: A Rare Form with Serum Negative and Tissue Positive PLA2R Ab

Nephron ◽  
2021 ◽  
pp. 1-4
Author(s):  
Emel Isiktas Sayilar ◽  
Saba Kiremitci ◽  
Ihsan Ergun ◽  
Arzu Ensari
Keyword(s):  
Nephrotic Syndrome ◽  
Light Chain ◽  
Membranous Nephropathy ◽  
Capillary Wall ◽  
Glomerular Capillary Wall ◽  
Glomerular Capillary ◽  
Phospholipase A2 Receptor ◽  
Antibody Positivity ◽  
Immunoglobulin Deposits ◽  
Light Chain Deposition

Membranous nephropathy (MN) is the most common cause of nephrotic syndrome in adults. Subepithelial polyclonal immunoglobulin deposits and >70% M-type phospholipase A2 receptor antibody positivity are typical findings in idiopathic MN. A 58-year-old female patient was admitted with clinical presentation of nephrotic syndrome. Autoimmune diseases, infections, and malignancies were ruled out after clinical and laboratory evaluations. Diagnostic work-up revealed serum PLA2R antibody negativity and diffuse thickening of glomerular capillary wall on biopsy, while glomerular capillary wall IgG, C3, and Lambda monotypic light chain deposition and PLA2R1 positivity were detected by immunofluorescence and immunohistochemical examination, respectively. Following prednisolone treatment, creatinine and proteinuria were markedly regressed. The MN cases with a light chain deposits are rare and experience regarding their treatment are insufficient.

Sialoglycoproteins and filtration barriers in the glomerular capillary wall

1975 ◽  
Vol 51 (3) ◽  
pp. 354-376 ◽  
Author(s):  
Harrison Latta ◽  
William H. Johnston ◽  
Thomas M. Stanley
Keyword(s):  
Capillary Wall ◽  
Glomerular Capillary Wall ◽  
Glomerular Capillary

Glomerular endothelial activation, C4d deposits and microangiopathy in immunoglobulin A nephropathy

2019 ◽  
Author(s):  
Hernán Trimarchi ◽  
Rosanna Coppo
Keyword(s):  
Immunoglobulin A ◽  
Endothelial Activation ◽  
Capillary Wall ◽  
Vascular Damage ◽  
Therapeutic Interventions ◽  
Immunoglobulin A Nephropathy ◽  
Glomerular Capillary Wall ◽  
Glomerular Capillary ◽  
Definition Of ◽  
First Contact

Abstract Immunoglobulin A nephropathy (IgAN) is considered as mesangiopathy since it initiates in the mesangium; however, other glomerular components are involved and the glomerular capillary wall offers the first contact to circulating macromolecular IgA1. Acute and active forms of IgAN are associated with endocapillary hypercellularity and vascular damage of various degrees, in severe cases with microangiopathy (MA) without or with thrombosis [thrombotic microangiopathy (TMA)]. Vascular damage activates complement and coagulation cascades. A defective complement regulation has recently been detected in active and progressive cases of IgAN. C4d deposits in renal biopsies have been found to be an early risk factor. These observations have raised interest in manifestation of MA and TMA in progressive cases of IgAN. MA–TMA lesions have been found in various percentages (2–53%) of patients with IgAN according to patients’ selection and pathology definition of TMA. The association with hypertension (HTN) was so strong that it led to the hypothesis that MA/TMA in IgAN was a mere consequence of severe HTN. Old and new clinical and experimental data indicate that in IgAN the interaction of the glomerular capillary wall with immune reactants and complement uncontrolled activation leading to C4b deposits favours the development of MA–TMA, which plays a role in progression and renal function decline. The central role of complement activation is relevant also for the new therapeutic interventions offered by the pharma.

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