Membranous Nephropathy

Couser, William G.

doi:10.1681/asn.2005010087

Cited by 22 publications

(22 citation statements)

References 20 publications

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“…Data from rat models (Heymann nephritis) that closely simulate human disease (19) and the case of infants with a rare form of membranous nephropathy secondary to immunization with maternal antibodies (20) suggest that damage to the podocyte is initiated by IgG binding to native antigens expressed on the membrane of podocyte foot processes (21). These antibodyantigen complexes that are typically detectable as immune deposits in the subepithelial space are likely to activate complement by the recruitment of later-acting C5, C6, and C5b-9 and insertion of sublytic amounts of the membrane attack complex into podocytes, with cell injury and loss of the glomerular barrier to protein filtration (22)(23)(24). Conceivably, rituximab might interrupt this process upstream to the synthesis of pathogenic autoantibodies (5-7).…”

Section: Discussionmentioning

confidence: 99%

Effects of Rituximab on Morphofunctional Abnormalities of Membranous Glomerulopathy

Ruggenenti¹,

Cravedi²,

Sghirlanzoni³

et al. 2008

Clinical Journal of the American Society of Nephrology

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Section: Discussionmentioning

confidence: 99%

Effects of Rituximab on Morphofunctional Abnormalities of Membranous Glomerulopathy

Ruggenenti¹,

Cravedi²,

Sghirlanzoni³

et al. 2008

Clinical Journal of the American Society of Nephrology

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“…The pathological mechanism of MN is mostly associated with phospholipase A2 receptor antibody; a combination of phospholipase A2 receptor antibody and corresponding antigen on the podocytes forms in the immune complex and then activates the C5b-9 complex through the relative channels, damages the podocytes, destroys the glomerular filtration barrier, and generates proteinuria [ 5 – 7 ]. This disease has been reported to contribute to an immune response to the self-antigens expressed on the podocyte cell and is similar to many immune diseases [ 8 ]. Nowadays, there are no specific diagnostic biomarkers in MN.…”

Section: Introductionmentioning

confidence: 99%

miR-217 Is a Useful Diagnostic Biomarker and Regulates Human Podocyte Cells Apoptosis via Targeting TNFSF11 in Membranous Nephropathy

Liu

Xue³

et al. 2017

BioMed Research International

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Background MicroRNAs have recently been verified as useful diagnostic biomarkers in various diseases. In this study, we investigated whether miR-217 is a useful diagnostic biomarker and the possible pathological mechanism of miR-217 in this disease. Methods Patients with focal segmental glomerulosclerosis (FSGS), membranous nephropathy (MN), and diabetic nephropathy (DN) and control patients were enrolled in this study. The miR-217 inhibitor and mimics were transfected into human podocyte cells to investigate the pathological mechanism of miR-217 in this disease. Relevant indicators were detected and tested. Results Compared with control patients, miR-217 was significantly downregulated and TNFSF11 was significantly upregulated in MN. Then, miR-217 had obvious separation between patients with MN and control patients, with an AUC of 0.941, a cutoff value of <750.0 copies/ul, and sensitivity and specificity of 88.9% and 75.9%. In addition, the TNFSF11 was confirmed to be the target gene of miR-217. Finally, in in vitro experiments, the upregulation of miR-217 could decrease the expression of TNFSF11 and not induce human podocyte cells apoptosis; however, the downregulation of miR-217 could bring about an opposite change. Conclusions miR-217 is a useful diagnostic biomarker and is involved in human podocyte cells apoptosis via targeting TNFSF11 in membranous nephropathy.

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“…The mental stress and economic burden brought by ESFR were enormous, which necessitated exploration of eligible biomarkers for IMN treatment [7,8]. Of note, IMN was explicitly proposed as a disease featured by antigen-specificity of podocyte membrane [9], and injury of podocytes could give rise to proteinuria, a characteristic manifestation of IMN [10]. These linkages of podocytes with IMN suggested that etiologies underlying malfunctioning of podocytes might also explain the onset of IMN.…”

Section: Introductionmentioning

confidence: 99%

Application of miR-193a/WT1/PODXL axis to estimate risk and prognosis of idiopathic membranous nephropathy

Zhang

Ren

2019

Renal Failure

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Background: This investigation was managed to explore whether miR-193a in combination with two podocytes, namely, Wilms tumor type 1 (WT1) and podocalyxin (PODXL), were feasible in estimating onset and prognosis of idiopathic membranous nephropathy (IMN). Methods: We recruited a total of 189 healthy controls and 364 IMN patients, whose urine samples were prepared to measure the expression of miR-193a and PODXL. Meanwhile, renal tissues collected from above-mentioned IMN patients (n ¼ 364) and renal cell carcinoma patients (n ¼ 189) were arranged to determine the expression of WT1. Ultimately, receiver operating characteristic curves were constructed to appraise the performance of miR-193a, WT1, and PODXL in predicting renal survival of IMN patients. Results: The IMN patients were measured with up-regulated miR-193a expression and downregulated WT1/PODXL expression, when compared with healthy controls (p < 0.05). Moreover, highly expressed miR-193a, lowly expressed WT1/PODXL, elevated amounts of proteinuria (>3.79 g/24 h)/serum creatinine (>174.63 lmol/L), and declined GFR (68.13 mL/min/1.73 m 2) were implicated as prominent biomarkers for the poor renal survival of IMN patients (all p < 0.05). Notably, miR-193a combined with PODXL and WT1 generated optimal effects in differentiating IMN patients from healthy controls (AUC ¼ 0.994) and also in anticipating the renal survival state of IMN patients (AUC ¼ 0.824), when compared with strategies that merely employed 2 of the biomarkers. Conclusion: The combination of miR-193a, WT1, and PODXL might serve as a favorable strategy for expecting IMN prognosis.

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Membranous Nephropathy

Cited by 22 publications

References 20 publications

Effects of Rituximab on Morphofunctional Abnormalities of Membranous Glomerulopathy

Effects of Rituximab on Morphofunctional Abnormalities of Membranous Glomerulopathy

miR-217 Is a Useful Diagnostic Biomarker and Regulates Human Podocyte Cells Apoptosis via Targeting TNFSF11 in Membranous Nephropathy

Application of miR-193a/WT1/PODXL axis to estimate risk and prognosis of idiopathic membranous nephropathy

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