Crescentic glomerulonephritis and membranous nephropathy: a rare coexistence

Balafa, Olga; Kalaitzidis, Rigas; Liapis, Georgios; Xiromeriti, Sofia; Zarzoulas, F.; Baltatzis, George; Elisaf, Moses

doi:10.1007/s11255-015-1031-z

Cited by 13 publications

(14 citation statements)

References 28 publications

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“…The coexistence of MGN with other renal diseases was already reported [3][4][5][6] including MGN and FSGS 7,8 , with FSGS cellular 9 and collapsing variants 10,11 . Therefore, we report the case of a patient with morphological characteristics of two primary glomerular diseases, MGN and FSGS.…”

Section: Introductionmentioning

confidence: 99%

Focal and Segmental Glomerulosclerosis and Membranous Nephropathy overlapping in a patient with Nephrotic Syndrome: a case report

et al. 2020

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Introduction: Some cases of membranous nephropathy (MGN) present focal segmental glomerulosclerosis (FSGS) typically associated with disease progression. However, we report a case of a patient who seemed to have MGN and FSGS, both primary. Case presentation: A 17-year-old female, Caucasian, presenting lower extremity edema associated with episodes of foamy urine and high blood pressure, had physical and laboratorial exams indicating nephrotic syndrome. A renal biopsy was performed and focal and segmental glomerulosclerosis were observed under light microscopy in some glomeruli presented as tip lesion, and in others it was accompanied by podocyte hypertrophy and podocyte detachment in urinary space, compatible with podocytopathy FSGS. Besides, there were thickened capillary loops with basement membrane irregularities due to "spikes" compatible with MGN stage II. Immunofluorescence showed finely granular IgG, IgG4, and PLA2R deposits in capillary loops and, in electron microscopy, subepithelial deposits and foot process effacement. These morphological findings are compatible with FSGS and MGN stage II. Conclusions: In the present case, clinical and morphological characteristics showed a possible overlap of primary FSGS and MGN as focal and segmental glomerulosclerosis does not seem to be related with MGN progression but with the podocytopathy FSGS.

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Section: Introductionmentioning

confidence: 99%

Focal and Segmental Glomerulosclerosis and Membranous Nephropathy overlapping in a patient with Nephrotic Syndrome: a case report

et al. 2020

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“…Membranous nephropathy (MN), also called membranous glomerulonephritis, is a non‐inflammatory immune kidney disorder that often results in nephrotic syndrome, in which IgG antibodies form glomerular subepithelial immune complexes (Aaltonen & Honkanen, ; Balafa et al., ). The aetiology of membranous nephropathy involves glomerular injury caused by in situ formation of subepithelial immune deposits and C5b‐9 formation and insertion into podocytes (Nangaku, Shankland, & Couser, ).…”

Section: Introductionmentioning

confidence: 99%

Down‐regulation of the long non‐coding RNA XIST ameliorates podocyte apoptosis in membranous nephropathy via the miR‐217–TLR4 pathway

Jin

Pan

et al. 2018

Experimental Physiology

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New Findings What is the central question of this study?What is the role of the long non‐coding RNA X‐inactive specific transcript (XIST), which is up‐regulated in injured podocytes and membranous nephropathy, in the pathogenesis of membranous nephropathy? What is the main finding and its importance?XIST was up‐regulated in kidney tissue with membranous nephropathy and in injured podocytes. Down‐regulation of XIST inhibited podocyte apoptosis. XIST negatively regulated miR‐217, and miR‐217 modulated Toll‐like receptor 4. Inhibition of XIST suppressed podocyte apoptosis induced by angiotensin II via miR‐217. Abstract Membranous nephropathy is often characterized by glomerular podocyte injury. Up‐regulation of the long non‐coding RNA (lncRNA) X‐inactive specific transcript (XIST) has been verified in membranous nephropathy and in injured podocytes. Here the role of XIST in podocyte injury and membranous nephropathy was explored. Quantitative real‐time PCR and western blot were performed to detect the expression of XIST and miR‐217, and Toll‐like receptor 4 (TLR4) protein, respectively. Podocyte apoptosis was evaluated with flow cytometry. Interaction between XIST and miR‐217 was analysed by RNA immunoprecipitation and RNA pull‐down assay. A dual luciferase reporter assay was used to examine the interplay between miR‐217 and TLR4. Up‐regulation of the lncRNA XIST and angiotensin II (Ang II) and kidney and podocyte injury were indicated in kidney tissue of patients with membranous nephropathy. Increase of XIST and apoptosis were induced by Ang II in podocytes. Down‐regulation of XIST reversed podocyte apoptosis induced by Ang II. MiR‐217 was negatively regulated by XIST. MiR‐217 controlled TLR4 by targeting its 3′‐untranslated region. XIST modulated TLR4 through miR‐217 and inhibition of XIST reduced podocyte apoptosis induced by Ang II via regulating miR‐217. Down‐regulation of XIST ameliorates podocyte apoptosis via the miR‐217–TLR4 pathway, which may improve membranous nephropathy.

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“…Most of the cases have been reported with the presence of anti-GBM antibodies or ANCA. [11,12] However, there are patients of MN and crescent formation without any signs of vasculitis, lupus, or anti-GBM disease. [13] Although the percentage of crescents in glomeruli was low of 5% (2%–17%), [14] these patients with crescents showed unfavorable therapeutic response and tended to have worse renal outcomes.…”

Section: Introductionmentioning

confidence: 99%

Plasma exchange and rituximab treatments in primary membranous nephropathy combined with crescentic glomerulonephritis

et al. 2019

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Rationale: Crescent formation is rare in primary membranous nephropathy (MN). Anti-phospholipase A2 receptor (PLA2R) antibodies are detectable in these patients. The mechanism and treatments are unknown. Patient concerns: A 72-year-old female patient who presented with nephrotic syndrome, hematuria, and rapidly progressive kidney dysfunction. Diagnoses: Kidney biopsy was performed and the diagnosis was MN in combination with crescentic glomerulonephritis. Circulating anti-PLA2R IgG3 and IgG4 were detected of high level. Interventions: The patient received plasma exchange and rituximab besides corticosteroids. Outcomes: The patient achieved complete remission of proteinuria and recovery of kidney function after the clearance of anti-PLA2R antibodies. Lesson: This case suggests a pathogenic role of anti-PLA2R antibodies in the mechanism of crescent formation in MN, which may need intensive therapy to eliminate the antibodies quickly.

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Crescentic glomerulonephritis and membranous nephropathy: a rare coexistence

Cited by 13 publications

References 28 publications

Focal and Segmental Glomerulosclerosis and Membranous Nephropathy overlapping in a patient with Nephrotic Syndrome: a case report

Focal and Segmental Glomerulosclerosis and Membranous Nephropathy overlapping in a patient with Nephrotic Syndrome: a case report

Down‐regulation of the long non‐coding RNA XIST ameliorates podocyte apoptosis in membranous nephropathy via the miR‐217–TLR4 pathway

Plasma exchange and rituximab treatments in primary membranous nephropathy combined with crescentic glomerulonephritis

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