&lt;b&gt;&lt;i&gt;Mannose-Binding Lectin2&lt;/i&gt;&lt;/b&gt; Gene Polymorphism and IgG4 in Membranous Nephropathy

Costa, Denise Maria do Nascimento; Valente, Lucila Maria; Vajgel, Gisele; Sandrin-Garcia, Paula; Cruz, Heidi Lacerda Alves da; Crovella, Sérgio; Cavalcante, Antônio Henrique Santana; Cavalcante, Maria Alina Gomes de Mattos; Oliveira, Camila Barbosa Lyra de; Vasconcelos, Carolina de Andrade Jordão de; Sarinho, Emanuel

doi:10.1159/000486552

Cited by 8 publications

(8 citation statements)

References 44 publications

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“…There is evidence that MBL can bind to the Fc portion of IgG, which lacks galactose residues (such as in rheumatoid arthritis) and thereby activate the LP [42]. Recently polymorphisms in the MBL2 gene in idiopathic MN and lupus MN were suggested to be associated with LP activation in MN [43].…”

Section: Membranous Nephropathymentioning

confidence: 99%

C4d in Native Glomerular Diseases

Chandra¹

2019

Am J Nephrol

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Complement activation occurs in many glomerular diseases, the exact pathway(s) of activation has been studied in detail in some diseases but not in all. C4d is generated by the activation of classical and lectin pathways, and its presence can point to the activation of either of these pathways. This review aims to summarize the available data with regard to the deposition of glomerular C4d in native kidney biopsies in different glomerular pathologies that may be useful for future research into the role of complement activation in glomerular diseases. While there is more information on C4d in certain diseases (e.g., Immunoglobulin A (IgA) nephropathy), there is scant data in other diseases (such as focal segmental glomerulosclerosis).

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Section: Membranous Nephropathymentioning

confidence: 99%

C4d in Native Glomerular Diseases

Chandra¹

2019

Am J Nephrol

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“…Complete remission as defined by proteinuria endpoints was more likely to occur in seropositive patients (treated with various combinations of corticosteroids, cyclophosphamide, cyclosporine and/or tacrolimus) who had lower levels of MBL, MASP-1 and MASP2 at baseline (65). Polymorphisms in the MBL2 gene were more commonly observed in patients with primary MN in one study, although correlations between MBL2 genotype, circulating MBL levels, anti-PLA2R seropositivity, and proteinuria were not made in this study (66).…”

Section: Mannose-binding Lectin and Alternative Pathway Activation In...mentioning

confidence: 56%

The role of the complement system in primary membranous nephropathy: A narrative review in the era of new therapeutic targets

Chan

Yap

et al. 2022

Front. Immunol.

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Primary membranous nephropathy (MN) is an important cause of nephrotic syndrome and chronic kidney disease (CKD) in the adult population. Although the discovery of different autoantibodies against glomerular/podocytic antigens have highlighted the role of B cells in the pathogenesis of MN, suboptimal response or even resistance to B cell-directed therapies occurs, suggesting that other pathophysiological mechanisms are involved in mediating podocyte injury. The complement system plays an important role in the innate immune response to infection, and dysregulation of the complement system has been observed in various kidney diseases. There is compelling evidence of complement cascade activation in primary MN, with the mannose-binding lectin (MBL) and alternative pathways particularly implicated. With appropriate validation, assays of complements and associated activation products could hold promise as adjunctive tools for non-invasive disease monitoring and prognostication. While there is growing interest to target the complement system in MN, there is concern regarding the risk of infection due to encapsulated organisms and high treatment costs, highlighting the need for clinical trials to identify patients most likely to benefit from complement-directed therapies.

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“…As previously discussed, the lectin pathway plays an important role in disease pathogenesis [30]. In a case-control Brazilian study, an association was noted between membranous nephropathy and mannose-binding lectin 2(MBL2) polymorphism in patients carrying O allele, in particular, A/O genotype [31]. Investigators also found a defective MBL production in patients with YA/O, XA/O, and O/O genotypes.…”

Section: Role Of Complements In the Disease Pathophysiologymentioning

confidence: 83%

Unraveling Primary Membranous Nephropathy Using Proteogenomic Studies

Ragy¹,

Hamilton²,

Kanigicherla³

2022

Urinary Tract Infection and Nephropathy - Insights Into Potential Relationship

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Membranous nephropathy is one of the leading causes of nephrotic syndrome in adults. The disease manifests in different forms with varying severity and outcomes range from spontaneous remission to rapid disease progression. The effects of the disease are so far best understood using conventional histopathological morphology and clinical phenotype. Being an autoimmune condition subject to a multi-hit hypothesis, the notion of underlying genetic risks is being examined in recent times. Current evidence points to significant heterogeneity in the gene expression profiles in both the immune system and at the glomerular level, with potential implications for disease management. Further proteomic and transcriptomic analysis can instruct classification, prognostication, and treatment pathways. This chapter focuses on the links identified between primary membranous nephropathy and underlying gene polymorphism, and pathways using both proteomics and transcriptomic analysis. We discuss the potential impact this could have on future management to try to minimize the patient’s immunosuppression exposure and find the most effective targeted immunosuppressive therapy.

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<b><i>Mannose-Binding Lectin2</i></b> Gene Polymorphism and IgG4 in Membranous Nephropathy

Cited by 8 publications

References 44 publications

C4d in Native Glomerular Diseases

C4d in Native Glomerular Diseases

The role of the complement system in primary membranous nephropathy: A narrative review in the era of new therapeutic targets

Unraveling Primary Membranous Nephropathy Using Proteogenomic Studies

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