scholarly journals The Role of IgA in the Pathogenesis of IgA Nephropathy

2019 ◽  
Vol 20 (24) ◽  
pp. 6199 ◽  
Author(s):  
Martina Perše ◽  
Željka Večerić-Haler
Keyword(s):  
Iga Nephropathy ◽  
Genetic Factors ◽  
Immunoglobulin A ◽  
Symbiotic Relationship ◽  
Biological Functions ◽  
Antibody Isotype ◽  
Microbial Invasion ◽  
Iga Antibodies ◽  
Interaction With Receptors

Immunoglobulin A (IgA) is the most abundant antibody isotype produced in humans, predominantly present in the mucosal areas where its main functions are the neutralization of toxins, prevention of microbial invasion across the mucosal epithelial barrier, and simultaneous maintenance of a physiologically indispensable symbiotic relationship with commensal bacteria. The process of IgA biosynthesis, interaction with receptors, and clearance can be disrupted in certain pathologies, like IgA nephropathy, which is the most common form of glomerulonephritis worldwide. This review summarizes the latest findings in the complex characteristics of the molecular structure and biological functions of IgA antibodies, offering an in-depth overview of recent advances in the understanding of biochemical, immunologic, and genetic factors important in the pathogenesis of IgA nephropathy.

Aggregation of erythrocyte sodium/lithium countertransport activity in families of patients with immunoglobulin A nephropathy

1992 ◽  
Vol 83 (2) ◽  
pp. 241-245 ◽  
Author(s):  
A. Fabbri ◽  
R. Boero ◽  
E. Degli Esposti ◽  
C. Guarena ◽  
A. Lucatello ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Iga Nephropathy ◽  
Poor Prognosis ◽  
Genetic Factors ◽  
Immunoglobulin A ◽  
Mean Blood Pressure ◽  
Immunoglobulin A Nephropathy ◽  
Normal Range ◽  
Erythrocyte Sodium

1. We evaluated the inheritance of erythrocyte Na+/Li+ countertransport activity in IgA nephropathy by assessing this parameter in 19 patients with biopsy-proven IgA nephropathy and in their 53 relatives (32 parents and 21 siblings). The possible use of erythrocyte Na+/Li+ countertransport activity as a marker of poor prognosis was also evaluated. 2. A significant correlation was found between ‘familial’ and proband Na+/Li+ countertransport activity, but not between that of spouses. 3. Mean blood pressure, although within the normal range, and Na+/Li+ countertransport activity were significantly higher in patients with proteinuria than in those without proteinuria. 4. Parents of proteinuric patients had a higher Na+/Li+ countertransport activity than parents of non-proteinuric patients. 5. In IgA nephropathy the inheritance of erythrocyte Na+/Li+ countertransport activity was preserved. Therefore genetic factors could play a role in the non-immunological progression of IgA nephropathy.

scholarly journals Fcα Receptor (Cd89) Mediates the Development of Immunoglobulin a (Iga) Nephropathy (Berger's Disease)

1999 ◽  
Vol 191 (11) ◽  
pp. 1999-2010 ◽  
Author(s):  
Pierre Launay ◽  
Béatrice Grossetête ◽  
Michelle Arcos-Fajardo ◽  
Emmanuelle Gaudin ◽  
Sonia P. Torres ◽  
...  
Keyword(s):  
Iga Nephropathy ◽  
Molecular Mechanism ◽  
Severe Combined Immunodeficiency ◽  
Immunoglobulin A ◽  
In Vivo Model ◽  
Matrix Expansion ◽  
Recombination Activating Gene ◽  
New Treatments

The pathogenesis of immunoglobulin A (IgA) nephropathy (IgAN), the most prevalent form of glomerulonephritis worldwide, involves circulating macromolecular IgA1 complexes. However, the molecular mechanism(s) of the disease remain poorly understood. We report here the presence of circulating soluble FcαR (CD89)-IgA complexes in patients with IgAN. Soluble CD89 was identified as a glycoprotein with a 24-kD backbone that corresponds to the expected size of CD89 extracellular domains. To demonstrate their pathogenic role, we generated transgenic (Tg) mice expressing human CD89 on macrophage/monocytes, as no CD89 homologue is found in mice. These mice spontaneously developed massive mesangial IgA deposition, glomerular and interstitial macrophage infiltration, mesangial matrix expansion, hematuria, and mild proteinuria. The molecular mechanism was shown to involve soluble CD89 released after interaction with IgA. This release was independent of CD89 association with the FcRγ chain. The disease was induced in recombination activating gene (RAG)2−/− mice by injection of serum from Tg mice, and in severe combined immunodeficiency (SCID)-Tg mice by injection of patients' IgA. Depletion of soluble CD89 from serum abolished this effect. These results reveal the key role of soluble CD89 in the pathogenesis of IgAN and provide an in vivo model that will be useful for developing new treatments.

scholarly journals The mucosal immune system and IgA nephropathy

2021 ◽  
Author(s):  
Loreto Gesualdo ◽  
Vincenzo Di Leo ◽  
Rosanna Coppo
Keyword(s):  
Immune Response ◽  
Mucosal Immunity ◽  
Lymphoid Tissue ◽  
Genetic Factors ◽  
Immunoglobulin A ◽  
Mucosal Immune Response ◽  
Immunoglobulin A Nephropathy ◽  
Food Antigen ◽  
The Relationship

Abstract The precise pathogenesis of immunoglobulin A nephropathy (IgAN) is still not clearly established but emerging evidence confirms a pivotal role for mucosal immunity. This review focuses on the key role of mucosa-associated lymphoid tissue (MALT) in promoting the onset of the disease, underlying the relationship among microbiota, genetic factors, food antigen, infections, and mucosal immune response. Finally, we evaluate potential therapies targeting microbes and mucosa hyperresponsiveness in IgAN patients.

C4d in Native Glomerular Diseases

2019 ◽  
Vol 49 (1) ◽  
pp. 81-92 ◽  
Author(s):  
Preeti Chandra
Keyword(s):  
Iga Nephropathy ◽  
Focal Segmental Glomerulosclerosis ◽  
Complement Activation ◽  
Immunoglobulin A ◽  
Future Research ◽  
Glomerular Diseases ◽  
Segmental Glomerulosclerosis ◽  
Native Kidney

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).

scholarly journals Measurement of Chlamydia pneumoniae-Specific Immunoglobulin A (IgA) Antibodies by the Microimmunofluorescence (MIF) Method: Comparison of Seven Fluorescein-Labeled Anti-Human IgA Conjugates in an In-House MIF Test Using One Commercial MIF and One Enzyme Immunoassay Kit

2003 ◽  
Vol 10 (1) ◽  
pp. 8-12 ◽  
Author(s):  
Mika Paldanius ◽  
Aini Bloigu ◽  
Maija Leinonen ◽  
Pekka Saikku
Keyword(s):  
Enzyme Immunoassay ◽  
Chlamydia Pneumoniae ◽  
Immunoglobulin A ◽  
Method Comparison ◽  
Serum Samples ◽  
Iga Antibodies ◽  
Specific Immunoglobulin ◽  
Antibody Titers ◽  
Iga Antibody

ABSTRACT For the serological diagnosis of acute Chlamydia pneumoniae infection, the microimmunofluorescence (MIF) test is the most commonly used method and also the “gold standard” for the measurement of immunoglobulin G (IgG) and IgM antibodies. The role of IgA antibodies in diagnosis has not been established. Commercially available fluorescein-labeled anti-human IgA conjugates have not been systematically compared to each other, and this situation may cause considerable variations in IgA results. Therefore, we tested 261 serum samples from 122 patients with pneumonia for IgA antibodies by using six α-chain-specific anti-IgA conjugates in our in-house MIF test, one commercial MIF test, and one enzyme immunoassay (EIA). Interfering IgG antibodies were removed with Gullsorb reagent before the measurement of IgA antibodies. Altogether, 14 significant IgA antibody increases in serum samples between the acute phase and the convalescent phase were detected by at least one of the conjugates in the MIF test, while no increases were found in the IgA EIA. Only one patient showed a significant IgA antibody increase with all of the fluorescein-labeled conjugates. Five significant titer changes were detected by at least two conjugates, and in nine instances, the titer increase was detected by one conjugate only. The titer agreement indicated by kappa coefficients was very good or good for all of the fluorescein-labeled conjugates and the EIA with low antibody titers but decreased with increasing titers.

Epigenetic factors and molecular markers of the risk of early pregnancy losses

GYNECOLOGY ◽  
2019 ◽  
Vol 21 (3) ◽  
pp. 9-16
Author(s):  
Nataly I Frolova ◽  
Tatiana E Belokrinitskaya
Keyword(s):  
Early Pregnancy ◽  
Genetic Factors ◽  
Molecular Genetic ◽  
Pregnancy Complication ◽  
Common Complication ◽  
Epigenetic Factors ◽  
Genetic Determination ◽  
Periconceptional Period ◽  
Combined Impact

Background. Miscarriage is a common complication in early pregnancy. Current studies have shown a higher prevalence of miscarriage, ranging from 10 to 20%. The review is devoted to modern concepts of etiology and pathogenesis of early pregnancy losses. Aim. Assess the role of epigenetic factors and molecular-genetic markers in the pathogenesis and prediction of early pregnancy losses Materials and methods. In order to write this review domestic and foreign publications were searched in Russian and international search systems (PubMed, eLibrary, etc.) for the last 10-15 years. Relevant articles from the peer-reviewed literature and clinical practice guidelines were included. Results. Many recent studies have proved the contribution of various epigenetic factors to the pathogenesis of spontaneous miscarriages, and the molecular-genetic determination such kinds of pregnancy complication has been confirmed. Conclusion. The miscarriage in early gestation is driven by combined impact of epigenetic and molecular-genetic factors, as well as the presence of intergenic interactions. It is may lead to deterioration of physiological functions, and maternal pathologenic pathways could be changed as during her periconceptional period as so during the pregnancy.

Role of genetic factors in the development of hypertension in young patients with metabolic syndrome

2020 ◽  
pp. 23-32
Author(s):  
Elena Korneeva ◽  
Mikhail Voevoda ◽  
Sergey Semaev ◽  
Vladimir Maksimov
Keyword(s):  
Metabolic Syndrome ◽  
High Risk ◽  
Arterial Hypertension ◽  
Genetic Factors ◽  
Young Patients ◽  
Integrin Αiibβ3 ◽  
Ace Gene ◽  
The Metabolic Syndrome

Results of the study related to polymorphism of ACE gene (rs1799752)‎, integrin αIIbβ3, and CSK gene (rs1378942) influencing development of arterial hypertension in young patients with metabolic syndrome are presented. Hypertension as a component of the metabolic syndrome was detected in 15.0% of young patients. Prevalence of mutant alleles of the studied genes among the examined patients was quite high, so homozygous DD genotype was found in 21.6%, and mutant D allele of the ACE gene in 47.4%. A high risk of hypertension in patients with MS was detected in carriers of the T allele of the CSK (rs1378942) gene – 54.8%, which was most often observed in a combination of polymorphic ACE and CSK gene loci (p = 0.0053).

Prevalence of IgA Nephropathy: A 10 Years’ Experience from Jinnah Postgraduate Medical Centre, Karachi, Pakistan

2020 ◽  
Keyword(s):  
Body Mass Index ◽  
Iga Nephropathy ◽  
Body Mass ◽  
Immunoglobulin A ◽  
Medical Centre ◽  
Male Dominance ◽  
Clinical Indication ◽  
Glomerular Lesion ◽  
Female Ratio ◽  
Nephritic Syndrome

Background: Immunoglobulin A (IgA) is considered the most frequently dealt primary glomerulonephritis, worldwide. The Berger’s disease or IgA nephropathy is a mesangial proliferative glomerulonephritis characterized by deposition of immunoglobulin A in kidneys. The aim of the study was to report the prevalence of IgA nephropathy and the associated parameters (age, gender, and body mass index) in our population. Methods: This was a retrospective study, accomplished at Jinnah Postgraduate Medical Centre, Karachi, Pakistan, from June 2009-May 2019. The histopathology and immunofluorescence of renal biopsies of 519 patients were studied and the prevalence of biopsy proven IgA nephropathy was determined. The Chi-square test was used for association of biopsy proven IgA nephropathy with age, gender, and body mass index. A p-value of 0.05 or less was considered statistically significant. Results: A total of 519 biopsies were studied, out of those, only 4 (0.8%) had IgA nephropathy with male dominance in the last 10 years at Karachi, Pakistan. Male to female ratio was found to be 3:1. The most common clinical indication for renal biopsy was isolated hematuria in 50% of the cases followed by acute kidney injury and nephritic syndrome with 25% each respectively. Most of the patients suffering from proteinuria (> 3.5gm/24 hours), microscopic hematuria in 80% cases, high blood pressure in 50% cases, with other associated symptoms including edema, gastrointestinal, and skin-related symptoms reported. Conclusion: Immunoglobulin A (IgA) nephropathy is not a commonly diagnosed glomerular lesion. Further large-scale cohorts can aid in determining the other factors associated with a low frequency of IgA nephropathy. Keywords: Biopsy; Glomerulonephritis; Immunoglobulin A; Nephropathy.

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