Mechanisms that potentially contribute to the development of post-streptococcal glomerulonephritis

Mohammad Raguib Munif; Robert A Hart; Rukshan A M Rafeek; Amali C Mallawaarachchi; Lyndal Anderson; David J McMillan; Kadaba S Sriprakash; Natkunam Ketheesan

doi:10.1093/femspd/ftae024

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Mechanisms that potentially contribute to the development of post-streptococcal glomerulonephritis

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Mechanisms that potentially contribute to the development of post-streptococcal glomerulonephritis

Mohammad Raguib Munif, Robert A Hart, Rukshan A M Rafeek, Amali C Mallawaarachchi, Lyndal Anderson, David J McMillan, Kadaba S Sriprakash and Natkunam Ketheesan

Pathogens and Disease, Vol.82, pp.1-13

2024

DOI: https://doi.org/10.1093/femspd/ftae024

PMID: 39341789

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Abstract

chronic kidney disease

post-streptococcal glomerulonephritis

streptococcal pyrogenic exotoxin B

animal model

streptococcal inhibitor of complement

nephritis associated plasmin receptor

Post-streptococcal glomerulonephritis (PSGN) is primarily associated with preceding Group A streptococcal skin or throat infections, now mainly observed in economically disadvantaged communities. This condition significantly predisposes individuals to later-life chronic kidney disease and concurrent renal complications, with the elderly experiencing increased severity and less favourable outcomes. Streptococcal pyrogenic exotoxin B and nephritis associated plasmin receptor are identified nephritogenic antigens (nephritogens). Pathogenesis of PSGN is multifactorial. It can involve the formation of antigen-antibody immune complexes, causing inflammatory damage to renal glomeruli. Deposition of circulating immune complexes or in situ formation of immune complexes in glomeruli, or both, results in glomerulonephritis. Additionally, molecular mimicry is hypothesised as a mechanism, wherein cross-reactivity between anti-streptococcal antibodies and glomerular intrinsic matrix proteins leads to glomerulonephritis. Besides, as observed in clinical studies, streptococcal inhibitor of complement, a streptococcal-secreted protein, can also be associated with PSGN. However, the interplay between these streptococcal antigens in the pathogenesis of PSGN necessitates further investigation. Despite the clinical significance of PSGN, the lack of credible animal models poses challenges in understanding the association between streptococcal antigens and the disease process. This review outlines the postulated mechanisms implicated in the development of PSGN with possible therapeutic approaches.

Details

Title: Mechanisms that potentially contribute to the development of post-streptococcal glomerulonephritis
Authors: Mohammad Raguib Munif - University of New England
Robert A Hart (Author) - University of New England
Rukshan A M Rafeek - University of New England
Amali C Mallawaarachchi - UNSW Sydney
Lyndal Anderson - The University of Sydney
David J McMillan - University of the Sunshine Coast, Queensland, School of Science, Technology and Engineering
Kadaba S Sriprakash - University of New England
Natkunam Ketheesan (Corresponding Author) - University of the Sunshine Coast, Queensland, School of Science, Technology and Engineering
Publication details: Pathogens and Disease, Vol.82, pp.1-13
Publisher: Oxford University Press
Date published: 2024
DOI: 10.1093/femspd/ftae024
ISSN: 2049-632X
PMID: 39341789
Copyright note: © The Author(s) 2024. Published by Oxford University Press on behalf of FEMS. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
Data Availability: All data are presented within this manuscript.
Grants: Preclinical evaluation of a streptococcal peptide based specific diagnostic for rheumatic fever and the identification of proteins responsible for the pathogenesis of rheumatic heart disease, 2010336, National Health and Medical Research Council (Australia, Canberra) - NHMRC
Organisation Unit: School of Science, Technology and Engineering; Centre for Bioinnovation
Language: English
Record Identifier: 991066196802621
Output Type: Journal article

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