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Infection Related Glomerulonephritis (IRGN)

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Pathology of Glomerular Diseases
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Abstract

Infection related glomerulonephritis include post-infectious (post-streptococcal) glomerulonephritis, IgA dominant post-infectious glomerulonephritis, endocarditis associated glomerulonephritis etc. Post-infectious (post-streptocoocal) glomerulonephritis (PIGN) is the leading cause of acute nephritic syndrome/acute glomerulonephritis in children. It is less often seen in adults. It is usually caused secondary to upper respiratory tract streptococcal infection with a latent period of 1–2 weeks. Streptococcal pyrogenic exotoxin B and nephritis-associated plasmin receptor are two common antigens that cause activation of the alternate complement pathway and are involved in the pathogenesis of PIGN. In adults, it is usually seen in association with risk factors such as diabetes, alcohol abuse, malignancies, etc. It can also be caused by other bacteria such as staphylococci and pneumococcal infection. Gram-negative bacteria and certain viral and parasitic infections associated PIGN have also been described. The most common presentation is nephritic syndrome, but nephrotic syndrome and rapidly progressive glomerulonephritis can also be seen. Light microscopic appearances show enlarged glomeruli with lobular accentuation and diffuse proliferative glomerulonephritis with endocapillary hyperplasia along with neutrophilic infiltration. Crescents can also be seen. In the resolving phase of the disease, glomeruli are less cellular with only mesangial proliferation. Subepithelial humps can be observed in some cases under oil immersion in Masson’s trichrome-stained sections. On immunofluorescence, typical cases show coarse granular deposits of IgG and complement C3 along glomerular capillary wall. In the resolving phase mesangial granular IgG and C3 deposits are seen or sometimes only C3 deposits can be evident. On electron microscopy, characteristic finding is the presence of electron-dense deposits in the form of subepithelial humps. Endothelial cell swelling, mesangial cell swelling, and polymorphs are also visualized.

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Further Reading

  • Balasubramanian R, Marks SD. Post-infectious glomerulonephritis. Paediatr Int Child Health. 2017;37:240–7.

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  • D’Agati VD, Jennette JC, Olson JL. Heptinstall’s pathology of the kidney. 7th ed. Wolters Kluwer; 2014.

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  • Glassock RJ, Alvarado A, Prosek J, Hebert C, Parikh S, Satoskar A, Nadasdy T, Forman J, Rovin B, Hebert LA. Staphylococcus-related glomerulonephritis and poststreptococcal glomerulonephritis: why defining “post” is important in understanding and treating infection-related glomerulonephritis. Am J Kidney Dis. 2015;65:826–32.

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  • Khalighi MA, Wang S, Henriksen KJ, Bock M, Keswani M, Meehan SM, Chang A. Revisiting post-infectious glomerulonephritis in the emerging era of C3 glomerulopathy. Clin Kidney J. 2016;9:397–402.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Gupta, P., Gupta, R.K. (2022). Infection Related Glomerulonephritis (IRGN). In: Pathology of Glomerular Diseases. Springer, Singapore. https://doi.org/10.1007/978-981-19-1430-0_7

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  • DOI: https://doi.org/10.1007/978-981-19-1430-0_7

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  • Publisher Name: Springer, Singapore

  • Print ISBN: 978-981-19-1429-4

  • Online ISBN: 978-981-19-1430-0

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