Post-streptococcal glomerulonephritis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

Overview

It is thought that post-streptococcal glomerulonephritis (PSGN) is caused by nephritogenic strains of group A beta-hemolytic streptococcus (GAS). The mechanism which leads to immunologic injury to the glomerulus include deposition of immune complexes with streptococcal antigenic components, then immune complexes are deposited in glomerular basement membrane and antibodies bind to the GBM.

Pathophysiology

It is thought that post-streptococcal glomerulonephritis (PSGN) is caused by nephritogenic strains of group A beta-hemolytic streptococcus (GAS)
Other strains of Group A streptococci which cause PSGN include:
- Group A streptococci M protein types 47, 49, 55, 2, 60
- Group A streptococci M types 1, 2, 4, 3, 25, 49, and 12
Two antigens isolated from nephritogenic streptococci are commonly implicated are:^[1]^[2]
- Streptococcal pyrogenic exotoxin B
- Nephritis-associated plasmin receptor

The mechanism which leads to immunologic injury to the glomerulus are:^[3]

There is deposition of immune complexes with streptococcal antigenic components
Immune complexes are deposited in glomerular basement membrane and antibodies bind to the GBM
Further antigen reacts with antibodies bind to GBM and cross glomerular membranes

Gross Pathology

On gross pathology, following features are seen:
- Kidney are enlarged and pale in color

Microscopic Pathology

On microscopic histopathological analysis:

Glomeruli are enlarged and hypercellular due to the deposition of neutrophils and macrophages
There is a proliferation of mesangial and endothelial cells
There is a swelling of endothelial cells and presence of inflammatory cells obstructs capillary lumina
There is an accumulation of mononuclear leukocytic infiltrate and edema in the interstitium

Immunofluorescence findings

During the early phase of post-infectious glomerulonephritis, there is the starry sky appearance due to deposition of C3 and IgG in the capillary walls and mesangial areas
In later stages, there is a predominance of C3 deposition in mesangium^[4]

References

↑ Yoshizawa N, Yamakami K, Fujino M, Oda T, Tamura K, Matsumoto K, Sugisaki T, Boyle MD (July 2004). “Nephritis-associated plasmin receptor and acute poststreptococcal glomerulonephritis: characterization of the antigen and associated immune response”. J. Am. Soc. Nephrol. 15 (7): 1785–93. PMID 15213266.
↑ Oda T, Yoshizawa N, Yamakami K, Tamura K, Kuroki A, Sugisaki T, Sawanobori E, Higashida K, Ohtomo Y, Hotta O, Kumagai H, Miura S (September 2010). “Localization of nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis”. Hum. Pathol. 41 (9): 1276–85. doi:10.1016/j.humpath.2010.02.006. PMID 20708459.
↑ Rodríguez-Iturbe B, Batsford S (June 2007). “Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet”. Kidney Int. 71 (11): 1094–104. doi:10.1038/sj.ki.5002169. PMID 17342179.
↑ Sorger K, Gessler U, Hübner FK, Köhler H, Schulz W, Stühlinger W, Thoenes GH, Thoenes W (March 1982). “Subtypes of acute postinfectious glomerulonephritis. Synopsis of clinical and pathological features”. Clin. Nephrol. 17 (3): 114–28. PMID 7067173.

Overview