Post-streptococcal glomerulonephritis pathophysiology: Difference between revisions
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==Microscopic Pathology== | ==Microscopic Pathology== | ||
On microscopic histopathological analysis: | On microscopic histopathological analysis: | ||
*Glomeruli are enlarged and hypercellular due to the deposition of neutrophils and macrophages | *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 leucocytic infiltrate and edema in the interstitium | |||
==References== | ==References== | ||
Revision as of 14:11, 22 May 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]
Overview
Pathophysiology
Pathogenesis
- 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 in APSGN:[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
Associated Conditions
Gross Pathology
- On gross pathology, following features are seen:
- Kidney are enlarged and pale in color.
- Glomeruli is having red dots
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 leucocytic infiltrate and edema in the interstitium
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.