Post-streptococcal glomerulonephritis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*It is thought that post-streptococcal glomerulonephritis (PSGN) is caused by nephritogenic strains of group A beta-hemolytic streptococcus (GAS) | *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 | *Other strains of [[Group A streptococcal infection|Group A streptococc]]<nowiki/>i which cause PSGN include: | ||
**Group A streptococci M protein types 47, 49, 55, 2, 60 | **Group A streptococci M protein types 47, 49, 55, 2, 60 | ||
**Group A streptococci M types 1, 2, 4, 3, 25, 49, and 12 | **Group A streptococci M types 1, 2, 4, 3, 25, 49, and 12 | ||
*Two antigens isolated from nephritogenic streptococci are commonly implicated | *Two antigens isolated from nephritogenic [[Streptococcus|streptococci]] are commonly implicated are:<ref name="pmid15213266">{{cite journal |vauthors=Yoshizawa N, Yamakami K, Fujino M, Oda T, Tamura K, Matsumoto K, Sugisaki T, Boyle MD |title=Nephritis-associated plasmin receptor and acute poststreptococcal glomerulonephritis: characterization of the antigen and associated immune response |journal=J. Am. Soc. Nephrol. |volume=15 |issue=7 |pages=1785–93 |date=July 2004 |pmid=15213266 |doi= |url=}}</ref><ref name="pmid20708459">{{cite journal |vauthors=Oda T, Yoshizawa N, Yamakami K, Tamura K, Kuroki A, Sugisaki T, Sawanobori E, Higashida K, Ohtomo Y, Hotta O, Kumagai H, Miura S |title=Localization of nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis |journal=Hum. Pathol. |volume=41 |issue=9 |pages=1276–85 |date=September 2010 |pmid=20708459 |doi=10.1016/j.humpath.2010.02.006 |url=}}</ref> | ||
**Streptococcal pyrogenic exotoxin B | **[[Streptococcal Infections|Streptococcal]] pyrogenic [[Exotoxins|exotoxin]] B | ||
**Nephritis-associated plasmin receptor | **[[Nephritis]]-associated plasmin receptor | ||
The mechanism which leads to immunologic injury to the glomerulus are:<ref name="pmid17342179">{{cite journal |vauthors=Rodríguez-Iturbe B, Batsford S |title=Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet |journal=Kidney Int. |volume=71 |issue=11 |pages=1094–104 |date=June 2007 |pmid=17342179 |doi=10.1038/sj.ki.5002169 |url=}}</ref> | The mechanism which leads to [[Immunological|immunologic]] injury to the [[glomerulus]] are:<ref name="pmid17342179">{{cite journal |vauthors=Rodríguez-Iturbe B, Batsford S |title=Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet |journal=Kidney Int. |volume=71 |issue=11 |pages=1094–104 |date=June 2007 |pmid=17342179 |doi=10.1038/sj.ki.5002169 |url=}}</ref> | ||
*There is deposition of immune complexes with streptococcal antigenic components | *There is deposition of [[immune complexes]] with [[streptococcal]] antigenic components | ||
*Immune complexes are deposited in glomerular basement membrane and antibodies bind to the GBM | *[[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 | *Further antigen reacts with [[antibodies]] bind to GBM and cross glomerular membranes | ||
==Associated Conditions== | ==Associated Conditions== | ||
Revision as of 20:24, 14 June 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 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
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.