Post-streptococcal glomerulonephritis pathophysiology: Difference between revisions
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{{CMG}} {{AE}} {{MKK}} | {{CMG}} {{AE}} {{MKK}} | ||
==Overview== | ==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 [[Immunological|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== | ==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 streptococcal infection|Group A streptococc]]<nowiki/>i which cause PSGN include: | |||
*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 | |||
**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 | ||
==Gross Pathology== | ==Gross Pathology== | ||
*On gross pathology, following features are seen: | *On gross pathology, following features are seen: | ||
**Kidney are enlarged and pale in color | **[[Kidney]] are enlarged and pale in color | ||
==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 [[Neutrophil|neutrophils]] and [[macrophages]] | ||
*There is a proliferation of mesangial and endothelial cells | *There is a proliferation of [[Mesangial cells|mesangial]] and [[endothelial cells]] | ||
*There is a swelling of endothelial cells and presence of inflammatory cells obstructs capillary lumina | *There is a swelling of [[endothelial cells]] and presence of [[inflammatory cells]] obstructs [[capillary]] lumina | ||
*There is an accumulation of mononuclear | *There is an accumulation of [[Mononuclear cells|mononuclear]] leukocytic infiltrate and [[edema]] in the [[interstitium]] | ||
[[Image:Post-infectious glomerulonephritis - very high mag (1).jpg|200px|centre|Source:By Nephron - Own work<ref/ https://commons.wikimedia.org/w/index.php?curid=17591464 ref>>]] | |||
I'''mmunofluorescence findings''' | |||
*During the early phase of [[Post-streptococcal glomerulonephritis|post-infectious glomerulonephritis]], there is the starry sky appearance due to deposition of [[C3 (complement)|C3]] and [[IgG]] in the [[capillary]] walls and [[Mesangial cell|mesangial]] areas | |||
*In later stages, there is a predominance of [[C3 (complement)|C3]] deposition in [[mesangium]]<ref name="pmid7067173">{{cite journal |vauthors=Sorger K, Gessler U, Hübner FK, Köhler H, Schulz W, Stühlinger W, Thoenes GH, Thoenes W |title=Subtypes of acute postinfectious glomerulonephritis. Synopsis of clinical and pathological features |journal=Clin. Nephrol. |volume=17 |issue=3 |pages=114–28 |date=March 1982 |pmid=7067173 |doi= |url=}}</ref> | |||
==References== | ==References== | ||
Latest revision as of 14:59, 18 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
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
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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.