Post-streptococcal glomerulonephritis pathophysiology
Post-streptococcal glomerulonephritis Microchapters |
Differentiating Post-streptococcal glomerulonephritis from other Diseases |
---|
Diagnosis |
Treatment |
Case Studies |
Post-streptococcal glomerulonephritis pathophysiology On the Web |
American Roentgen Ray Society Images of Post-streptococcal glomerulonephritis pathophysiology |
FDA on Post-streptococcal glomerulonephritis pathophysiology |
CDC on Post-streptococcal glomerulonephritis pathophysiology |
Post-streptococcal glomerulonephritis pathophysiology in the news |
Blogs on Post-streptococcal glomerulonephritis pathophysiology |
Directions to Hospitals Treating Post-streptococcal glomerulonephritis |
Risk calculators and risk factors for 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
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: streptococcal pyrogenic exotoxin B (SPEB) and nephritis-associated plasmin receptor (NAPlr).
- Following infection with nephritogenic strains of group A beta-hemolytic streptococcus,
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
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
Overview
Pathophysiology
The exact pathology remains unclear, but it is believed to be Type III hypersensitivity reaction. Immune complexes (antigen-antibody complexes formed during an infection) become lodged in the glomerular basement membrane. Complement activation leads to the destruction of the basement membrane. It has also been proposed that specific antigens from certain nephrotoxic streptococcal infections have a high affinity for basement membrane proteins, giving rise to particularly severe, long-lasting antibody response.