Hematuria pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
It is understood that [[glomerular]] hematuria is caused by either the dysfunction or damage of the [[glomerular filtration barrier]](GFB).<ref name="pmid25949932">{{cite journal |vauthors=Yuste C, Gutierrez E, Sevillano AM, Rubio-Navarro A, Amaro-Villalobos JM, Ortiz A, Egido J, Praga M, Moreno JA |title=Pathogenesis of glomerular haematuria |journal=World J Nephrol |volume=4 |issue=2 |pages=185–95 |date=May 2015 |pmid=25949932 |pmc=4419128 |doi=10.5527/wjn.v4.i2.185 |url=}}</ref> | It is understood that [[glomerular]] hematuria is caused by either the dysfunction or damage of the [[glomerular filtration barrier]](GFB).<ref name="pmid25949932">{{cite journal |vauthors=Yuste C, Gutierrez E, Sevillano AM, Rubio-Navarro A, Amaro-Villalobos JM, Ortiz A, Egido J, Praga M, Moreno JA |title=Pathogenesis of glomerular haematuria |journal=World J Nephrol |volume=4 |issue=2 |pages=185–95 |date=May 2015 |pmid=25949932 |pmc=4419128 |doi=10.5527/wjn.v4.i2.185 |url=}}</ref> | ||
Revision as of 21:54, 19 July 2021
Template:Pathophysiology Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Adnan Ezici, M.D[2]
Overview
Pathophysiology
Pathogenesis
It is understood that glomerular hematuria is caused by either the dysfunction or damage of the glomerular filtration barrier(GFB).[1]
- Major components of GFB include:
- Endothelial surface layer (composed of glycosaminoglycans)
- Endothelial cells
- Glomerular basement membrane (GBM)
- Slit diaphragms
- Subpodocyte space
The pathophsiologic mechanism of glomerular hematuria might be further classified into 6 subtype depends on the primary and histopathologic localization.[1]
- Injuries of the glomerular endothelial cell and surface layer
- Primary and secondary GBM disorders
- Diseases that can cause mesangial deposition
- Diseases that can cause subendothelial and subepithelial deposition
- Podocyte-associated disorders
- Miscellaneous
Genetics
Molecular defects involved in the pathogenesis of glomerular hematuria include:[1]
Diseases with structural GBM damage
- In the pathogenesis of alport syndrome:
- COL4A5 (X linked)
- COL4A3/COL4A4 (autosomal recessive)
- In the pathogenesis of thin basement membrane disease:
- COL4A3/COL4A4
- In the pathogenesis of hereditary angiopathy, nephropathy, aneurysms, and muscle cramps syndrome:
- COL4A1
Diseases with structural podocyte damage
- In the pathogenesis of MYH9-related disorder:
- Non muscle myosin IIA heavy chain
Storage disorders
- In the pathogenesis of fibronectin glomerulonephritis:
- Fibronectin
- In the pathogenesis of fibrillary glomerulonephritis:
- 10-30 nm fibrils
- In the pathogenesis of fabry’s disease:
- lysosomal storage
- In the pathogenesis of immunotactoid glomerulonephritis:
- Fibrils that are > 30 nm
Autoimmune disorders
- In the pathogenesis of ANCA (antineutrophil cytoplasmic antibodies):
- Antibodies against endothelium
- In the pathogenesis of anti-GBM:
- Antibodies against COL4
Complement mediated disorders
- In the pathogenesis of C3 glomerulopathy:
- Alternative pathway
Infectious (endocapillary) diseases
- In the pathogenesis of IgA nephritis:
- Galactose-deficient IgA1
Gross Pathology
Microscopic Pathology
References
- ↑ 1.0 1.1 1.2 Yuste C, Gutierrez E, Sevillano AM, Rubio-Navarro A, Amaro-Villalobos JM, Ortiz A, Egido J, Praga M, Moreno JA (May 2015). "Pathogenesis of glomerular haematuria". World J Nephrol. 4 (2): 185–95. doi:10.5527/wjn.v4.i2.185. PMC 4419128. PMID 25949932.