Lupus nephritis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
Immune system, genetic, and environmental factors are considered in the pathogenesis of SLE. | |||
- Immune system: | |||
* Plasma cells and B lymphocytes: | |||
Numbers of plasma cells(PC) are high in the kidney medulla of patients with severe lupus nephritis( LN). PCs and B cells produce auto antibodies. Increased number and activation of B cells may cause worsening proteinuria and severe damage. | |||
B cells in LN patients have more MicroRNAs (miRNAs) which modulate gene expression <ref name="pmid15211354">{{cite journal |vauthors=He L, Hannon GJ |title=MicroRNAs: small RNAs with a big role in gene regulation |journal=Nat. Rev. Genet. |volume=5 |issue=7 |pages=522–31 |date=July 2004 |pmid=15211354 |doi=10.1038/nrg1379 |url=}}</ref>. Over expression of the miR-30a could lower the level of Lyn (type of protein tyrosine kinases), and lower level of Lyn may cause deposition of immune complexes in the kidney <ref name="pmid11166177">{{cite journal |vauthors=Yu CC, Yen TS, Lowell CA, DeFranco AL |title=Lupus-like kidney disease in mice deficient in the Src family tyrosine kinases Lyn and Fyn |journal=Curr. Biol. |volume=11 |issue=1 |pages=34–8 |date=January 2001 |pmid=11166177 |doi= |url=}}</ref><ref name="pmid23450709">{{cite journal |vauthors=Liu Y, Dong J, Mu R, Gao Y, Tan X, Li Y, Li Z, Yang G |title=MicroRNA-30a promotes B cell hyperactivity in patients with systemic lupus erythematosus by direct interaction with Lyn |journal=Arthritis Rheum. |volume=65 |issue=6 |pages=1603–11 |date=June 2013 |pmid=23450709 |doi=10.1002/art.37912 |url=}}</ref>. | |||
* Macrophages: | |||
Increase expression of Sialoadhesin (Sn), a macrophage-restricted adhesion molecule may play a role in causing sever LN. | |||
* Inflammatory cytokines: | |||
TNF-like weak inducer of apoptosis (TWEAK), a member of the TNF superfamily. TWEAK is an inflammatory cytokine that is believed to play an important role in LN. | |||
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3]. | *It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3]. | ||
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host. | *[Pathogen name] is usually transmitted via the [transmission route] route to the human host. | ||
Revision as of 17:54, 12 June 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2], Raviteja Guddeti, M.B.B.S. [3]
Overview
Pathophysiology
Systemic lupus erythematosus (SLE, or lupus) is an autoimmune disease. This means there is a problem with the body's immune system.
Normally, the immune system helps protect the body from harmful substances. But in patients with an autoimmune disease, the immune system cannot tell the difference between harmful substances and healthy ones. As a result, the immune system attacks otherwise healthy cells and tissue.
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
Immune system, genetic, and environmental factors are considered in the pathogenesis of SLE.
- Immune system:
- Plasma cells and B lymphocytes:
Numbers of plasma cells(PC) are high in the kidney medulla of patients with severe lupus nephritis( LN). PCs and B cells produce auto antibodies. Increased number and activation of B cells may cause worsening proteinuria and severe damage.
B cells in LN patients have more MicroRNAs (miRNAs) which modulate gene expression [1]. Over expression of the miR-30a could lower the level of Lyn (type of protein tyrosine kinases), and lower level of Lyn may cause deposition of immune complexes in the kidney [2][3].
- Macrophages:
Increase expression of Sialoadhesin (Sn), a macrophage-restricted adhesion molecule may play a role in causing sever LN.
- Inflammatory cytokines:
TNF-like weak inducer of apoptosis (TWEAK), a member of the TNF superfamily. TWEAK is an inflammatory cytokine that is believed to play an important role in LN.
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
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, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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Videos
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References
- ↑ He L, Hannon GJ (July 2004). "MicroRNAs: small RNAs with a big role in gene regulation". Nat. Rev. Genet. 5 (7): 522–31. doi:10.1038/nrg1379. PMID 15211354.
- ↑ Yu CC, Yen TS, Lowell CA, DeFranco AL (January 2001). "Lupus-like kidney disease in mice deficient in the Src family tyrosine kinases Lyn and Fyn". Curr. Biol. 11 (1): 34–8. PMID 11166177.
- ↑ Liu Y, Dong J, Mu R, Gao Y, Tan X, Li Y, Li Z, Yang G (June 2013). "MicroRNA-30a promotes B cell hyperactivity in patients with systemic lupus erythematosus by direct interaction with Lyn". Arthritis Rheum. 65 (6): 1603–11. doi:10.1002/art.37912. PMID 23450709.