Focal segmental glomerulosclerosis causes: Difference between revisions
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==Causes== | ==Causes== | ||
According to D'Agati and colleagues<ref name="pmid12704572">{{cite journal| author=D'Agati V| title=Pathologic classification of focal segmental glomerulosclerosis. | journal=Semin Nephrol | year= 2003 | volume= 23 | issue= 2 | pages= 117-34 | pmid=12704572 | doi=10.1053/snep.2003.50012 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12704572 }} </ref>, FSGS may be primary of secondary. Primary FSGS is defined as idiopathic FSGS, whereas secondary FSGS is defined as FSGS | According to D'Agati and colleagues<ref name="pmid12704572">{{cite journal| author=D'Agati V| title=Pathologic classification of focal segmental glomerulosclerosis. | journal=Semin Nephrol | year= 2003 | volume= 23 | issue= 2 | pages= 117-34 | pmid=12704572 | doi=10.1053/snep.2003.50012 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12704572 }} </ref>, FSGS may be primary of secondary. Primary FSGS is defined as idiopathic FSGS, whereas secondary FSGS is defined as FSGS other etiologies.<ref name="pmid12704572">{{cite journal| author=D'Agati V| title=Pathologic classification of focal segmental glomerulosclerosis. | journal=Semin Nephrol | year= 2003 | volume= 23 | issue= 2 | pages= 117-34 | pmid=12704572 | doi=10.1053/snep.2003.50012 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12704572 }} </ref> | ||
The following list shows all the causes of FSGS<ref name="pmid23871408">{{cite journal| author=Beck L, Bomback AS, Choi MJ, Holzman LB, Langford C, Mariani LH et al.| title=KDOQI US commentary on the 2012 KDIGO clinical practice guideline for glomerulonephritis. | journal=Am J Kidney Dis | year= 2013 | volume= 62 | issue= 3 | pages= 403-41 | pmid=23871408 | doi=10.1053/j.ajkd.2013.06.002 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23871408 }} </ref>: | |||
===Primary (Idiopathic) FSGS=== | |||
* | ===Secondary FSGS=== | ||
* | ====Familial==== | ||
* | *Mutations in alpha actinin 4 | ||
* | *Mutations in NPHS1 (nephrin) | ||
** | *Mutations in NPHS2 (podocin) | ||
** | *Mutations in WT-1 | ||
*Mutations in TRPC6 | |||
* | *Mutations in SCARB2 (LIMP2) | ||
** | *Mutations in INF2 (formin) | ||
* | *Mutations in CD2-associated protein | ||
*Mitochondrial cytopathies | |||
* | ====Virus Associated==== | ||
**Reduced | *HIV | ||
*Parvovirus B19 | |||
*CMV | |||
* | ====Medication==== | ||
* | *Heroin | ||
*Interferon-alpha | |||
*Lithium | |||
* | *Pamidronate/aledronate | ||
*Anabolic steroids | |||
====Adaptive Structural-Functional Responses==== | |||
=====Reduced Kidney Size===== | |||
*Oligomeganephronia | |||
*Unilateral kidney agenesis | |||
*Kidney dysplasia | |||
*Cortical necrosis | |||
* | *Reflux nephropathy | ||
*Surgical kidney ablation | |||
*Chronic allograft nephropathy | |||
*Any advanced kidney disease with reduction in functioning nephrons | |||
=====Initially Normal Kidney Mass===== | |||
** | *Diabetes mellitus | ||
** | *Hypertension | ||
*Obesity | |||
*Cyanotic congenital heart disease | |||
**Thrombotic | *Sickle cell anemia | ||
====Malignancy==== | |||
*Lymphoma | |||
====Nonspecific Pattern of FSGS Caused by Kidney Scarring in Glomerular Disease==== | |||
*Focal proliferative glomerulonephritis | |||
**IgA nephropathy | |||
**Lupus nephritis | |||
**Pauci-immune focal necrotizing and crescentic glomerulonephritis | |||
**Alport's syndrome (hereditary nephritis) | |||
**Membranous nephropathy | |||
**Thrombotic microangiopathy | |||
==References== | ==References== | ||
Revision as of 23:56, 3 December 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief:’’’ Cafer Zorkun, M.D., Ph.D. [2]
Overview
Causes
According to D'Agati and colleagues[1], FSGS may be primary of secondary. Primary FSGS is defined as idiopathic FSGS, whereas secondary FSGS is defined as FSGS other etiologies.[1] The following list shows all the causes of FSGS[2]:
Primary (Idiopathic) FSGS
Secondary FSGS
Familial
- Mutations in alpha actinin 4
- Mutations in NPHS1 (nephrin)
- Mutations in NPHS2 (podocin)
- Mutations in WT-1
- Mutations in TRPC6
- Mutations in SCARB2 (LIMP2)
- Mutations in INF2 (formin)
- Mutations in CD2-associated protein
- Mitochondrial cytopathies
Virus Associated
- HIV
- Parvovirus B19
- CMV
Medication
- Heroin
- Interferon-alpha
- Lithium
- Pamidronate/aledronate
- Anabolic steroids
Adaptive Structural-Functional Responses
Reduced Kidney Size
- Oligomeganephronia
- Unilateral kidney agenesis
- Kidney dysplasia
- Cortical necrosis
- Reflux nephropathy
- Surgical kidney ablation
- Chronic allograft nephropathy
- Any advanced kidney disease with reduction in functioning nephrons
Initially Normal Kidney Mass
- Diabetes mellitus
- Hypertension
- Obesity
- Cyanotic congenital heart disease
- Sickle cell anemia
Malignancy
- Lymphoma
Nonspecific Pattern of FSGS Caused by Kidney Scarring in Glomerular Disease
- Focal proliferative glomerulonephritis
- IgA nephropathy
- Lupus nephritis
- Pauci-immune focal necrotizing and crescentic glomerulonephritis
- Alport's syndrome (hereditary nephritis)
- Membranous nephropathy
- Thrombotic microangiopathy
References
- ↑ 1.0 1.1 D'Agati V (2003). "Pathologic classification of focal segmental glomerulosclerosis". Semin Nephrol. 23 (2): 117–34. doi:10.1053/snep.2003.50012. PMID 12704572.
- ↑ Beck L, Bomback AS, Choi MJ, Holzman LB, Langford C, Mariani LH; et al. (2013). "KDOQI US commentary on the 2012 KDIGO clinical practice guideline for glomerulonephritis". Am J Kidney Dis. 62 (3): 403–41. doi:10.1053/j.ajkd.2013.06.002. PMID 23871408.