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__NOTOC__
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{{HIV associated nephropathy}}
{{HIV associated nephropathy}}
{{CMG}}{{APM}};{{AE}}{{KW}}
{{CMG}}{{APM}};{{AE}}{{KW}}{{SHA}}
==Overview==
==Overview==
Currently there are no known established causes of HIV-associated nephropathy. However, the genetic component, a key to the pathogenesis of the disease in blacks but not in other races is a factor that is seen in HIV-associated nephropathy.<ref name="pmid104693892">{{cite journal| author=Klotman PE| title=HIV-associated nephropathy. | journal=Kidney Int | year= 1999 | volume= 56 | issue= 3 | pages= 1161-76 | pmid=10469389 | doi=10.1046/j.1523-1755.1999.00748.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10469389  }}</ref>
Currently there are no known established causes of HIV-associated nephropathy.<ref name="pmid104693893" /> However, the [[Genetics|genetic]] component, a key to the pathogenesis of the disease in blacks but not in other races is a factor that is seen in HIV-associated nephropathy. High risk [[Allele|alleles]] G1 (a missense [[mutation]]) and G2 (a frameshift deletion) for [[APOL1|Apolipoprotein 1 (APOL1)]] are associated with HIVAN (APOL1 gene is on [[chromosome]] 22).<ref name="pmid21997394" />


==Causes==
==Causes==
Currently there are no known established causes of HIV-associated nephropathy. However, the genetic component, a key to the pathogenesis of the disease in blacks but not in other races is a factor that is seen in HIV-associated nephropathy.<ref name="pmid104693893">{{cite journal| author=Klotman PE| title=HIV-associated nephropathy. | journal=Kidney Int | year= 1999 | volume= 56 | issue= 3 | pages= 1161-76 | pmid=10469389 | doi=10.1046/j.1523-1755.1999.00748.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10469389  }}</ref> Another cause for HIV-associated nephropathy is the lack of a deletion mutation of CCR5 or CCR2, which is protective form HIV-1 infection.<ref name="pmid8756719">{{cite journal| author=Liu R, Paxton WA, Choe S, Ceradini D, Martin SR, Horuk R et al.| title=Homozygous defect in HIV-1 coreceptor accounts for resistance of some multiply-exposed individuals to HIV-1 infection. | journal=Cell | year= 1996 | volume= 86 | issue= 3 | pages= 367-77 | pmid=8756719 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8756719  }}</ref>  
Currently there are no known established causes of HIV-associated nephropathy. However, the [[Genetics|genetic]] component, a key to the pathogenesis of the disease in blacks but not in other races is a factor that is seen in HIV-associated nephropathy.<ref name="pmid104693893">{{cite journal| author=Klotman PE| title=HIV-associated nephropathy. | journal=Kidney Int | year= 1999 | volume= 56 | issue= 3 | pages= 1161-76 | pmid=10469389 | doi=10.1046/j.1523-1755.1999.00748.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10469389  }}</ref> Another cause for HIV-associated nephropathy is the lack of a deletion [[mutation]] of CCR5 or CCR2, which is protective form HIV-1 infection.<ref name="pmid8756719">{{cite journal| author=Liu R, Paxton WA, Choe S, Ceradini D, Martin SR, Horuk R et al.| title=Homozygous defect in HIV-1 coreceptor accounts for resistance of some multiply-exposed individuals to HIV-1 infection. | journal=Cell | year= 1996 | volume= 86 | issue= 3 | pages= 367-77 | pmid=8756719 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8756719  }}</ref>  


Other factors that are attributed to the development of HIV-associated nephropathy is the use of intravenous drugs, however, this is inconclusive as patients with HIV-associated nephropathy are not all intravenous drug users.<ref name="pmid10469389">{{cite journal| author=Klotman PE| title=HIV-associated nephropathy. | journal=Kidney Int | year= 1999 | volume= 56 | issue= 3 | pages= 1161-76 | pmid=10469389 | doi=10.1046/j.1523-1755.1999.00748.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10469389  }}</ref>
Other factors that are attributed to the development of HIV-associated nephropathy is the use of intravenous drugs, however, this is inconclusive as patients with HIV-associated [[nephropathy]] are not all [[Intravenous drug use|intravenous drug users]].<ref name="pmid3599656">{{cite journal| author=Pardo V, Meneses R, Ossa L, Jaffe DJ, Strauss J, Roth D et al.| title=AIDS-related glomerulopathy: occurrence in specific risk groups. | journal=Kidney Int | year= 1987 | volume= 31 | issue= 5 | pages= 1167-73 | pmid=3599656 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3599656  }}</ref><ref name="pmid10469389">{{cite journal| author=Klotman PE| title=HIV-associated nephropathy. | journal=Kidney Int | year= 1999 | volume= 56 | issue= 3 | pages= 1161-76 | pmid=10469389 | doi=10.1046/j.1523-1755.1999.00748.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10469389  }}</ref><ref name="pmid3561458">{{cite journal| author=Rao TK, Friedman EA, Nicastri AD| title=The types of renal disease in the acquired immunodeficiency syndrome. | journal=N Engl J Med | year= 1987 | volume= 316 | issue= 17 | pages= 1062-8 | pmid=3561458 | doi=10.1056/NEJM198704233161705 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3561458  }}</ref>
 
High risk alleles G1 (a missense mutation) and G2 (a frameshift deletion) for [[APOL1|Apolipoprotein 1 (APOL1)]] are associated with HIVAN ([[APOL1]] gene is on [[chromosome]] 22).<ref name="pmid21997394">{{cite journal| author=Kopp JB, Nelson GW, Sampath K, Johnson RC, Genovese G, An P | display-authors=etal| title=APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy. | journal=J Am Soc Nephrol | year= 2011 | volume= 22 | issue= 11 | pages= 2129-37 | pmid=21997394 | doi=10.1681/ASN.2011040388 | pmc=3231787 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21997394  }} </ref>


==References==
==References==
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[[Category:HIV/AIDS]]
[[Category:HIV/AIDS]]
[[Category:Immune system disorders]]
[[Category:Immune system disorders]]
[[Category:Infectious disease]]
 
[[category:viral diseases]]
[[category:viral diseases]]

Latest revision as of 19:19, 30 June 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Ali Poyan Mehr, M.D. [2];Associate Editor(s)-in-Chief: Krzysztof Wierzbicki M.D. [3]Shakiba Hassanzadeh, MD[4]

Overview

Currently there are no known established causes of HIV-associated nephropathy.[1] However, the genetic component, a key to the pathogenesis of the disease in blacks but not in other races is a factor that is seen in HIV-associated nephropathy. High risk alleles G1 (a missense mutation) and G2 (a frameshift deletion) for Apolipoprotein 1 (APOL1) are associated with HIVAN (APOL1 gene is on chromosome 22).[2]

Causes

Currently there are no known established causes of HIV-associated nephropathy. However, the genetic component, a key to the pathogenesis of the disease in blacks but not in other races is a factor that is seen in HIV-associated nephropathy.[1] Another cause for HIV-associated nephropathy is the lack of a deletion mutation of CCR5 or CCR2, which is protective form HIV-1 infection.[3]

Other factors that are attributed to the development of HIV-associated nephropathy is the use of intravenous drugs, however, this is inconclusive as patients with HIV-associated nephropathy are not all intravenous drug users.[4][5][6]

High risk alleles G1 (a missense mutation) and G2 (a frameshift deletion) for Apolipoprotein 1 (APOL1) are associated with HIVAN (APOL1 gene is on chromosome 22).[2]

References

  1. 1.0 1.1 Klotman PE (1999). "HIV-associated nephropathy". Kidney Int. 56 (3): 1161–76. doi:10.1046/j.1523-1755.1999.00748.x. PMID 10469389.
  2. 2.0 2.1 Kopp JB, Nelson GW, Sampath K, Johnson RC, Genovese G, An P; et al. (2011). "APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy". J Am Soc Nephrol. 22 (11): 2129–37. doi:10.1681/ASN.2011040388. PMC 3231787. PMID 21997394.
  3. Liu R, Paxton WA, Choe S, Ceradini D, Martin SR, Horuk R; et al. (1996). "Homozygous defect in HIV-1 coreceptor accounts for resistance of some multiply-exposed individuals to HIV-1 infection". Cell. 86 (3): 367–77. PMID 8756719.
  4. Pardo V, Meneses R, Ossa L, Jaffe DJ, Strauss J, Roth D; et al. (1987). "AIDS-related glomerulopathy: occurrence in specific risk groups". Kidney Int. 31 (5): 1167–73. PMID 3599656.
  5. Klotman PE (1999). "HIV-associated nephropathy". Kidney Int. 56 (3): 1161–76. doi:10.1046/j.1523-1755.1999.00748.x. PMID 10469389.
  6. Rao TK, Friedman EA, Nicastri AD (1987). "The types of renal disease in the acquired immunodeficiency syndrome". N Engl J Med. 316 (17): 1062–8. doi:10.1056/NEJM198704233161705. PMID 3561458.

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