HIV associated nephropathy pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathogenesis== | ==Pathogenesis== | ||
The pathogenesis of HIV-associated nephropathy is heavily dependent upon viral, genetic, and enviornmental co factors. | The pathogenesis of HIV-associated nephropathy is heavily dependent upon viral, genetic, and enviornmental co factors.<ref name="pmid9692355">{{cite journal| author=Schwartz EJ, Klotman PE| title=Pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy. | journal=Semin Nephrol | year= 1998 | volume= 18 | issue= 4 | pages= 436-45 | pmid=9692355 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9692355 }}</ref> | ||
'''Viral:''' | '''Viral:''' | ||
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Environmental factors that are associated with HIV-associated nephropathy, include intravenous drug abuse, men having sex with other men, and those who have more than one sexual partner are at increased risk in the development of HIV. | Environmental factors that are associated with HIV-associated nephropathy, include intravenous drug abuse, men having sex with other men, and those who have more than one sexual partner are at increased risk in the development of HIV. | ||
The development of HIV-associated nephropathy, is suggestive upon HIV-1 affecting the renal epithelium. This reasoning provides that localized replication of the virus in the renal epithelium is needed for the development of HIV-associated nephropathy. However, the mechanism of how the virus induces renal injure is still not conclusive. However, what is known is that in order for the virus to proliferate, the virus's gene products trigger the process of apoptosis. In some studies conducted, HIV protease that is encoded in the pol gene, is found to cleave Bcl-2, which lead to apoptosis of the renal cells in a monkey. However, this still not well established. The role cytokines play in the mechanism of HIV-associated nephropathy is still not clearly known, and is seen as non essential in HIV-associated nephropathy. | The development of HIV-associated nephropathy, is suggestive upon HIV-1 affecting the renal epithelium. This reasoning provides that localized replication of the virus in the renal epithelium is needed for the development of HIV-associated nephropathy. However, the mechanism of how the virus induces renal injure is still not conclusive. However, what is known is that in order for the virus to proliferate, the virus's gene products trigger the process of apoptosis. In some studies conducted, HIV protease that is encoded in the pol gene, is found to cleave Bcl-2, which lead to apoptosis of the renal cells in a monkey. However, this still not well established.<ref name="pmid8790371">{{cite journal| author=Strack PR, Frey MW, Rizzo CJ, Cordova B, George HJ, Meade R et al.| title=Apoptosis mediated by HIV protease is preceded by cleavage of Bcl-2. | journal=Proc Natl Acad Sci U S A | year= 1996 | volume= 93 | issue= 18 | pages= 9571-6 | pmid=8790371 | doi= | pmc=38469 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8790371 }}</ref> The role cytokines play in the mechanism of HIV-associated nephropathy is still not clearly known, and is seen as non essential in HIV-associated nephropathy.<ref name="pmid9692355" /> | ||
==Associated Conditions== | ==Associated Conditions== | ||
Revision as of 17:56, 20 December 2016
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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]
Overview
Pathogenesis
The pathogenesis of HIV-associated nephropathy is heavily dependent upon viral, genetic, and enviornmental co factors.[1]
Viral:
HIV-1 is the strongest risk factor that is associated with the development of HIV-associated nephropathy. It has been found through murine studies, that showed HIV-1 infected mice expressed similar renal disease clinical and pathological characteristics of patients who had HIV-associated nephropathy.
Genetic and Enviornmental Co factors:
Genetic factors most certainly play an intricate role in disease progression. Approximately 90% of patient infected with HIV-associated nephropathy are black. This suggests a strong racial predilection for HIV-associated nephropathy. It is also important to note that through genetic tests APOL1 gene that is found on chromosome 22 is found more commonly in blacks than in any other races.
Environmental factors that are associated with HIV-associated nephropathy, include intravenous drug abuse, men having sex with other men, and those who have more than one sexual partner are at increased risk in the development of HIV.
The development of HIV-associated nephropathy, is suggestive upon HIV-1 affecting the renal epithelium. This reasoning provides that localized replication of the virus in the renal epithelium is needed for the development of HIV-associated nephropathy. However, the mechanism of how the virus induces renal injure is still not conclusive. However, what is known is that in order for the virus to proliferate, the virus's gene products trigger the process of apoptosis. In some studies conducted, HIV protease that is encoded in the pol gene, is found to cleave Bcl-2, which lead to apoptosis of the renal cells in a monkey. However, this still not well established.[2] The role cytokines play in the mechanism of HIV-associated nephropathy is still not clearly known, and is seen as non essential in HIV-associated nephropathy.[1]
Associated Conditions
The following are conditions that are associated with HIV-associated nephropathy:
Gross Pathology
On gross pathology, HIV-associated nephropathy is characterized as the renal being pale, unevenly enlarged, having a smooth cortical surface and tubulars that are dilatated.
Microscopic Pathology
On microscopic histological analysis, focal segmental glomerulosclerosis, tubuointerstital injury, and microcystic tubular dilation are characteristics findings of HIV-associated nephropathy.[3]
References
- ↑ 1.0 1.1 Schwartz EJ, Klotman PE (1998). "Pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy". Semin Nephrol. 18 (4): 436–45. PMID 9692355.
- ↑ Strack PR, Frey MW, Rizzo CJ, Cordova B, George HJ, Meade R; et al. (1996). "Apoptosis mediated by HIV protease is preceded by cleavage of Bcl-2". Proc Natl Acad Sci U S A. 93 (18): 9571–6. PMC 38469. PMID 8790371.
- ↑ D'Agati V, Suh JI, Carbone L, Cheng JT, Appel G (1989). "Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study". Kidney Int. 35 (6): 1358–70. PMID 2770114.