<s>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></s>
'''<s>Viral:</s>'''
<s>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 HIV-1 infected mice expressed similar clinical and pathological characteristics to those affected by HIV-associated nephropathy.</s>
<s>'''Genetic and Enviornmental Co factors''':</s>
<s>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 found on chromosome 22 is more commonly found in blacks than in any other race.</s>
<s>Environmental factors associated with HIV-associated nephropathy:</s>
| bgcolor="#94e65d"|'''<s>Increased risk of developing HIV</s>'''
|-
| bgcolor="#ffffff"|<s>Intravenous drug use</s>
|-
| bgcolor="#ffffff"|<s>Men having sex with men</s>
|-
| bgcolor="#ffffff"|<s>Having more than one sexual partner</s>
|}
<s><br />
It is hypothesized that HIV-associated nephropathy is attributed to the HIV-1 virus attacking the renal epithelium, suggesting that a localized replication of the virus of the renal epithelium is needed. However, the mechanism of how the virus induces renal injure is still inconclusive. However, what is known is that in order for the virus to proliferate, the virus induces apoptosis. In various conducted studies, HIV protease (encoded in the pol gene) is found to cleave Bcl-2 and inducing apoptosis of the renal cells monkeys. 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" /></s>
HIV associated nephropathy (HIVAN) is mostly seen in patients of African decent.<ref name="pmid24655211" />
HIV associated nephropathy (HIVAN) is mostly seen in patients of African decent.<ref name="pmid24655211" />
| bgcolor="#ececec"|<s>characteristically seen as a visceral epithelium that displays hyperplasia and hypertrophy; due a segmental or global glomerular tuft collapse. When examining the hypertrophic portions of the visceral epithelium protein droplets are seen.</s>|| bgcolor="#ececec" |<s>a glomerular basement membrane that is wrinkled and collapsed; displaying vacuoles and protein droplets hypertrophic and hyperplastic portions of the visceral epithelium, foot process effacements that are quite extensive and tubuloreticular aggregates that are present in endothelial cells. However, not all patients display tubuloreticular aggregates as the pattern is no seen in patients who express low viral loads (due to combined antiretroviral therapy).</s>|| bgcolor="#ececec" |<s>Immune deposits that show a limited nonspecific deposition (IgM and C3 in collapsed segments) or no deposits. Visceral</s>
|}
On [[microscopic]] [[pathology]], kidneys in HIV-associated nephropathy have the following features:<ref name="pmid2770114" />
On [[microscopic]] [[pathology]], kidneys in HIV-associated nephropathy have the following features:<ref name="pmid2770114" />
HIV associated nephropathy (HIVAN) is mostly seen in patients of African decent. Some factors involving HIV associated nephropathy (HIVAN) pathology includes: HIV-1 replication in the kidney, HIV-1 gene products, increased proliferation, apoptosis and dedifferentiation of podocytes and polymorphysim of Apolipoprotein 1 (APOL1) polymorphysim gene.
Pathogenesis
HIV associated nephropathy (HIVAN) is mostly seen in patients of African decent.[1]
Some factors involving HIV associated nephropathy (HIVAN) pathology includes:[1]
Pathogenesis
Viral Factors
Proviral DNA has been reported in the renal tissue of all patients with HIV associated nephropathy (HIVAN) even in those with negative HIV-1 RNA levels in plasma.[2]
HIV-1 can replicate in the kidney even in those patients who are on treatment.[3]
HIV-1 gene products such as nef (negative effector) and vpr (viral protein r) are reported to be involved in the pathogenesis.[4]
Increased proliferation, apoptosis and dedifferentiation of podocytes have been reported in HIVAN.[3]
Genetic Factor
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).[5]
Gross Pathology
On gross pathology, kidneys in HIV-associated nephropathy have the following features:[6]
Pale
Unevenly enlarged
Smooth cortical surface.
Microscopic Pathology
On microscopicpathology, kidneys in HIV-associated nephropathy have the following features:[6]