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On gross pathology, HIV-associated nephropathy is characterized as the renal being pale, unevenly enlarged, having a smooth cortical surface and tubulars that are dilated.<ref name="pmid2770114">{{cite journal| author=D'Agati V, Suh JI, Carbone L, Cheng JT, Appel G| title=Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study. | journal=Kidney Int | year= 1989 | volume= 35 | issue= 6 | pages= 1358-70 | pmid=2770114 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2770114  }}</ref>  
On gross pathology, HIV-associated nephropathy is characterized as the renal being pale, unevenly enlarged, having a smooth cortical surface and tubulars that are dilated.<ref name="pmid2770114">{{cite journal| author=D'Agati V, Suh JI, Carbone L, Cheng JT, Appel G| title=Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study. | journal=Kidney Int | year= 1989 | volume= 35 | issue= 6 | pages= 1358-70 | pmid=2770114 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2770114  }}</ref>  
==Microscopic Pathology==
==Microscopic Pathology==
{| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
| bgcolor="#94e65d"|'''Light Microscopy'''<ref name="pmid274773643">{{cite journal| author=Fogo AB, Lusco MA, Najafian B, Alpers CE| title=AJKD Atlas of Renal Pathology: HIV-Associated Immune Complex Kidney Disease (HIVICK). | journal=Am J Kidney Dis | year= 2016 | volume= 68 | issue= 2 | pages= e9-e10 | pmid=27477364 | doi=10.1053/j.ajkd.2016.06.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27477364  }}</ref>|| bgcolor="#94e65d"|'''Electron Microscopy'''<ref name="pmid274773642">{{cite journal| author=Fogo AB, Lusco MA, Najafian B, Alpers CE| title=AJKD Atlas of Renal Pathology: HIV-Associated Immune Complex Kidney Disease (HIVICK). | journal=Am J Kidney Dis | year= 2016 | volume= 68 | issue= 2 | pages= e9-e10 | pmid=27477364 | doi=10.1053/j.ajkd.2016.06.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27477364  }}</ref> || bgcolor="#94e65d"|'''Immunofluorescence'''<ref name="pmid274773644">{{cite journal| author=Fogo AB, Lusco MA, Najafian B, Alpers CE| title=AJKD Atlas of Renal Pathology: HIV-Associated Immune Complex Kidney Disease (HIVICK). | journal=Am J Kidney Dis | year= 2016 | volume= 68 | issue= 2 | pages= e9-e10 | pmid=27477364 | doi=10.1053/j.ajkd.2016.06.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27477364  }}</ref>
|-
| bgcolor="#ececec"|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.|| bgcolor="#ececec"|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). || bgcolor="#ececec" |Immune deposits that show a limited nonspecific deposition (IgM and C3 in collapsed segments) or no deposits. Visceral 
|}
On microscopic histological analysis, focal segmental glomerulosclerosis, tubuointerstital injury, and microcystic tubular dilation are characteristics findings of HIV-associated nephropathy.<ref name="pmid2770114">{{cite journal| author=D'Agati V, Suh JI, Carbone L, Cheng JT, Appel G| title=Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study. | journal=Kidney Int | year= 1989 | volume= 35 | issue= 6 | pages= 1358-70 | pmid=2770114 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2770114  }}</ref>
On microscopic histological analysis, focal segmental glomerulosclerosis, tubuointerstital injury, and microcystic tubular dilation are characteristics findings of HIV-associated nephropathy.<ref name="pmid2770114">{{cite journal| author=D'Agati V, Suh JI, Carbone L, Cheng JT, Appel G| title=Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study. | journal=Kidney Int | year= 1989 | volume= 35 | issue= 6 | pages= 1358-70 | pmid=2770114 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2770114  }}</ref>



Revision as of 16:24, 17 March 2017

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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 HIV-1 infected mice expressed similar clinical and pathological characteristics to those affected by 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 found on chromosome 22 is more commonly found in blacks than in any other race.

Environmental factors associated with HIV-associated nephropathy:


Increased risk of developing HIV
Intravenous drug use
Men having sex with men
Having more than one sexual partner


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.[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 dilated.[3]

Microscopic Pathology

Light Microscopy[4] Electron Microscopy[5] Immunofluorescence[6]
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. 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). Immune deposits that show a limited nonspecific deposition (IgM and C3 in collapsed segments) or no deposits. Visceral





On microscopic histological analysis, focal segmental glomerulosclerosis, tubuointerstital injury, and microcystic tubular dilation are characteristics findings of HIV-associated nephropathy.[3]

References

  1. 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.
  2. 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.
  3. 3.0 3.1 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.
  4. Fogo AB, Lusco MA, Najafian B, Alpers CE (2016). "AJKD Atlas of Renal Pathology: HIV-Associated Immune Complex Kidney Disease (HIVICK)". Am J Kidney Dis. 68 (2): e9–e10. doi:10.1053/j.ajkd.2016.06.003. PMID 27477364.
  5. Fogo AB, Lusco MA, Najafian B, Alpers CE (2016). "AJKD Atlas of Renal Pathology: HIV-Associated Immune Complex Kidney Disease (HIVICK)". Am J Kidney Dis. 68 (2): e9–e10. doi:10.1053/j.ajkd.2016.06.003. PMID 27477364.
  6. Fogo AB, Lusco MA, Najafian B, Alpers CE (2016). "AJKD Atlas of Renal Pathology: HIV-Associated Immune Complex Kidney Disease (HIVICK)". Am J Kidney Dis. 68 (2): e9–e10. doi:10.1053/j.ajkd.2016.06.003. PMID 27477364.

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