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HIV associated nephropathy pathophysiology

Introduction

Overview

Overview

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.[1]

Pathogenesis

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

Gross Pathology

On gross pathology, kidneys in HIV-associated nephropathy have the following features:[6]

  • Pale
  • Unevenly enlarged
  • Smooth cortical surface.
Microscopic Pathology

Microscopic Pathology

On microscopic pathology, kidneys in HIV-associated nephropathy have the following features:[6]

Histopathology of HIV-associated nephropathy
Light Microscopy[6] Electron Microscopy[6] Immunofluorescence[6]
    • Wrinkling and folding of the glomerular basement membrane (GBM)
    • Hypertrophied visceral epithelial cells  
    • Visceral epithelial cells foot process effacement.  
    • Numerous tubuloreticular inclusions (TRI)
    • Nuclear bodies

 

References

References

  1. ↑ 1.0 1.1 1.2 Waheed S, Atta MG (2014). “Predictors of HIV-associated nephropathy”. Expert Rev Anti Infect Ther. 12 (5): 555–63. doi:10.1586/14787210.2014.901170. PMID 24655211.
  2. ↑ Izzedine H, Acharya V, Wirden M, Cluzel P, Sene D, Lucas GM; et al. (2011). “Role of HIV-1 DNA levels as clinical marker of HIV-1-associated nephropathies”. Nephrol Dial Transplant. 26 (2): 580–3. doi:10.1093/ndt/gfq414. PMID 20624771.
  3. ↑ 3.0 3.1 Medapalli RK, He JC, Klotman PE (2011). “HIV-associated nephropathy: pathogenesis”. Curr Opin Nephrol Hypertens. 20 (3): 306–11. doi:10.1097/MNH.0b013e328345359a. PMC 3153858. PMID 21358326.
  4. ↑ Atta MG (2010). “Diagnosis and natural history of HIV-associated nephropathy”. Adv Chronic Kidney Dis. 17 (1): 52–8. doi:10.1053/j.ackd.2009.08.005. PMID 20005489.
  5. ↑ 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.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 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.

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