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HIV associated nephropathy

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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: Shakiba Hassanzadeh, MD[3]Krzysztof Wierzbicki M.D. [4]

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Overview

AIDS was first reported in 1981. The first reported cases of HIV-associated nephropathy (HIVAN) were described in 1984. HIV-associated nephropathy (HIVAN) is mostly seen in male patients and of African decent. It is associated with polymorphysim of Apolipoprotein 1 (APOL1) gene. Renal biopsy is the diagnostic study of choice in HIVAN. The treatment of HIV associated nephropathy (HIVAN) includes: combined antiretroviral therapy (cART), renin–angiotensin–aldosterone system (RAAS) blockade, corticosteroids and renal replacement with dialysis.

Historical Perspective

  • AIDS was first reported in 1981.[1][2]
  • The first reported cases of HIV-associated nephropathy (HIVAN) were described in 1984.[3]

Pathophysiology

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.[4]

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.[5]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).[6]

Differentiating HIV associated nephropathy from other Diseases

HIV-associated nephropathy must be differentiated form other diseases that cause focal segmental glomerulonephritis, high grade proteinuria, and elevated serum creatinine levels.

Epidemiology and Demographics

HIV-associated nephropathy (HIVAN) is mostly seen in male patients and of African decent. The prevalence of HIVAN in the population of patients with African descent has been reported to be 3% to 12%.[7]

Risk Factors

The risk factors that attribute to HIV-associated nephropathy are similar to those seen with HIV. Positive predicators for HIV-associated nephropathy include: polymorphysim of Apolipoproetin-1 (APOL1) gene, high viral load, low CD-4 count, proteinuria (nephrotic range), and higher level of renal echogenicity on ultrasound.[4]

Screening

Screening for kidney disease is recommended in high risk populations in all patients with seropositive HIV-1 (upon detection).[8]

Natural History, Complications and Prognosis

HIV-associated nephropathy (HIVAN) will progress to end-stage renal disease (ESRD) in a few weeks to months without treatment. However, early diagnosis and treatment has shown better outcome.[9]

Diagnosis

History and Symptoms

Obtaining a complete history is an important aspect in making a clinical diagnosis of HIV-associated nephropathy. The initial symptoms that are seen in patients presenting with HIV-associated nephropathy are non specific in nature as other glomerular diseases may express similar clinical presentations. The following are symptoms that are seen in HIV-associated nephropathy: fatigue, malaise, anorexia and pruritus.[10]

Physical Examination

A complete physical examination in a patient with HIV-associated nephropathy is dependent on the stage of the disease. Physical examinations findings seen in patients are typically similar to those who are infected with HIV but do not present with renal involvement.

Diagnostic Study of Choice

Renal biopsy is the diagnostic study of choice for HIV-associated nephropathy (HIVAN). Renal biopsy reveals the following findings: collapsing focal segmental glomerulonephritis, significant tubulointerstitial injury, interstitial fibrosis and inflammation and microcystic tubular dilation.[11]

Laboratory Findings

Laboratory findings in HIV-associated nephropathy include: proteinuria, elevated serum creatinine levels, decreased GFR, dyslipidemia, and CD4 counts below 200 cells/mm3.[12][13]

KUB X-ray

There are no x-ray findings associated with HIV associated nephropathy.

CT

There are no CT findings associated with HIV associated nephropathy.

MRI

There are no MRI findings associated with HIV associated nephropathy.

Ultrasound

Renal ultrasound in patients with HIV-associated nephropathy (HIVAN) reveals higher renal echogenicity.[14]

Other Imaging Findings

There are no other imaging findings associated with HIV associated nephropathy.

Other Diagnostic Studies

There are no other diagnostic studies associated with HIV associated nephropathy.

Treatmennt

Medical Therapy

The treatment of HIV associated nephropathy (HIVAN) includes: combined antiretroviral therapy (cART), renin–angiotensin–aldosterone system (RAAS) blockade, corticosteroids and renal replacement with dialysis.[15]

Surgery

Prevention

HIV-positive patients should be screened for chronic kidney disease (CKD). Interventions in HIV-positive patients with renal disease should be done in order to slow the progress and prevent end stage renal disease (ESRD) and they should be referred to a nephrologist.[8][20]

Cost-Effectiveness of Therapy

There is insufficient information about the cost-effectiveness of therapy in HIV associated nephropathy. The World Health Organization (WHO) data on HIV/AIDS for 2018 is 37.9 million people living with HIV/AIDS worldwide and 770 000 deaths due to HIV-related illnesses worldwide.[21]

Future or Investigational Therapies

References

  1. ↑ Gottlieb MS, Schroff R, Schanker HM, Weisman JD, Fan PT, Wolf RA; et al. (1981). “Pneumocystis carinii pneumonia and mucosal candidiasis in previously healthy homosexual men: evidence of a new acquired cellular immunodeficiency”. N Engl J Med. 305 (24): 1425–31. doi:10.1056/NEJM198112103052401. PMID 6272109.
  2. ↑ Centers for Disease Control (CDC) (1982). “A cluster of Kaposi’s sarcoma and Pneumocystis carinii pneumonia among homosexual male residents of Los Angeles and Orange Counties, California”. MMWR Morb Mortal Wkly Rep. 31 (23): 305–7. PMID 6811844.
  3. ↑ Rao TK, Filippone EJ, Nicastri AD, Landesman SH, Frank E, Chen CK; et al. (1984). “Associated focal and segmental glomerulosclerosis in the acquired immunodeficiency syndrome”. N Engl J Med. 310 (11): 669–73. doi:10.1056/NEJM198403153101101. PMID 6700641.
  4. ↑ 4.0 4.1 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.
  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. ↑ 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.
  7. ↑ 7.0 7.1 Menez S, Hanouneh M, McMahon BA, Fine DM, Atta MG (2018). “Pharmacotherapy and treatment options for HIV-associated nephropathy”. Expert Opin Pharmacother. 19 (1): 39–48. doi:10.1080/14656566.2017.1416099. PMC 6381591. PMID 29224373.
  8. ↑ 8.0 8.1 8.2 Palau L, Menez S, Rodriguez-Sanchez J, Novick T, Delsante M, McMahon BA; et al. (2018). “HIV-associated nephropathy: links, risks and management”. HIV AIDS (Auckl). 10: 73–81. doi:10.2147/HIV.S141978. PMC 5975615. PMID 29872351.
  9. ↑ Atta MG, Lucas GM, Fine DM (2008). “HIV-associated nephropathy: epidemiology, pathogenesis, diagnosis and management”. Expert Rev Anti Infect Ther. 6 (3): 365–71. doi:10.1586/14787210.6.3.365. PMID 18588500.
  10. ↑ Brook MG, Miller RF (2001). “HIV associated nephropathy: a treatable condition”. Sex Transm Infect. 77 (2): 97–100. PMC 1744263. PMID 11287685.
  11. ↑ 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.
  12. ↑ Lescure FX, Flateau C, Pacanowski J, Brocheriou I, Rondeau E, Girard PM; et al. (2012). “HIV-associated kidney glomerular diseases: changes with time and HAART”. Nephrol Dial Transplant. 27 (6): 2349–55. doi:10.1093/ndt/gfr676. PMID 22248510.
  13. ↑ Bigé N, Lanternier F, Viard JP, Kamgang P, Daugas E, Elie C; et al. (2012). “Presentation of HIV-associated nephropathy and outcome in HAART-treated patients”. Nephrol Dial Transplant. 27 (3): 1114–21. doi:10.1093/ndt/gfr376. PMID 21745806.
  14. ↑ Atta MG, Longenecker JC, Fine DM, Nagajothi N, Grover DS, Wu J; et al. (2004). “Sonography as a predictor of human immunodeficiency virus-associated nephropathy”. J Ultrasound Med. 23 (5): 603–10, quiz 612-3. doi:10.7863/jum.2004.23.5.603. PMID 15154526.

    Other Imaging Findings

    There are no other imaging findings associated with HIV associated nephropathy.

    Other Diagnostic Studies

    There are no other diagnostic studies associated with HIV associated nephropathy.

    Treatment

    Medical Therapy

    The treatment of HIV associated nephropathy (HIVAN) includes: combined antiretroviral therapy (cART), renin–angiotensin–aldosterone system (RAAS) blockade, corticosteroids and renal replacement with dialysis.<ref name=”pmidpmid29872351″>Palau L, Menez S, Rodriguez-Sanchez J, Novick T, Delsante M, McMahon BA; et al. (2018). “HIV-associated nephropathy: links, risks and management”. HIV AIDS (Auckl). 10: 73–81. doi:10.2147/HIV.S141978. PMC 5975615. PMID pmid29872351 Check |pmid= value (help).

  15. ↑ Palau L, Menez S, Rodriguez-Sanchez J, Novick T, Delsante M, McMahon BA; et al. (2018). “HIV-associated nephropathy: links, risks and management”. HIV AIDS (Auckl). 10: 73–81. doi:10.2147/HIV.S141978. PMC 5975615. PMID pmid29872351 Check |pmid= value (help).
  16. ↑ Stock PG, Barin B, Murphy B, Hanto D, Diego JM, Light J; et al. (2010). “Outcomes of kidney transplantation in HIV-infected recipients”. N Engl J Med. 363 (21): 2004–14. doi:10.1056/NEJMoa1001197. PMC 3028983. PMID 21083386.
  17. ↑ Invalid <ref> tag; no text was provided for refs named pmid26061701
  18. ↑ 18.0 18.1 Muller E, Barday Z, Mendelson M, Kahn D (2015). “HIV-positive-to-HIV-positive kidney transplantation–results at 3 to 5 years”. N Engl J Med. 372 (7): 613–20. doi:10.1056/NEJMoa1408896. PMC 5090019. PMID 25671253.
  19. ↑ 19.0 19.1 Durand CM, Segev D, Sugarman J (2016). “Realizing HOPE: The Ethics of Organ Transplantation From HIV-Positive Donors”. Ann Intern Med. 165 (2): 138–42. doi:10.7326/M16-0560. PMC 4949150. PMID 27043422.
  20. ↑ Fine DM, Perazella MA, Lucas GM, Atta MG (2008). “Kidney biopsy in HIV: beyond HIV-associated nephropathy”. Am J Kidney Dis. 51 (3): 504–14. doi:10.1053/j.ajkd.2007.12.005. PMID 18295067.
  21. ↑ “WHO | HIV/AIDS”.

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Historical Perspective

Historical Perspective

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]

Overview

AIDS was first reported in 1981.[1][2] The first reported cases of HIV-associated nephropathy (HIVAN) were described in 1984.[3]

Historical Perspective

  • AIDS was first reported in 1981.[1][2]
  • The first reported cases of HIV-associated nephropathy (HIVAN) were described in 1984.[3]
  • HIV-associated nephropathy (HIVAN) was formerly known as ‘AIDS-associated nephropathy‘.

References

  1. ↑ 1.0 1.1 Gottlieb MS, Schroff R, Schanker HM, Weisman JD, Fan PT, Wolf RA; et al. (1981). “Pneumocystis carinii pneumonia and mucosal candidiasis in previously healthy homosexual men: evidence of a new acquired cellular immunodeficiency”. N Engl J Med. 305 (24): 1425–31. doi:10.1056/NEJM198112103052401. PMID 6272109.
  2. ↑ 2.0 2.1 Centers for Disease Control (CDC) (1982). “A cluster of Kaposi’s sarcoma and Pneumocystis carinii pneumonia among homosexual male residents of Los Angeles and Orange Counties, California”. MMWR Morb Mortal Wkly Rep. 31 (23): 305–7. PMID 6811844.
  3. ↑ 3.0 3.1 Rao TK, Filippone EJ, Nicastri AD, Landesman SH, Frank E, Chen CK; et al. (1984). “Associated focal and segmental glomerulosclerosis in the acquired immunodeficiency syndrome”. N Engl J Med. 310 (11): 669–73. doi:10.1056/NEJM198403153101101. PMID 6700641.

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Pathophysiology

Pathophysiology

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]

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

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 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

  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.

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Causes

Causes

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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Differentiating HIV associated nephropathy from other Diseases

Differentiating HIV associated nephropathy from other Diseases

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

HIV-associated nephropathy must be differentiated form other diseases that cause focal segmental glomerulonephritis, high grade proteinuria, and elevated serum creatinine levels.

Differential Diagnosis

HIV-associated nephropathy must be differentiated form other diseases that cause focal segmental glomerulonephritis, high grade proteinuria, and elevated serum creatinine levels.

Differentiating HIV-Associated Nephropathy from Other Diseases

Glomerular disease that present with similar characteristics of HIV-associated nephropathy must be differentiated from other glomerular disease that may occur in patients that are HIV-1 affected. They are:[1]

References

  1. ↑ Atta MG, Lucas GM, Fine DM (2008). “HIV-associated nephropathy: epidemiology, pathogenesis, diagnosis and management”. Expert Rev Anti Infect Ther. 6 (3): 365–71. doi:10.1586/14787210.6.3.365. PMID 18588500.

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Epidemiology and Demographics

Epidemiology and Demographics

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]

Overview

HIV-associated nephropathy (HIVAN) is mostly seen in male patients and of African decent. The prevalence of HIVAN in the population of patients with African descent has been reported to be 3% to 12%.[1]

Epidemiology

The prevalence of HIV-associated nephropathy (HIVAN) in the population of patients with African descent has been reported to be 3% to 12%.[1]

Demographics

Age

The average age at which patients are affected with HIV-associated nephropathy has been reported to be around 40.8 years of age in a study.[2]

Gender

HIV-associated nephropathy affects men more than women.[2]

Race

HIVAN is mostly seen in patients of African descent.[2]

References

  1. ↑ 1.0 1.1 Menez S, Hanouneh M, McMahon BA, Fine DM, Atta MG (2018). “Pharmacotherapy and treatment options for HIV-associated nephropathy”. Expert Opin Pharmacother. 19 (1): 39–48. doi:10.1080/14656566.2017.1416099. PMC 6381591. PMID 29224373.
  2. ↑ 2.0 2.1 2.2 Atta MG, Lucas GM, Fine DM (2008). “HIV-associated nephropathy: epidemiology, pathogenesis, diagnosis and management”. Expert Rev Anti Infect Ther. 6 (3): 365–71. doi:10.1586/14787210.6.3.365. PMID 18588500.

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Overview

The risk factors that attribute to HIV-associated nephropathy are similar to those seen with HIV. Positive predicators for HIV-associated nephropathy include: polymorphysim of Apolipoproetin-1 (APOL1) gene, high viral load, low CD-4 count, proteinuria (nephrotic range), and higher level of renal echogenicity on ultrasound.[1]

Risk Factors

The majority of patients developing HIV-associated nephropathy, is through the acquisition of HIV-1. The acquisition of the disease can be attributed to unprotected sexual relations between partners (one partner having HIV), sharing of needles, and or contaminated blood transfusions. However, the greatest risk factor attributed to development of HIV-associated nephropathy is the black race.[2][3][4]

The predictors for the development of HIV-associated nephropathy include:[1]

Positive predictors for the development of HIV-associated nephropathy  

Negative predictors for the development of HIV-associated nephropathy  

References

  1. ↑ 1.0 1.1 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. ↑ Szczech LA (2001). “Renal diseases associated with human immunodeficiency virus infection: epidemiology, clinical course, and management”. Clin Infect Dis. 33 (1): 115–9. doi:10.1086/320893. PMID 11389504.
  3. ↑ Naicker S, Fabian J (2010). “Risk factors for the development of chronic kidney disease with HIV/AIDS”. Clin Nephrol. 74 Suppl 1 ( ): S51–6. PMID 20979964.
  4. ↑ Foy MC, Estrella MM, Lucas GM, Tahir F, Fine DM, Moore RD; et al. (2013). “Comparison of risk factors and outcomes in HIV immune complex kidney disease and HIV-associated nephropathy”. Clin J Am Soc Nephrol. 8 (9): 1524–32. doi:10.2215/CJN.10991012. PMC 3805081. PMID 23685946.
  5. ↑ Bigé N, Lanternier F, Viard JP, Kamgang P, Daugas E, Elie C; et al. (2012). “Presentation of HIV-associated nephropathy and outcome in HAART-treated patients”. Nephrol Dial Transplant. 27 (3): 1114–21. doi:10.1093/ndt/gfr376. PMID 21745806.
  6. ↑ Genovese G, Friedman DJ, Ross MD, Lecordier L, Uzureau P, Freedman BI; et al. (2010). “Association of trypanolytic ApoL1 variants with kidney disease in African Americans”. Science. 329 (5993): 841–5. doi:10.1126/science.1193032. PMC 2980843. PMID 20647424.
  7. ↑ Lescure FX, Flateau C, Pacanowski J, Brocheriou I, Rondeau E, Girard PM; et al. (2012). “HIV-associated kidney glomerular diseases: changes with time and HAART”. Nephrol Dial Transplant. 27 (6): 2349–55. doi:10.1093/ndt/gfr676. PMID 22248510.
  8. ↑ Atta MG, Choi MJ, Longenecker JC, Haymart M, Wu J, Nagajothi N; et al. (2005). “Nephrotic range proteinuria and CD4 count as noninvasive indicators of HIV-associated nephropathy”. Am J Med. 118 (11): 1288. doi:10.1016/j.amjmed.2005.05.027. PMID 16271919.
  9. ↑ 9.0 9.1 Berliner AR, Fine DM, Lucas GM, Rahman MH, Racusen LC, Scheel PJ; et al. (2008). “Observations on a cohort of HIV-infected patients undergoing native renal biopsy”. Am J Nephrol. 28 (3): 478–86. doi:10.1159/000112851. PMID 18176076.
  10. ↑ 10.0 10.1 Atta MG, Longenecker JC, Fine DM, Nagajothi N, Grover DS, Wu J; et al. (2004). “Sonography as a predictor of human immunodeficiency virus-associated nephropathy”. J Ultrasound Med. 23 (5): 603–10, quiz 612-3. doi:10.7863/jum.2004.23.5.603. PMID 15154526.
  11. ↑ Atta MG, Estrella MM, Kuperman M, Foy MC, Fine DM, Racusen LC; et al. (2012). “HIV-associated nephropathy patients with and without apolipoprotein L1 gene variants have similar clinical and pathological characteristics”. Kidney Int. 82 (3): 338–43. doi:10.1038/ki.2012.111. PMC 3463138. PMID 22495294.
  12. ↑ Estrella M, Fine DM, Gallant JE, Rahman MH, Nagajothi N, Racusen LC; et al. (2006). “HIV type 1 RNA level as a clinical indicator of renal pathology in HIV-infected patients”. Clin Infect Dis. 43 (3): 377–80. doi:10.1086/505497. PMID 16804855.
  13. ↑ 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.

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Screening

Screening

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]

Overview

Screening for kidney disease is recommended in high risk populations in all patients with seropositive HIV-1 (upon detection).[1]  

Screening

Screening for kidney disease is recommended in high risk populations in all patients with seropositive HIV-1 (upon detection).[1]

HIV screening

  • According to the U.S. Preventive Service Task Force, clinicians should screen for HIV in:
    • Adolescents and adults ages 15 to 65
    • Pregnant Persons
  • Center of Disease Control (CDC) recommendations for HIV screening:
    • People between the ages of 13 and 64 should get tested for HIV at least once.
    • Those with risk factors for HIV are recommended to be screened more frequently. The CDC suggests that people with risk factors should be tested at least once a year.
    • Asymptomatic sexually active men who have sex with men (MSM) should be screened once a year. The benefits of more frequent screening ( once every 3 or 6 months) for MSM at increased risk for HIV infection should be considered.

References

  1. ↑ 1.0 1.1 Palau L, Menez S, Rodriguez-Sanchez J, Novick T, Delsante M, McMahon BA; et al. (2018). “HIV-associated nephropathy: links, risks and management”. HIV AIDS (Auckl). 10: 73–81. doi:10.2147/HIV.S141978. PMC 5975615. PMID 29872351.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

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]

Overview

HIV-associated nephropathy (HIVAN) will progress to end stage renal disease (ESRD) in a few weeks to months without treatment. However, early diagnosis and treatment has shown better outcome.

Natural History

  • If left untreated, HIV-associated nephropathy (HIVAN) will progress to end stage renal disease (ESRD) in a few weeks to months.[1]
  • Treatment with cART has shown 60% reduction in the developement of HIVAN.[1]
  • Treatment with cART has shown 38% slowing in the progression of HIVAN towards ESRD.[1]
  • Early diagnosis and Immediate treatment has shown better outcome.[1]

Complications

Possible complications that are associated with HIV-associated nephropathy include:

Prognosis

  • Before the advent of cART therapy, the prognosis of HIV-associated nephropathy was fatal. The mortality rate during this time was 100% within 6 months.[1]
  • Today, the prognosis of HIVAN with the availability of cART therapy still remains grim,[1] however, treatment with cART has increased renal survival rate.[2]
  • Early diagnosis and Immediate treatment has shown better outcome.[1]
  • Treatment with cART has shown 60% reduction in the developement of HIVAN.[1]
  • Treatment with cART has shown 38% slowing in the progression of HIVAN towards ESRD.[1]
  • The current first and second year survival rate of HIV-associated nephropathy is estimated to be around 63% and 43% respectively, with the use of HAART therapy.[3]
  • Several factors have been associated with increased risk of progression of kidney disease in patients with HIVAN, which include:[4]

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 Atta MG, Lucas GM, Fine DM (2008). “HIV-associated nephropathy: epidemiology, pathogenesis, diagnosis and management”. Expert Rev Anti Infect Ther. 6 (3): 365–71. doi:10.1586/14787210.6.3.365. PMID 18588500.
  2. ↑ Atta MG, Fine DM, Kirk GD, Mehta SH, Moore RD, Lucas GM (2007). “Survival during renal replacement therapy among African Americans infected with HIV type 1 in urban Baltimore, Maryland”. Clin Infect Dis. 45 (12): 1625–32. doi:10.1086/523728. PMC 4096866. PMID 18190325.
  3. ↑ Atta MG, Choi MJ, Longenecker JC, Haymart M, Wu J, Nagajothi N; et al. (2005). “Nephrotic range proteinuria and CD4 count as noninvasive indicators of HIV-associated nephropathy”. Am J Med. 118 (11): 1288. doi:10.1016/j.amjmed.2005.05.027. PMID 16271919.
  4. ↑ Palau L, Menez S, Rodriguez-Sanchez J, Novick T, Delsante M, McMahon BA; et al. (2018). “HIV-associated nephropathy: links, risks and management”. HIV AIDS (Auckl). 10: 73–81. doi:10.2147/HIV.S141978. PMC 5975615. PMID 29872351.

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Diagnosis

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