HIV-Associated Nephropathy (HIVAN)

📋 Key Information Summary

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HIV-associated nephropathy (HIVAN) is a collapsing variant of focal segmental glomerulosclerosis (FSGS) occurring in HIV-1-positive patients with low CD4 counts (<200 cells/µL) and high viral loads.
HIVAN is the third leading cause of end-stage renal failure (ESRF) in African Americans aged 20–64; in Australia it remains an important differential in HIV-positive patients presenting with proteinuria or renal impairment.
Direct HIV-1 infection of renal tubular epithelial cells and podocytes drives the pathogenesis via viral gene products (Nef, Vpr, Tat) causing dedifferentiation, proliferation, and apoptosis.
Clinically presents with heavy proteinuria (often nephrotic-range >3.5 g/day), rapidly progressive renal impairment, and large echogenic kidneys on ultrasound.
Renal biopsy is the gold standard — demonstrating collapsing glomerulopathy (collapsing FSGS), microcystic tubular dilatation, and interstitial inflammation.
Antiretroviral therapy (ART) is the cornerstone of management — early initiation can halt or reverse renal injury and dramatically reduces ESRF risk.
ACE inhibitors (ACEi) or angiotensin receptor blockers (ARB) are recommended to reduce proteinuria and slow disease progression, irrespective of blood pressure.
Tenofovir disoproxil fumarate (TDF) carries nephrotoxic risk — tenofovir alafenamide (TAF) is preferred when available; monitor renal function if TDF is used.
Corticosteroids (prednisolone) may be considered in severe or refractory cases, though evidence is limited and not from large RCTs.
Aboriginal and Torres Strait Islander peoples have higher rates of HIV late diagnosis and concurrent renal disease — culturally safe, early screening is essential.
All HIV-positive patients should have baseline and annual urine albumin-to-creatinine ratio (uACR) and eGFR monitoring.
Referral to nephrology is recommended for all patients with suspected HIVAN for biopsy consideration and multidisciplinary care.

Introduction & Australian Epidemiology

HIV-associated nephropathy (HIVAN) is a distinct clinicopathological entity and the most common renal complication directly attributable to HIV-1 infection. It is characterised by a collapsing variant of focal segmental glomerulosclerosis (FSGS), microcystic tubular dilatation, and interstitial nephritis. HIVAN typically presents with heavy proteinuria and rapidly progressive renal impairment, and without treatment may progress to end-stage renal failure (ESRF) within weeks to months.

HIVAN was first described in 1984 among Black patients in the United States and remains overwhelmingly more prevalent in individuals of African descent, owing to genetic susceptibility variants in the APOL1 gene (G1 and G2 risk alleles). In Australia, HIVAN is an important but under-recognised diagnosis. The Kirby Institute reported approximately 29,045 people living with HIV in Australia as of 2022, with growing proportions of sub-Saharan African-born migrants and Aboriginal and Torres Strait Islander peoples — populations with higher background rates of renal disease and, in the case of African-born individuals, higher APOL1 risk allele prevalence.

In the pre-ART era, HIVAN accounted for up to 10–12% of ESRF in HIV-positive patients. Since the widespread adoption of combination ART, the incidence has declined substantially, but HIVAN persists — particularly among those with late HIV diagnosis, poor ART adherence, or advanced immunosuppression (CD4 <200 cells/µL). Australian data from tertiary renal units suggest HIVAN remains in the differential for collapsing FSGS, particularly in patients of African ancestry.

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Late diagnosis: Approximately 30% of new HIV diagnoses in Australia are classified as late (CD4 <350 cells/µL). These patients are at highest risk of HIVAN and should have baseline renal assessment at diagnosis.

Pathophysiology — Direct HIV Infection of Podocytes

HIVAN is unique among HIV-related renal diseases because it results from direct infection of renal parenchymal cells by HIV-1, rather than from immune complex deposition or drug toxicity. The pathogenesis involves several key mechanisms:

Viral Entry & Tropism

HIV-1 infects renal tubular epithelial cells and, critically, glomerular podocytes. Unlike CD4+ T cells, renal cells lack the canonical CD4 receptor; viral entry occurs via alternative pathways including mannose receptors, galactosylceramide, and C-type lectins. Once integrated, HIV-1 proviral DNA persists within the renal epithelium, forming a renal reservoir independent of circulating viral load.

Viral Gene Products

Nef: Expressed on podocyte surfaces, Nef activates Src kinase signalling (Src, Rac, STAT3), causing podocyte dedifferentiation, proliferation (a hallmark of collapsing FSGS), and loss of the mature podocyte phenotype (reduced synaptopodin, WT-1 expression).
Vpr: A secreted protein that induces G2 cell-cycle arrest and apoptosis in tubular epithelial cells. Vpr is detectable in the urine of HIVAN patients and correlates with disease activity.
Tat: Promotes tubular cell proliferation and fibrosis via upregulation of TGF-β and PDGF pathways.
Gag/Pol: Contribute to endoplasmic reticulum stress and the unfolded protein response, driving tubular injury.

Host Genetic Susceptibility

Variants in the APOL1 gene (G1: rs73885319, rs60910145; G2: rs71785313) are the strongest host risk factors. Individuals carrying two APOL1 risk alleles have a 50-fold increased risk of HIVAN. These alleles are almost exclusive to individuals of recent African ancestry. In Australia, clinicians should consider APOL1 risk in patients of sub-Saharan African descent presenting with unexplained proteinuria in the setting of HIV.

Downstream Effects

Infected podocytes lose their differentiated phenotype and re-enter the cell cycle, leading to the characteristic collapsing glomerular tuft. Concurrently, microcystic tubular dilatation develops due to tubular epithelial proliferation and obstruction. Interstitial inflammation (CD8+ T-cell infiltrate) contributes to fibrosis and progressive renal scarring. The net result is rapid loss of nephron function, heavy proteinuria, and accelerated progression to ESRF.

Clinical Features & Diagnosis

Typical Presentation

HIVAN classically presents in patients with advanced HIV (CD4 <200 cells/µL, high viral loads, often ART-naïve). However, it may also occur in patients on suboptimal ART or with poor adherence. Key features include:

Nephrotic-range proteinuria: Often >3.5 g/day; urine protein-to-creatinine ratio (uPCR) >350 mg/mmol.
Rapidly progressive renal impairment: Creatinine may rise over days to weeks, mimicking acute kidney injury.
Normal or low blood pressure: Unlike typical FSGS, hypertension is uncommon in HIVAN.
Oedema and nephrotic syndrome: Peripheral oedema, hypoalbuminaemia, hypercholesterolaemia.
Large, echogenic kidneys on ultrasound: Bilateral renal enlargement with increased cortical echogenicity — a useful bedside clue differentiating HIVAN from other causes of CKD where kidneys are typically small.

Diagnostic Criteria

There are no universally agreed clinical diagnostic criteria; however, HIVAN should be strongly suspected in an HIV-positive patient with:

Proteinuria >1 g/day (or uPCR >100 mg/mmol) on at least two occasions
Declining eGFR not attributable to prerenal, obstructive, or drug-related causes
Large echogenic kidneys on renal ultrasound
Absence of another glomerular disease (e.g., IgA nephropathy, lupus nephritis, diabetic nephropathy)

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Do not rely on clinical criteria alone: A renal biopsy is required to confirm HIVAN and exclude other HIV-associated renal diseases (immune complex GN, thrombotic microangiopathy, drug-induced interstitial nephritis). Empirical treatment without biopsy risks missing a coexisting, treatable condition.

Differential Diagnosis of Renal Disease in HIV

Condition	Key Features	Biopsy Finding
HIVAN (collapsing FSGS)	Nephrotic proteinuria, large kidneys, low CD4	Collapsing FSGS, microcystic tubules
HIV immune complex kidney disease (HIVICK)	Variable proteinuria, may have haematuria	MPGN pattern, subendothelial deposits
IgA nephropathy	Visible haematuria, moderate proteinuria	Mesangial IgA deposits
Tenofovir nephrotoxicity	Proximal tubulopathy, declining eGFR	Proximal tubular injury, crystals
Thrombotic microangiopathy	AKI, microangiopathic haemolytic anaemia, thrombocytopenia	Thrombi in arterioles/glomeruli
Diabetic nephropathy	Long-standing DM, gradual proteinuria	Kimmelstiel–Wilson nodules, GBM thickening

Investigations & Biopsy — Collapsing FSGS

Baseline Investigations

ESSENTIAL

Urine albumin-to-creatinine ratio (uACR)

First-void morning specimen. MBS Item 66838. ACR >3.5 mg/mmol (males) or >2.5 mg/mmol (females) indicates significant albuminuria.

ESSENTIAL

Serum creatinine, eGFR (CKD-EPI)

MBS Item 66506. Monitor trajectory — a decline >5 mL/min/1.73 m² over 3 months warrants urgent review.

ESSENTIAL

Renal ultrasound with Doppler

MBS Item 55042. Look for bilaterally enlarged, echogenic kidneys. Exclude obstruction and renal vein thrombosis.

AVAILABLE

HIV viral load & CD4 count

Confirm HIV status, quantify immunosuppression. Low CD4 (<200) and high viral load (>100,000 copies/mL) increase HIVAN risk.

AVAILABLE

Serum albumin, lipid panel, urine microscopy

Assess nephrotic syndrome. Urine microscopy may show oval fat bodies; haematuria suggests alternative diagnosis (HIVICK, IgA).

AVAILABLE

Hepatitis B & C serology

Co-infection is common and may contribute to renal disease (HBV-associated membranous nephropathy, HCV-associated MPGN).

SPECIALIST

APOL1 genotyping

Available through research or specialist referral. Consider in patients of African ancestry with unexplained renal disease. Not routinely funded on MBS.

REFERRAL

Renal biopsy

Gold standard for HIVAN diagnosis. Should be performed by nephrology. Risk of bleeding assessed individually. Histopathology: collapsing FSGS, microcystic tubular dilatation, interstitial nephritis, endothelial tubuloreticular inclusions on EM.

Renal Biopsy — Histopathological Features

The hallmark of HIVAN on renal biopsy is collapsing glomerulopathy, classified under the Columbia classification as a variant of FSGS. Key features include:

Light microscopy: Collapse of glomerular capillary tufts with hypertrophy and hyperplasia of overlying podocytes (often with cytoplasmic vacuolisation). Microcystic dilatation of tubules is prominent. Interstitial inflammation with CD8+ T lymphocytes and mild fibrosis.
Immunofluorescence: Typically negative or nonspecific (focal IgM, C3 in sclerotic segments). The absence of dominant immune complex deposits distinguishes HIVAN from HIVICK.
Electron microscopy: Endothelial tubuloreticular inclusions (TRI) — pathognomonic structures within capillary endothelial cytoplasm, induced by interferon-α. Podocyte foot process effacement is widespread.

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Tubuloreticular inclusions: These IFN-α-induced structures on EM are highly suggestive of HIVAN but not pathognomonic (can occur in lupus nephritis). Clinical correlation with HIV status is essential.

Risk Stratification

Risk factors for developing HIVAN and for progression to ESRF include:

Lower Risk

Suppressed on ART

Undetectable viral load, CD4 >350 cells/µL, normal baseline uACR, eGFR >60. Risk of HIVAN is low but not zero — continue annual screening.

Setting: GP annual review with uACR + eGFR

Moderate Risk

Late Diagnosis or Suboptimal ART

CD4 200–350, detectable viral load, uACR 3–30 mg/mmol, eGFR 30–60. Risk of progression — urgent ART optimisation, ACEi initiation, nephrology referral.

Setting: Specialist-led outpatient with nephrology involvement

High Risk

Advanced HIVAN

CD4 <200, viral load >100,000, nephrotic-range proteinuria (>3.5 g/day), eGFR <30, large echogenic kidneys. High risk of ESRF — urgent ART, consider biopsy, consider corticosteroids.

Setting: Tertiary nephrology + infectious disease joint management

Predictors of Poor Outcome

Degree of interstitial fibrosis on biopsy (>40% fibrosis = poor prognosis)
Presentation with ESRF requiring dialysis at diagnosis
Failure to achieve viral suppression on ART
Homozygous APOL1 G1/G2 risk alleles
Coexistent hepatitis B or C co-infection

Management — ART & ACE Inhibitors

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Key principle: ART is the single most important intervention in HIVAN. Initiation or optimisation of ART should occur urgently — do not wait for biopsy results if clinical suspicion is high. ART reduces ESRF risk by up to 60%.

Antiretroviral Therapy (ART)

All patients with suspected or confirmed HIVAN should be on suppressive ART. Regimen selection should account for renal function and potential nephrotoxicity.

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Dolutegravir (DTG)

Tivicay® · INSTI (integrase inhibitor)

Adult dose 50 mg PO once daily (no renal adjustment needed)

Paediatric dose Weight-based: ≥30 kg — 50 mg daily

Renal adjustment None required — preferred agent in CKD

PBS status ✔ PBS General Benefit

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Tenofovir alafenamide (TAF)

Vemlidy® · NRTI (preferred over TDF)

Adult dose 25 mg PO once daily (as component of co-formulated ART)

Renal adjustment Safer than TDF in CKD; avoid if eGFR <15 mL/min (limited data)

Key note TAF has significantly less nephrotoxicity than TDF — preferred in HIVAN

PBS status ✔ PBS General Benefit (as co-formulated ART)

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Bictegravir/Emtricitabine/TAF

Biktarvy® · Complete single-tablet regimen

Adult dose 1 tablet PO once daily (BIC 50 mg/FTC 200 mg/TAF 25 mg)

Renal adjustment No dose adjustment; caution if eGFR <30 (TAF component). Avoid if on dialysis.

PBS status ✔ PBS General Benefit

⚠️

Tenofovir disoproxil fumarate (TDF) caution: TDF causes proximal tubular dysfunction (Fanconi syndrome) and reduces eGFR. In patients with HIVAN and declining renal function, switch from TDF to TAF or a non-tenofovir regimen. If TDF must be used, monitor serum phosphate and uACR every 3 months.

ACE Inhibitors & ARBs

ACE inhibitors (ACEi) or angiotensin receptor blockers (ARB) are recommended for all patients with HIVAN and proteinuria >1 g/day, regardless of blood pressure. They reduce intraglomerular pressure, proteinuria, and podocyte injury.

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Ramipril

Tritace® · ACE inhibitor — 1st-line

Adult dose 2.5 mg PO once daily, titrate to 5–10 mg daily as tolerated

Monitoring Check K⁺ and creatinine at 1–2 weeks after initiation/dose change

Renal adjustment Start at 1.25 mg if eGFR <30 mL/min; titrate cautiously

PBS status ✔ PBS General Benefit

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Perindopril

Coversyl® · ACE inhibitor — alternative

Adult dose 2–4 mg PO once daily, titrate to 8 mg daily

PBS status ✔ PBS General Benefit

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Losartan

Cozaar® · ARB (if ACEi-intolerant)

Adult dose 50 mg PO once daily, titrate to 100 mg daily

Indication Use if ACEi not tolerated (cough, angioedema)

PBS status ✔ PBS General Benefit

Corticosteroids

Corticosteroids may be considered in severe HIVAN (eGFR <30 or rapidly declining) that is not responding to ART optimisation within 2–4 weeks. Evidence is based on small cohort studies and case series; there are no large RCTs. Use only under specialist supervision.

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Prednisolone

Solone® · Corticosteroid — specialist use

Adult dose 1 mg/kg/day PO (max 60–80 mg/day) for 2–3 months, then taper

Cautions Increased infection risk in immunocompromised patients. Ensure adequate ART cover before starting. Monitor glucose, BP, opportunistic infections.

PBS status ✔ PBS General Benefit

Supportive Measures

Sodium and fluid restriction: <2 g sodium/day if oedematous.
Diuretics: Frusemide (Lasix®) 20–80 mg PO/IV daily for volume overload; add spironolactone if refractory (monitor K⁺).
Statin therapy: Atorvastatin 10–40 mg PO daily for cardiovascular risk reduction (high CV burden in CKD + HIV). PBS General Benefit.
Anticoagulation: Consider in nephrotic patients with serum albumin <20 g/L due to thrombotic risk (LMWH or warfarin).
Vaccination: Ensure pneumococcal (Prevenar 13®, Pneumovax 23®), influenza, hepatitis B vaccination are up to date.
Renal replacement therapy: Dialysis or transplant referral if progression to ESRF. HIV-positive patients can safely receive renal transplants with suppressed viral loads.

Management Timeline

Day 0

Suspect HIVAN in HIV-positive patient with proteinuria + renal impairment. Order uACR, eGFR, renal U/S. Initiate or optimise ART. Start ACEi (ramipril 2.5 mg). Refer nephrology.

Week 1–2

Nephrology review. Renal biopsy performed if safe. Check K⁺ and creatinine post-ACEi initiation. Reassess ART regimen — switch TDF to TAF if applicable.

Week 4–6

Biopsy results available. Confirm HIVAN diagnosis. Titrate ACEi to maximum tolerated dose. Check HIV viral load — expect >1 log reduction if ART adherent.

Month 3

Repeat uACR, eGFR. Assess proteinuria response. If >50% reduction in uPCR → continue current therapy. If minimal response → consider prednisolone (specialist decision).

Month 6–12

Ongoing monitoring every 3 months. Undetectable viral load should be target. Renal recovery (eGFR improvement, proteinuria reduction) may continue for 12+ months on ART.

Monitoring

Ongoing monitoring is essential in HIVAN to assess treatment response and detect complications:

Parameter	Frequency	Target / Action
Serum creatinine / eGFR	Every 2–4 weeks (initially), then 3-monthly	Stabilisation or improvement; >5 mL/min decline → reassess ART, consider biopsy
uACR / uPCR	Monthly (initially), then 3-monthly	>50% reduction in proteinuria by 6 months is favourable
HIV viral load	At ART initiation, 4 weeks, 3 months, then 6-monthly	Undetectable (<20 copies/mL) by 6 months
CD4 count	Every 3–6 months	Recovery to >350 cells/µL; >500 is ideal
Serum potassium	1–2 weeks after ACEi/ARB start/change, then 3-monthly	K⁺ <5.5 mmol/L; reduce/hold ACEi if hyperkalaemia
Serum phosphate, bicarbonate	3-monthly if on TDF	Detect proximal tubulopathy (Fanconi syndrome)
Lipid panel	Baseline and annually	Statin if indicated for CV risk
Blood pressure	Every visit	Target <130/80 mmHg (KDIGO CKD guidelines)

Special Populations

🤰 Pregnancy

ART: Continue ART through pregnancy — dolutegravir is now considered safe (WHO preferred). Avoid efavirenz in first trimester if alternatives available.

ACEi/ARB: CONTRAINDICATED — teratogenic (renal dysgenesis, oligohydramnios). Discontinue and use methyldopa, labetalol, or nifedipine for BP control.

Steroids: Avoid if possible; use only if life-threatening disease under obstetric/nephrology supervision.

Monitoring: Increased frequency of uACR and eGFR — pregnancy alters renal haemodynamics and may unmask or worsen proteinuria.

👶 Paediatrics

Epidemiology: HIVAN can occur in vertically infected children, typically presenting age 2–5 years if untreated. More common in children of African descent.

ART: Initiate ART promptly in all HIV-positive children — efavirenz-based or PI-based regimens per current Australian paediatric ART guidelines. Dolutegravir now approved for children ≥20 kg.

ACEi: Enalapril 0.1 mg/kg/day PO, titrate as needed. Monitor growth and K⁺.

Referral: All cases to paediatric nephrology and paediatric infectious disease specialist centres.

👴 Elderly

Considerations: Increased risk of AKI with ACEi in patients with pre-existing CKD or bilateral renal artery stenosis. Start low, titrate slowly.

Polypharmacy: Review drug interactions — many antiretrovirals have CYP3A4 interactions. Dolutegravir has fewer interactions than PIs.

Frailty: Consider goals of care early — dialysis may not confer survival benefit in frail elderly patients with advanced HIVAN.

🫘 Renal Impairment

eGFR 30–60: Use TAF-based ART. ACEi safe with monitoring. Avoid TDF.

eGFR 15–30: Dolutegravir + emtricitabine (dose-adjusted) + TAF. Nephrology co-management essential. Start planning for RRT.

Dialysis (eGFR <15): ART must be dialysis-adjusted. Dolutegravir does not require dose change. Emtricitabine dose reduce. HIV-positive patients can access peritoneal or haemodialysis.

Transplant: Renal transplantation is feasible and safe in HIV-positive patients with undetectable viral load and CD4 >200. Refer to transplant centres experienced with HIV.

🫁 Hepatic Impairment

HBV/HCV co-infection: Common — must be addressed. HBV-active ART (tenofovir or entecavir) must be continued indefinitely to avoid HBV flare. HCV treatment with DAAs (e.g., sofosbuvir/velpatasvir) is PBS-listed.

Drug adjustments: Dolutegravir is safe in mild-moderate hepatic impairment (Child-Pugh A/B). Avoid in severe (Child-Pugh C).

🛡️ Immunocompromised

Steroid caution: Prednisolone in severely immunosuppressed patients (CD4 <100) increases opportunistic infection risk — ensure prophylaxis (cotrimoxazole for PCP, fluconazole if indicated).

IRIS: Immune reconstitution inflammatory syndrome may occur 2–8 weeks after ART initiation — may transiently worsen renal function. Do not stop ART unless severe.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander peoples experience a disproportionate burden of both HIV and kidney disease in Australia. Late HIV diagnosis is more common, and concurrent risk factors for CKD — including diabetes, hypertension, and socioeconomic disadvantage — are prevalent. Culturally safe, community-led approaches to HIV testing and renal care are essential.

Late diagnosis

ATSI peoples are more likely to present with advanced HIV (CD4 <350), increasing HIVAN risk. Opt-out HIV testing should be routine in communities with higher prevalence, guided by local public health units.

Concurrent renal risk

Rates of CKD are 2–3× higher in ATSI populations. Diabetic kidney disease and hypertensive nephrosclerosis may coexist with HIVAN — biopsy is particularly important to delineate the primary pathology.

Remote & rural access

Access to nephrology, renal biopsy, and ART specialists may be limited in remote and very remote communities. Telehealth nephrology consultations (MBS Items 91822, 91823) are available. Point-of-care HIV viral load testing (e.g., Xpert HIV-1 Viral Load) may be accessible through some Aboriginal Community Controlled Health Services (ACCHS).

Stigma & cultural safety

HIV-related stigma is a significant barrier to testing and engagement with care. All services must be culturally safe, delivered with respect for cultural protocols, and ideally involve Aboriginal Health Workers and Practitioners in care teams. Yarning-based approaches to health education improve engagement.

Medication adherence

ART adherence is critical for HIVAN outcomes. Address practical barriers: medication storage in hot climates, blister packing, community pharmacy support, and integration with existing medication management for diabetes and cardiovascular disease.

Organisational partnerships

Collaborate with ACCHS, state/territory HIV/AIDS organisations (e.g., ACON, VAC, NAPWHA), and RHDAustralia. The National Guide to a Preventive Health Assessment for Aboriginal and Torres Strait Islander People (RACGP, 4th edition) provides comprehensive screening frameworks.

📚 References

1. Wyatt CM, Klotman PE, D'Agati VD. HIV-associated nephropathy: clinical presentation, pathology, and epidemiology in the era of antiretroviral therapy. Semin Nephrol. 2008;28(6):513–522.
2. Kopp JB, Nelson GW, Sampath K, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy. J Am Soc Nephrol. 2011;22(11):2129–2137.
3. Estrella M, Fine DM, Gallant JE, et al. HIV type 1 RNA level as a clinical indicator of renal disease in HIV-infected individuals. AIDS. 2007;21(3):355–360.
4. Lucas GM, Eustace JA, Sozio S, et al. Highly active antiretroviral therapy and the incidence of HIV-1-associated nephropathy: a 12-year cohort study. AIDS. 2004;18(3):541–546.
5. Rosenberg AZ, Naicker S, Winkler CA, Kopp JB. HIV-associated nephropathy: a review. Nephrol Dial Transplant. 2015;30(12):1991–1998.
6. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):S117–S314.
7. Australian Government Department of Health. Fifth National Aboriginal and Torres Strait Islander Blood-Borne Viruses and Sexually Transmissible Infections Strategy 2018–2022. Canberra: Commonwealth of Australia; 2018.
8. The Kirby Institute. HIV, viral hepatitis and sexually transmissible infections in Australia: Annual Surveillance Report 2023. Sydney: UNSW; 2023.
9. RACGP. National Guide to a Preventive Health Assessment for Aboriginal and Torres Strait Islander People. 4th edition. Melbourne: RACGP; 2018.
10. Australian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM). Antiretroviral Guidelines — Australian Commentary on the DHHS Guidelines. Sydney: ASHM; 2024.
11. Wearne N, Davidson B, Blockman M, Jones ESW, Dix-Peek T. HIV-associated nephropathy — a review of the current evidence. Curr Opin HIV AIDS. 2022;17(6):336–343.
12. Naicker S, Fabian J, Naidoo S, Muller E, Paget G, Cockburn I. Infection with human immunodeficiency virus (HIV) — end-stage renal disease: the experience in South Africa. J Ren Care. 2013;39(Suppl 1):3–9.
13. Campbell LJ, Ibrahim F, Fisher M, Holt SG, Post FA. Spectrum of chronic kidney disease in HIV-infected patients. HIV Med. 2009;10(6):329–336.
14. RHDAustralia (NACCHO & Menzies School of Health Research). Australian Guidelines for Sexual Health and Blood-borne Viruses — STI and BBV Management in Aboriginal and Torres Strait Islander Populations. Darwin: RHDAustralia; 2021.