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Renal Artery Stenosis

Last updated 31 May 2026 · Renal & nephrology guideline

📋 Key Information Summary

📋
  • Renal artery stenosis (RAS) is narrowing of one or both renal arteries, most commonly due to atherosclerosis (~85%) or fibromuscular dysplasia (~10%).
  • Atherosclerotic RAS typically affects the ostium and proximal third of the renal artery in patients aged ≥50 with widespread vascular disease (IHD, PVD, CVA).
  • Fibromuscular dysplasia (FMD) preferentially affects the mid-to-distal renal artery in young women (<50 years) and may be multifocal or focal.
  • Two major consequences: renovascular hypertension (RAAS-mediated) and ischaemic nephropathy (progressive nephron loss from chronic hypoperfusion).
  • Suspect RAS in resistant hypertension (requiring ≥3 agents), malignant hypertension, flash pulmonary oedema, unexplained renal function decline after ACE inhibitor/ARB, or asymmetric kidney size ≥1.5 cm difference.
  • Duplex Doppler ultrasonography is the preferred first-line screening investigation — non-invasive, widely available, and no contrast required.
  • CT angiography or MR angiography confirms diagnosis; conventional catheter angiography remains the gold standard when intervention is planned.
  • Medical management is first-line for atherosclerotic RAS: optimise antihypertensives, high-intensity statin, antiplatelet therapy, glycaemic control, and smoking cessation.
  • The CORAL and ASTRAL trials demonstrated no significant benefit of renal artery stenting over optimal medical therapy alone in most patients with atherosclerotic RAS.
  • Revascularisation (percutaneous transluminal angioplasty ± stenting) is indicated for: FMD-related RAS, flash pulmonary oedema with RAS, progressive renal failure despite medical therapy, and refractory hypertension with ≥70% stenosis.
  • Surgical revascularisation (renal endarterectomy or bypass grafting) is reserved for complex anatomy, failed angioplasty, or concurrent aortic surgery.
  • ACE inhibitors and ARBs are effective in atherosclerotic RAS but require close monitoring of creatinine and potassium; contraindicated in bilateral RAS or RAS in a solitary functioning kidney.
  • Aboriginal and Torres Strait Islander peoples have higher prevalence of CKD and vascular disease — maintain a low threshold for screening RAS in ATSI patients with unexplained hypertension.

Introduction & Australian Epidemiology

Renal artery stenosis (RAS) is the pathological narrowing of the renal artery, leading to reduced renal perfusion, activation of the renin–angiotensin–aldosterone system (RAAS), renovascular hypertension, and progressive ischaemic nephropathy. It remains one of the most common secondary causes of hypertension, though its true prevalence in the general population is debated.

RAS is frequently identified incidentally during angiography performed for other vascular indications. In Australia, RAS is encountered in approximately 5–10% of patients undergoing coronary angiography and up to 30–40% of patients with peripheral vascular disease. Among patients with resistant hypertension defined as uncontrolled blood pressure on three or more antihypertensives (including a diuretic), the prevalence of significant RAS ranges from 10–20%.

The disease burden is increasing in line with Australia's ageing population and the rising prevalence of diabetes, obesity, and dyslipidaemia. Atherosclerotic RAS predominantly affects men aged ≥50 years, while FMD-related RAS is far more common in women aged 15–50 years. Importantly, RAS contributes to 1–5% of all cases of end-stage kidney disease (ESKD) in Australia, and among the over-65 population starting dialysis, renovascular disease accounts for 10–15%.

⚠️
Important: RAS is not a benign condition. Unrecognised bilateral RAS or RAS in a solitary functioning kidney can precipitate acute kidney injury, flash pulmonary oedema, and malignant hypertension — all requiring urgent management.
Renal Artery Stenosis clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management
Tap or click image to enlarge — Renal Artery Stenosis: pathophysiology, clinical clues, diagnosis, imaging, and management.
Renal Artery Stenosis infographic, full size

Aetiology: Atherosclerotic vs Fibromuscular Dysplasia

The two predominant causes of RAS are atherosclerotic disease and fibromuscular dysplasia (FMD). Distinguishing between them is critical, as the prognosis, demographics, and treatment approaches differ significantly.

Feature Atherosclerotic RAS Fibromuscular Dysplasia
Proportion of all RAS ~85% ~10%
Demographics Men ≥50 years Women 15–50 years
Location Ostium and proximal third Mid-to-distal artery
Angiographic pattern Focal, irregular plaque String-of-beads (medial FMD) or focal stenosis
Risk factors Smoking, diabetes, dyslipidaemia, hypertension Female sex; less linked to traditional CVD risk factors
Associated vascular beds Coronary, carotid, iliac, aortic Carotid, vertebral, iliac, mesenteric
Bilateral 30–40% 35–50%
Progression Progressive with plaque growth Usually stable; aneurysm risk in renal artery
Preferred treatment Medical therapy first; angioplasty if indicated Percutaneous angioplasty (no stent usually)

Atherosclerotic Renal Artery Stenosis

Atherosclerotic RAS is a manifestation of systemic atherosclerosis. The stenosis typically involves the aortic ostium or the proximal third of the main renal artery. Risk factors mirror those for other atherosclerotic diseases: advancing age, smoking, hypertension, dyslipidaemia, diabetes mellitus, and chronic kidney disease. There is a strong association with coronary artery disease, peripheral vascular disease, and carotid stenosis. The disease tends to be progressive — approximately 50% of lesions with >60% stenosis at baseline will progress over 3–5 years if untreated.

Fibromuscular Dysplasia

FMD is a non-atherosclerotic, non-inflammatory arterial disease. The 2019 consensus statement classifies FMD into multifocal (the classic string-of-beads appearance, predominantly medial fibroplasia) and focal subtypes. Multifocal FMD accounts for approximately 80–90% of cases and is the more common form in the renal arteries. Focal FMD is less common but may present at a younger age and is more frequently associated with hypertension. FMD can involve multiple vascular beds, and up to two-thirds of patients with renal FMD have extrarenal involvement — most commonly carotid and vertebral arteries.

Other Causes (Rare)

  • Takayasu arteritis — large-vessel vasculitis affecting the aorta and its branches; more common in young Asian women.
  • Arterial dissection — spontaneous or traumatic.
  • Neurofibromatosis type 1 — vascular stenosis from intimal proliferation.
  • Radiation-induced arteriopathy — following abdominal or retroperitoneal radiotherapy.
  • Renal artery aneurysm with secondary stenosis.
  • Extrinsic compression — from tumours or retroperitoneal fibrosis.

Clinical Features & Presentation

Many patients with RAS are asymptomatic, and the condition is frequently discovered incidentally during imaging for other vascular pathology. When symptoms occur, they are related to the two major consequences of renal artery narrowing: renovascular hypertension and ischaemic nephropathy.

Presenting Features Suggestive of RAS

🚨
Red flags for RAS: Suspect RAS in any patient with flash pulmonary oedema, malignant hypertension (BP >180/120 with end-organ damage), unexplained acute kidney injury after starting an ACE inhibitor or ARB, or hypertension with an abdominal bruit.
Clinical Clue Details
Resistant hypertension Uncontrolled BP despite ≥3 antihypertensives (including a diuretic at adequate dose)
Malignant/accelerated hypertension BP >180/120 mmHg with papilloedema, haematuria, or renal impairment
New-onset hypertension <30 or >55 years Atypical age for primary hypertension; particularly young women (FMD)
Flash pulmonary oedema Acute pulmonary oedema with normal LV function; strongly suggests bilateral RAS
ACEi/ARB-induced AKI Rise in serum creatinine ≥30% within 1–2 weeks of starting RAAS blockade
Asymmetric kidney size Difference in renal length ≥1.5 cm on ultrasound
Unexplained renal impairment Progressive CKD without clear parenchymal cause; small, shrunken kidneys
Abdominal/renal bruit Systolic-diastolic bruit in the epigastrium or flank; specificity high but sensitivity low (~40%)
Widespread atherosclerosis Patients with known coronary, peripheral vascular, or cerebrovascular disease
Recurrent pulmonary oedema with renal failure Combined cardiorenal syndrome picture

Presentation Patterns by Aetiology

Atherosclerotic
Incidental or Gradual
Often found incidentally during angiography for coronary or peripheral vascular disease. Progressive hypertension and gradual renal function decline over months to years.
Setting: Outpatient / GP-initiated investigation
FMD
Young Woman with Hypertension
New-onset hypertension in a woman <50 years, often with headaches. May present with hypertensive urgency. Diagnosis delayed by 5–10 years on average.
Setting: GP or ED presentation
Emergency
Flash Pulmonary Oedema / Malignant HTN
Acute decompensation with pulmonary oedema (often bilateral RAS), malignant hypertension with end-organ damage, or AKI precipitated by RAAS inhibitor use.
Setting: Emergency / Intensive care

Pathophysiology

Understanding the pathophysiology of RAS is essential for rational management. Renal artery narrowing triggers a cascade of haemodynamic and neurohormonal responses that perpetuate both hypertension and renal injury.

The Two-Kidney, One-Clip Model

In unilateral RAS (the classic Goldblatt model), the stenosed kidney experiences reduced perfusion pressure. This leads to:

  • Juxtaglomerular apparatus activation: Renal ischaemia stimulates renin release from juxtaglomerular cells.
  • Angiotensin II elevation: Renin cleaves angiotensinogen to angiotensin I; ACE converts it to angiotensin II, causing systemic vasoconstriction and aldosterone secretion.
  • Sodium retention: Aldosterone promotes sodium reabsorption in the distal nephron, expanding plasma volume.
  • Systemic hypertension: The combination of vasoconstriction and volume expansion raises blood pressure, which the contralateral (non-stenosed) kidney must excrete. This is termed "renin-dependent" or "renovascular" hypertension.

The One-Kidney, One-Clip Model

In bilateral RAS or RAS in a solitary functioning kidney, both kidneys (or the only kidney) are underperfused. Sodium excretion is impaired because there is no "escape" kidney. Hypertension in this setting is primarily volume-dependent rather than renin-dependent, and RAAS blockade may precipitate AKI because the kidney relies on angiotensin II–mediated efferent arteriolar constriction to maintain glomerular filtration pressure.

Ischaemic Nephropathy

Chronic reduction in renal blood flow leads to tubular atrophy, interstitial fibrosis, and glomerulosclerosis. The tubulointerstitial changes are the hallmark of ischaemic nephropathy and may be irreversible even after successful revascularisation, explaining why revascularisation does not always restore renal function.

Investigations

Investigation of suspected RAS involves screening tests, confirmatory imaging, and functional assessment. Selection depends on clinical context, renal function, and local availability.

Screening & Confirmatory Investigations

Widely Available
Duplex Doppler Ultrasonography
First-line screening test. Measures renal artery peak systolic velocity (PSV), resistive index (RI), and renal-aortic ratio. PSV >200 cm/s suggests ≥60% stenosis; RI >0.80 predicts poor response to revascularisation. Non-invasive, no contrast, no radiation. Operator-dependent; limited by obesity, bowel gas. Medicare MBS item 55110.
Widely Available
CT Angiography (CTA)
Excellent spatial resolution for atherosclerotic RAS; demonstrates plaque morphology, aortic disease, and accessory renal arteries. Requires iodinated contrast (risk of contrast-induced AKI in eGFR <30). Radiation exposure. Sensitive for ostial and proximal disease. Not ideal for distal vessel or FMD. MBS item 57330 (CT aortography).
Widely Available
MR Angiography (MRA)
Gadolinium-enhanced MRA provides good visualisation of the renal arteries. Avoids iodinated contrast and radiation. Risk of nephrogenic systemic fibrosis with gadolinium in eGFR <30 (use low-risk macrocyclic agents only). May overestimate stenosis. Superior to CTA for visualising distal vessels and FMD. MBS item 63452.
Referral / Specialist
Digital Subtraction Angiography (DSA)
Gold standard for diagnosing RAS. Invasive, with access-site risks (haematoma, dissection) and contrast nephropathy risk. Reserved for cases where intervention (angioplasty ± stenting) is planned. Measures translesional pressure gradient — a mean gradient >10 mmHg (or systolic >20 mmHg) indicates haemodynamically significant stenosis.
Widely Available
Captopril Renal Scintigraphy
Functional test using 99mTc-MAG3 or 99mTc-DTPA with and without ACE inhibition. Delayed peak uptake and reduced uptake on the affected side after captopril suggests functionally significant RAS. Useful for predicting response to revascularisation. Less commonly performed in Australia since the CORAL trial shifted practice toward medical management.

Baseline Investigations

  • Serum creatinine and eGFR — assess baseline renal function and detect asymmetry.
  • Serum electrolytes — hypokalaemia may suggest hyperaldosteronism secondary to RAAS activation.
  • Plasma renin activity (PRA) and aldosterone — may be elevated in unilateral RAS (high renin hypertension).
  • Urinalysis — proteinuria, haematuria, casts to exclude parenchymal renal disease.
  • Full blood count — assess for secondary erythrocytosis (from elevated erythropoietin) or anaemia of CKD.
  • Lipid profile and HbA1c — assess cardiovascular risk factors that require optimisation.
  • Renal length on ultrasound — asymmetry of ≥1.5 cm suggests chronic ischaemia on the smaller side.
ℹ️
Imaging selection: In patients with eGFR >30, CT angiography provides rapid, high-resolution images. In patients with significant CKD (eGFR <30), MR angiography with a macrocyclic gadolinium agent or Doppler ultrasound (no contrast) is preferred. In patients with eGFR <15 or on dialysis, either CTA (with pre-hydration and N-acetylcysteine) or conventional angiography may be used.

Risk Stratification & Severity

Risk stratification guides the decision between conservative medical management and interventional revascularisation. The degree of stenosis alone is insufficient — clinical context, renal function trajectory, and blood pressure control must all be considered.

Low Risk
Stable <60%, Well Controlled
Incidental finding of <60% stenosis, well-controlled hypertension on ≤2 agents, stable eGFR, no end-organ damage.
Management: Medical therapy, surveillance imaging in 12–24 months
Moderate Risk
60–80%, Resistant HTN
60–80% stenosis with resistant hypertension (requiring ≥3 agents) or slowly progressive renal impairment. Atherosclerotic aetiology.
Management: Optimise medical therapy; consider angioplasty if no improvement at 3–6 months
High Risk
>80%, Complications
>80% stenosis with flash pulmonary oedema, refractory malignant hypertension, progressive AKI, or bilateral RAS/RAS in solitary kidney.
Management: Urgent angioplasty ± stenting; multidisciplinary vascular team

Predictors of Poor Response to Revascularisation

  • Resistive index (RI) >0.80 on Doppler ultrasound — suggests irreversible parenchymal damage.
  • Kidney length <7 cm — severely atrophied kidneys unlikely to recover function.
  • Long-standing renal impairment (>6 months of high creatinine).
  • Heavy proteinuria (>1 g/day) — may indicate coexisting parenchymal disease.
  • Diffuse small-vessel disease on angiography.

Management

Management of RAS requires a multidisciplinary approach involving nephrology, vascular surgery, interventional radiology, and the patient's general practitioner. The optimal strategy depends on aetiology, clinical severity, and comorbidities.

Medical Management (First-Line for Atherosclerotic RAS)

Following the landmark ASTRAL (2009) and CORAL (2014) randomised controlled trials, optimal medical therapy has become the cornerstone of management for most patients with atherosclerotic RAS. Neither trial demonstrated a significant benefit of renal artery stenting over medical therapy alone for the composite outcomes of cardiovascular events, renal events, or death.

💊
Ramipril
Tritace® · ACE inhibitor
Adult dose 2.5–10 mg PO daily; start low and titrate
Renal adjustment Start 1.25 mg daily if eGFR <30; monitor creatinine and K⁺ closely
Key caution Contraindicated in bilateral RAS or RAS in solitary functioning kidney — risk of AKI
PBS status ✔ PBS General Benefit
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Candesartan
Atacand® · Angiotensin receptor blocker
Adult dose 4–32 mg PO daily; titrate as tolerated
Renal adjustment Start 4 mg daily if eGFR <30
PBS status ✔ PBS General Benefit
💊
Atorvastatin
Lipitor® · Generic · HMG-CoA reductase inhibitor
Adult dose 40–80 mg PO daily (high-intensity statin)
Renal adjustment None required
PBS status ✔ PBS General Benefit
💊
Aspirin
Aspro Clear® · Generic · Antiplatelet
Adult dose 100 mg PO daily
PBS status ✔ PBS General Benefit
💊
Amlodipine
Norvasc® · Generic · Calcium channel blocker
Adult dose 2.5–10 mg PO daily
Role Second-line antihypertensive; effective in renovascular hypertension; no adverse renal haemodynamics
PBS status ✔ PBS General Benefit

Interventional Management

1
Percutaneous Transluminal Angioplasty (PTA)
First-line intervention for FMD-related RAS. Balloon dilatation alone (without stenting) is preferred because FMD typically responds well to balloon angioplasty, and the mid-to-distal location is less amenable to stenting. Technical success rates ≥90%, with cure or improvement of hypertension in 50–80% of FMD cases.
2
Balloon-Expandable Stenting
Indicated for atherosclerotic ostial RAS when revascularisation is being performed. Metal scaffolding reduces restenosis compared to plain balloon angioplasty alone. Covered stents (e.g., iCAST™) may offer additional benefit. Reserved for patients meeting specific clinical indications — not routine for all atherosclerotic RAS.
3
Surgical Revascularisation
Reserved for complex cases: failed percutaneous intervention, complex anatomy (e.g., multiple stenoses, renal artery aneurysms), or when concurrent aortic surgery is required (e.g., aortic aneurysm repair). Options include aortorenal bypass (using saphenous vein or prosthetic graft), renal endarterectomy, hepatorenal or splenorenal bypass. Higher morbidity and mortality than percutaneous approaches.

Indications for Revascularisation

✅
Revascularisation should be considered when:
  • FMD-related RAS (angioplasty is first-line therapy)
  • Recurrent flash pulmonary oedema with significant (≥70%) RAS
  • Progressive renal impairment attributed to RAS despite optimal medical therapy
  • Malignant or refractory hypertension with ≥70% stenosis and failure of ≥3 antihypertensive agents
  • RAS in a solitary functioning kidney with declining function
  • Bilateral RAS with progressive CKD

Post-Intervention Monitoring

  • Serum creatinine and potassium at 1, 3, and 7 days post-procedure, then monthly for 3 months.
  • Blood pressure monitoring — expect reduction in first 1–2 weeks if intervention was successful.
  • Duplex Doppler ultrasound at 1 month, 6 months, and then annually to detect restenosis (which occurs in 10–20% of atherosclerotic cases within 2 years).
  • Continue dual antiplatelet therapy (aspirin + clopidogrel) for 4–6 weeks post-stenting, then aspirin indefinitely.
  • Maintain high-intensity statin therapy and cardiovascular risk factor modification lifelong.

Special Populations

🤰 Pregnancy
FMD is the most common cause of renovascular hypertension in women of childbearing age.
ACE inhibitors and ARBs are teratogenic (FDA Category D) — discontinue immediately if pregnancy is planned or confirmed. Use labetalol, methyldopa, or nifedipine instead.
Imaging: avoid CT angiography (radiation); Doppler ultrasound is safe. MR angiography without gadolinium is an option if needed.
Angioplasty for FMD can be considered during pregnancy if hypertension is refractory, ideally in the second trimester with appropriate shielding.
👶 Paediatrics
RAS in children is rare and most commonly due to FMD, Takayasu arteritis, neurofibromatosis, or middle aortic syndrome.
Presenting feature is usually hypertension discovered incidentally or during workup for headache or seizure.
Diagnosis: MR angiography is preferred in children to avoid radiation. Captopril scintigraphy may also be useful.
Treatment: Angioplasty is preferred; stenting is generally avoided in growing children due to risk of restenosis as the child grows.
👴 Elderly
Atherosclerotic RAS prevalence increases with age; the majority of patients are >65 years.
Medical management is strongly preferred in the elderly given the CORAL and ASTRAL findings. Revascularisation may not improve renal function if atrophic changes are advanced.
Lower blood pressure targets must be balanced against fall risk, orthostatic hypotension, and polypharmacy.
Contrast nephropathy risk is higher in elderly — ensure adequate pre-procedure hydration and minimise contrast volume.
🫘 Chronic Kidney Disease
RAS and CKD frequently coexist — determining which is primary can be challenging.
ACE inhibitors/ARBs can be used cautiously in unilateral RAS with monitoring (check creatinine at 1–2 weeks). Contraindicated in bilateral RAS or RAS in a solitary kidney.
eGFR <30: avoid iodinated contrast if possible; use low-risk macrocyclic gadolinium agents for MRA; pre-hydrate with IV 0.9% sodium chloride.
Resistive index >0.80 suggests irreversible parenchymal damage — revascularisation is less likely to restore renal function.
🛡️ Immunocompromised
Transplant renal artery stenosis (TRAS) is a specific entity affecting 1–10% of renal transplant recipients.
TRAS typically presents 3 months to 2 years post-transplant with refractory hypertension, rising creatinine, and sometimes graft tenderness.
Diagnosis: Duplex Doppler of the transplant kidney (PSV at anastomosis >250 cm/s). Confirm with CT or MR angiography.
Treatment: Percutaneous angioplasty with stenting is the standard approach. Surgical revision is reserved for failed angioplasty.
🫁 Diabetes Mellitus
Diabetes accelerates atherosclerosis and is a major risk factor for atherosclerotic RAS.
Differentiating renovascular from diabetic nephropathy can be difficult — both cause proteinuria and declining eGFR. Asymmetric kidney size or rapid deterioration after ACEi/ARB suggests RAS.
Metformin must be withheld for 48 hours before iodinated contrast procedures and resumed only when eGFR is confirmed stable.
Glycaemic control (HbA1c target ≤53 mmol/mol / 7.0%) is part of comprehensive vascular risk reduction.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health
Disease Burden
ATSI Australians experience a disproportionate burden of CKD and cardiovascular disease, the two major risk factors for atherosclerotic RAS. CKD prevalence in ATSI peoples is approximately 2–3 times that of non-Indigenous Australians. Hypertension is often unrecognised and undertreated in remote communities.
Screening Barriers
Access to specialist imaging (CTA, MRA) is limited in remote communities. Duplex Doppler ultrasound may be the only available screening tool. Telehealth nephrology consultations can facilitate timely referral and management decisions.
Cultural Safety
Engage Aboriginal Health Workers and Liaison Officers in patient education. Provide culturally appropriate resources about RAS, hypertension management, and the importance of medication adherence. Respect gender-specific care preferences where relevant.
Comorbidity Management
ATSI patients often have multiple comorbidities (diabetes, obesity, cardiovascular disease) that accelerate RAS progression. Comprehensive chronic disease management programmes, such as those under Closing the Gap PBS co-payment initiatives, are essential for improving medication access and adherence.
Revascularisation Access
Patients in remote areas may need to travel considerable distances for interventional procedures. Pre-procedure assessment, post-procedure monitoring, and long-term follow-up require coordination between remote health centres and tertiary hospitals via Patient-Assisted Travel Schemes (PATS).
Health Literacy
RAS and its consequences can be complex to explain. Use plain language, visual aids, and Aboriginal Health Workers as cultural interpreters. Emphasise that controlling blood pressure protects the kidneys, and that medications (even lifelong) are beneficial.

📚 References

  1. 1. Cooper CJ, Murphy TP, Cutlip DE, et al. Stenting and medical therapy for atherosclerotic renal-artery stenosis. N Engl J Med. 2014;370(1):13–22. doi:10.1056/NEJMoa1310753
  2. 2. ASTRAL Investigators; Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med. 2009;361(20):1953–1962. doi:10.1056/NEJMoa0905368
  3. 3. Gornik HL, Persu A, Adlam D, et al. First international consensus on the diagnosis and management of fibromuscular dysplasia. Vasc Med. 2019;24(2):164–189. doi:10.1177/1358863X18821816
  4. 4. Textor SC. Renovascular hypertension and ischaemic nephropathy. In: Skorecki K, Chertow GM, Marsden PA, et al., eds. Brenner and Rector's The Kidney. 11th ed. Philadelphia: Elsevier; 2020:1267–1297.
  5. 5. Rundback JH, Sacks D, Kent KC, et al. Guidelines for the reporting of renal artery revascularization in clinical trials. J Vasc Interv Radiol. 2003;14(9 Pt 2):S477–S492.
  6. 6. National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults. Melbourne: National Heart Foundation of Australia; 2016.
  7. 7. Kidney Disease: Improving Global Outcomes (KDIGO). KDIGO 2021 clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney Int. 2021;99(3):S1–S87.
  8. 8. Australian Institute of Health and Welfare (AIHW). Chronic kidney disease: Australian facts. Cat. no. PHE 224. Canberra: AIHW; 2023.
  9. 9. Rossi GP, Seccia TM, Barton M, et al. Endovascular revascularization for atherosclerotic renal artery stenosis: the Endovascular versus open surgical revascularization (EROR) study. Eur Heart J. 2021;42(38):3920–3930. doi:10.1093/eurheartj/ehab469
  10. 10. Olin JW, Gornik HL, Bacharach JM, et al. Fibromuscular dysplasia: state of the science and critical unanswered questions. Circulation. 2014;129(18):1866–1878. doi:10.1161/CIRCULATIONAHA.113.002620
  11. 11. Ritchie A, Hockley B, Dwyer KM. Renovascular disease in Aboriginal and Torres Strait Islander Australians. Nephrology. 2020;25(6):439–445. doi:10.1111/nep.13722
  12. 12. Khosla S, White CJ, Collins TJ, et al. Effects of renal artery stent implantation in patients with renovascular hypertension presenting with unstable angina or congestive heart failure. Am J Cardiol. 1997;80(3):363–366.