Renal artery stenosis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, Serge Korjian
Overview
Renal artery stenosis is defined as the unilateral or bilateral progressive narrowing of the renal arteries or their proximal branches of more than 50% in diameter.[1] It is a heterogeneous group of diseases that most commonly include: fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS). Although renal artery stenosis may be an isolated asymptomatic condition, it may commonly lead to secondary hypertension that is thus called renovascular hypertension (RVHT), ischemic nephropathy, and chronic renal insufficiency.[2][3]
Approximately 90% of renal artery stenosis cases occur due to progressive atherosclerosis. The ostium and proximal third of the renal arteries are the most commonly involved regions in atherosclerosis.[4] Nonetheless, segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of chronic kidney disease and poor renal survival.[4]
Pathophysiology
The reduction in renal blood flow secondary to renal artery stenosis stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system. Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling.[5]
Causes
Renal artery stenosis is most commonly caused by development of atherosclerotic plaque in the renal arteries (termed atherosclerotic renal artery stenosis). Less frequently, it is caused by fibromuscular dysplasia.
Classification
Renal artery stenosis may be classified according to whether there is unilateral or bilateral involvement of the renal arteries. Additionally, renal artery stenosis is often classified anatomically according to severity of luminal narrowing. The following criteria are used according to most published studies about ARAS.[6][7]
| Severity | Luminal Narrowing |
| Normal | 0% |
| Mild | 1-49% |
| Moderate | 50-69% |
| Severe | 70-99% |
| Occluded | 100% |
To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.[8]
Another classification is based on hemodynamic function in RAS. This classification simply differentiates between hemodynamically insignificant RAS (< 75% stenosis) and hemodynamically significant RAS (> 75% stenosis).[9]
Epidemiology and Demographics
Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly. The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies. The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as diabetes mellitus, dyslipidemia, essential hypertension, and known coronary or peripheral artery disease.
Risk Factors
Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are those similar for other types of atherosclerosis, such as advanced age, dyslipidemia, diabetes mellitus, smoking, and hypertension.
Diagnosis
Non-invasive diagnosis is the first line for screening of ARAS. Doppler ultrasonography, CTA, and MRA may all be used to diagnose ARAS. Invasive diagnostic technique, such as renal angiography, is considered the gold standard for diagnosis and may be used when concomitant catheterizations are needed or when previously performed non-invasive techniques yielded equivocal results.
Diagnostic Criteria | History and Symptoms | Physical Examination | X Ray | CT | MRI | Echocardiography or Ultrasound
Treatment
Medical therapy is considered the first line of management for patients with ARAS. Several anti-hypertensive medications have proven to be efficacious in ARAS patients. According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have effect on both lowering BP and delaying renal disease. Other blood pressure lowering medications include beta-blockers, hydrazine, and chlorothiazide. Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.
Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical end points are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur in substantial costs without a significant public health advantage[10]
Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.
Medical Therapy | Angioplasty and Stenting | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
Related Chapters
- Renovascular hypertension
- Acute renal failure
- Atherosclerosis
- Chronic glomerulonephritis
- Hypersensitivity nephropathy
- Hypertension
- Malignant hypertension
- Nephrosclerosis
- Renovascular hypertension
- Uremia
External Links
- Bilateral Renal Artery Stenosis
{{#ev:youtube|xeV3lmYi1Hk}}
- Right Renal Artery Stenosis
{{#ev:youtube|4UzLFatOg1Q}}
References
- ↑ Simon G (2000). "What is critical renal artery stenosis? Implications for treatment". Am J Hypertens. 13 (11): 1189–93. PMID 11078179.
- ↑ Dworkin LD, Cooper CJ (2009). "Clinical practice. Renal-artery stenosis". N Engl J Med. 361 (20): 1972–8. doi:10.1056/NEJMcp0809200. PMID 19907044.
- ↑ Zierler RE, Bergelin RO, Isaacson JA, Strandness DE (1994). "Natural history of atherosclerotic renal artery stenosis: a prospective study with duplex ultrasonography". J Vasc Surg. 19 (2): 250–7, discussion 257-8. PMID 8114186.
- ↑ 4.0 4.1 Safian RD, Textor SC (2001). "Renal-artery stenosis". N Engl J Med. 344 (6): 431–42. doi:10.1056/NEJM200102083440607. PMID 11172181.
- ↑ Garovic, VD.; Textor, SC. (2005). "Renovascular hypertension and ischemic nephropathy". Circulation. 112 (9): 1362–74. doi:10.1161/CIRCULATIONAHA.104.492348. PMID 16129817. Unknown parameter
|month=ignored (help) - ↑ Kliewer MA, Tupler RH, Carroll BA, Paine SS, Kriegshauser JS, Hertzberg BS; et al. (1993). "Renal artery stenosis: analysis of Doppler waveform parameters and tardus-parvus pattern". Radiology. 189 (3): 779–87. doi:10.1148/radiology.189.3.8234704. PMID 8234704.
- ↑ Desberg AL, Paushter DM, Lammert GK, Hale JC, Troy RB, Novick AC; et al. (1990). "Renal artery stenosis: evaluation with color Doppler flow imaging". Radiology. 177 (3): 749–53. doi:10.1148/radiology.177.3.2243982. PMID 2243982.
- ↑ Lao D, Parasher PS, Cho KC, Yeghiazarians Y (2011). "Atherosclerotic renal artery stenosis--diagnosis and treatment". Mayo Clin Proc. 86 (7): 649–57. doi:10.4065/mcp.2011.0181. PMC 3127560. PMID 21719621.
- ↑ Kidney Disease Outcomes Quality Initiative (K/DOQI) (2004). "K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease". Am J Kidney Dis. 43 (5 Suppl 1): S1–290. PMID 15114537.
- ↑ Cooper CJ, Murphy TP, Cutlip DE, Jamerson K, Henrich W, Reid DM; et al. (2014). "Stenting and medical therapy for atherosclerotic renal-artery stenosis". N Engl J Med. 370 (1): 13–22. doi:10.1056/NEJMoa1310753. PMID 24245566.