- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Renal Artery Stenosis: Current Insights and Advances in Management
José C Rosario-Curcio1, Karthiga Vasudevan2, Chander Perkash Khatri3, Viraj Shetty4, Marcellina Nwosu5, Ruth Milena Machado6, Sahithya Ekasi7, Albine Djeagou8, Shanthanand Sreekar Chinthapally7, Yashita Arora9, Sossoh Patricia10, and Maria Isabel Gomez-Coral11*
1University of Medicine & Health Sciences, St. Kitts
2Yerevan State Medical University, Armenia
3Chandka Medical College
4Bangalore Medical College and Research Institute, India
5American University of Integrative Sciences, Barbados and Desert Regional Medical Center, USA
6Universidad Nacional Experimental Francisco de Miranda, Venezuela
7Pinnamaneni Siddhartha Institute of Medical Sciences and Research Foundation, India
8Faculty of Health sciences, University of Buea Cameroon
9Rajiv Gandhi Medical College and Chhatrapati Shivaji Maharaj Hospital, Thane, India
10Tongji Medical School of Huazhong University of Science and Technology, China
11Universidad del Valle, México
Submission: June 06, 2024;Published: June 21, 2024
*Corresponding author: Maria Isabel Gomez-Coral, Department of Medicine, Universidad del Valle de, Mexico
How to cite this article: José C R-C, Karthiga V, Chander Perkash K, Viraj S, Marcellina N, et al. Renal Artery Stenosis: Current Insights and Advances 004 in Management. JOJ Urology & Nephrology, 2024; 9(1): 555754. DOI:10.19080/JOJUN.2024.09.555754.
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Abstract
Renal artery stenosis (RAS) presents a significant challenge in clinical practice, often leading to treatment-resistant hypertension and renal dysfunction. This review provides a comprehensive overview of the current insights and advances in managing RAS, encompassing its pathophysiology, diagnosis, treatment strategies, recent research, and future directions. RAS, predominantly caused by atherosclerosis or fibromuscular dysplasia, poses a substantial burden on affected individuals, necessitating early diagnosis and intervention to mitigate its adverse effects on renal function and cardiovascular health. Recent advancements in diagnostic imaging modalities, such as contrast-enhanced magnetic resonance angiography (CE-MRA) and phase-contrast magnetic resonance angiography (PC-MRA), offer enhanced anatomical and functional insights into RAS without requiring invasive procedures. Furthermore, innovative interventional techniques, including drug-eluting stents and minimally invasive surgical approaches, demonstrate promising outcomes in addressing complex RAS cases. Clinical trials, notably the CORAL trial, provide valuable evidence for the efficacy and safety of various management strategies, guiding clinicians in making informed decisions tailored to individual patient needs. Future directions in RAS research may involve further refinement of imaging techniques, exploration of personalized medicine approaches, and the development of targeted therapies to address underlying pathophysiological mechanisms. Collaborative efforts between clinicians, researchers, and industry partners are essential in driving innovation and advancing the field toward improved outcomes and quality of life for patients with RAS. Through continued research and innovation, the prognosis for patients with RAS promises enhanced management strategies and improved long-term outcomes.
Keywords: Renal Artery Stenosis; RAS; Angiotensin-Converting Enzyme; Pathophysiology; ischemic nephropathy
Abbreviations: RAS: Renal Artery Stenosis; RAAS: Renin-Angiotensin-Aldosterone System; ACE: Angiotensin-Converting Enzyme; ARBs: Angiotensin Receptor Blockers; LDL: Low-Density Lipoprotein; DM: Diabetes Mellitus; PTA: Percutaneous Transluminal Angioplasty; CORAL: Cardiovascular Outcomes in Renal Atherosclerotic Lesions; CTA: Computed Tomography Angiography; MRA: Magnetic Resonance Angiography; FMD: Fibromuscular Dysplasia; CE-MRA: Contrast-Enhanced Magnetic Resonance Angiography; PC-MRA: Phase-Contrast Magnetic Resonance Angiography; CIN: Contrast-Induced Nephropathy; AKI: Acute Kidney Injury; ACEI: Angiotensin-Converting Enzyme Inhibitor; AT1R: Angiotensin II Type 1 Receptor; PAD: Peripheral Artery Disease
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Introduction
Renal artery stenosis is a disease characterized by stenosis of one of both renal arteries. This stenosis leads to reduced perfusion to the kidneys, which leads to activation of the renin-angiotensin-aldosterone system (RAAS), increasing more volume, which presents clinically as treatment-resistant hypertension. This condition is the most common cause of secondary hypertension, with up to 10% of the population having this etiology [1]. Although RAS can occur through several mechanisms, the most common is atherosclerosis, particularly in older adults with comorbid conditions, and fibromuscular dysplasia is the second most common cause, seen most in women younger than 50 [2]. Some less common causes of RAS include infrarenal aortic aneurysm, arterial dissection, thromboembolic disease, vasculitis, neurofibromatosis type 1, and retroperitoneal fibrosis [3]. RAS is also associated with other comorbidities, including carotid artery disease, stroke, coronary artery disease, myocardial infarction, abdominal aortic aneurysm, and other occlusive vascular diseases [4]. Because of the nature of the pathology, early diagnosis and management are integral for survival, as the mortality rate in patients with RAS was as high as 35% in some studies [5].
The scope of this study is to condense current insights and management of RAS and provide an updated and informative review of the treatment of this condition, which could appear relatively commonly in specific populations. RAS diagnosis and management continue to be of utmost importance, as understanding etiology and pathophysiology and combining them with current management will allow patients with secondary hypertension a chance to control it and prevent deterioration of renal function and other comorbidities that hypertension is associated with.
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Pathophysiology
Theoretically, renal artery stenosis contributes to renovascular hypertension and nephropathy based on its effects on the renin-angiotensin-aldosterone system (RAAS). The RAAS maintains vascular tone, water/salt balance, and cardiac function through interactions with the sympathetic nervous system and several hormones. It is activated by hypotension, decreased intravascular volume, hyponatremia, hypokalemia, and alterations in chloride based on intravascular volume through the Na+-K2+-Cl- co-transporter in the macula densa within the kidney. Once the RAAS is activated, the juxtaglomerular apparatus within the kidney releases renin, which cleaves angiotensinogen to angiotensin I. Angiotensin I is then further cleaved by angiotensin-converting enzyme (ACE) to angiotensin II, which binds to AT1 receptors within the kidney to cause vasoconstriction of the efferent arterioles, stimulation of aldosterone, and increased sodium reabsorption [6].
In RAS, decreased perfusion pressure to the kidneys is secondary to the stenotic renal artery, leading to RAAS activation. In activating the RAAS, the goal is to increase renal perfusion by increasing systemic blood pressure. In RAS, the vasoconstriction in the efferent arterioles of the glomeruli leads to short-term preservation of the glomerular filtration and protection from hypotension and relative hypoxia. While the RAAS provides short-term protection in RAS, over the long term, it leads to ischemic nephropathy in the affected kidney, hypertensive nephrosclerosis in the unaffected kidney, and glomerulosclerosis and tubule-interstitial fibrosis in both kidneys [7]. Glomerulosclerosis and tubule interstitial fibrosis are thought to be caused by elevated levels of angiotensin II, associated with inflammatory cytokines that lead to increased activation of inflammatory and profibrogenic pathways [8]. Additional processes associated with RAS include endothelial dysfunction causing impaired vascular relaxation, leading to tubule-interstitial fibrosis, and increased sympathetic adrenergic activity causing microvascular damage [9,10].
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
Renal artery stenosis (RAS) is a disease that consists of a broad spectrum of different entities with different pathophysiologies that require varied approaches to diagnosis and treatment. The two most common causes of RAS are fibromuscular dysplasia and atherosclerosis, which comprise approximately 10% and 90% of RAS [6]. These entities are unilateral (unilateral atherosclerotic renal artery stenosis, unilateral fibromuscular dysplasia, arterial embolus) or bilateral (bilateral atherosclerotic renal artery stenosis), and RAS may also occur as renal artery stenosis to a solitary kidney [11]. FMD is currently defined as an idiopathic, segmental, noninflammatory, and nonatherosclerotic disease of the musculature of arterial walls leading to stenosis, aneurysms, dissections, and occlusions of small‐ and medium‐sized arteries, namely the renal and carotid arteries. The disease involves the renal arteries with a frequency of 60% to 75%. The right renal artery is the dominant site of FMD, although a bilateral appearance is also possible in up to 40% of cases. The etiology of FMD is unknown, although various hormonal and mechanical factors have been suggested. Environmental factors such as smoking, exposure to endogenous or exogenous estrogens, and repeated stretching of the renal artery, as in kidney mobility, have also been associated with FMD, but the exact association remains unclear. It appears to be familial in 10% of cases, especially among Caucasians. In addition, an association between FMD and the HLA-DRw6 histocompatibility antigen has also been described [12]. On angiography, FMD has classically been described as having a “beads-on-a-string” appearance due to the contrast filling of consecutive aneurysms along the renal artery. FMD is generally associated with a good prognosis and usually does not progress to complete occlusion [13].
Atherosclerotic renal artery stenosis (ARAS) is predominantly seen in older patients as a part of systemic atherosclerosis and the presence of atherosclerotic changes in the abdominal aorta. ARAS is diagnosed mainly in men (male: female is 2:1) older than 50-55 years. Patients often present characteristic risk factors: diabetes, hypertension, dyslipidemia, smoking history, peripheral vascular disease, and coronary syndromes [14]. There is some genetic background predisposing to the development of ARAS. A significantly higher frequency of the angiotensin-converting enzyme (ACE) gene ACE-D allele when compared to matched control subjects was demonstrated in ARAS patients. The mechanism responsible for the increased risk of renal artery disease in patients with ACE-D allele may be linked to the overexpression of active angiotensin-converting enzyme in plasma or on endothelial cells (contributing to elevation of circulating and/or local angiotensin II levels and reduction in bradykinin level). Another genetic variant that could affect the renal vasculature is the angiotensin II type 1 receptor A1166C (AT1R A1166C) polymorphism. Patients homozygous for the C allele of this polymorphism have increased sensitivity to angiotensin II. They may, in combination with the ACE-D allele, have an increased risk of cardiovascular complications. Unlike FMD, atherosclerotic changes in the renal vessels often cause total obstruction of the renal artery and subsequent severe ischemic complications [15].
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
Kidneys are a relatively over perfused organ when referring to RBF’s metabolic requirements, and high RBF ensures the most important function of the kidneys as a filtering organ. Studies have demonstrated that only about 10% of the oxygen in a perfusing kidney's blood is necessary to maintain the energy demand of this organ [10,11,14]. Therefore, in a kidney affected by RAS, the blood flow may noticeably fall but without the inevitable threat to the viability of the kidney tissue. Moderate RBF reduction may be sufficient to disturb GFR. It may achieve a value below the level needed for renal autoregulation of RBF, which results in invariable activation of pressor mechanisms (RAAS activity) and initiation of RVH, with a subsequent diminishing of the kidney size while maintaining oxygen supply to both the cortex and the medulla of the stenotic kidney and without apparent rebuilding of the kidney tissues [10,12,14]. Therefore, the term “azotemic renovascular disease” is proposed by some authors as more adequate compared to the commonly used “ischemic nephropathy” for the description of such an entity [13-15]. The more severe and prolonged diminishing of RBF in the stenotic kidney may threaten the oxygen supply to the organ and viability of the tissues, eventually leading to kidney fibrosis. The inflammatory and profibrotic mechanisms prevailing in advanced RAS contribute to the advanced, pathological remodeling of the kidney structure, which evidences ongoing chronic kidney injury and ultimately accounts for up to 15–20% of the cases of chronic kidney disease developing [14].
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Epidemiology
The prevalence of Renal Artery Stenosis (RAS) is challenging to determine in the general population due to the necessity of advanced imaging techniques for accurate identification. This review compiles data from various research studies examining the prevalence of RAS across different populations. RAS has two leading causes, atherosclerotic and nonatherosclerotic. Atherosclerotic RAS accounts for 90% of cases, with the prevalence among individuals over 65 years of age reaching up to 7%, based on community-based screenings [16]. Nonatherosclerotic RAS, which includes fibromuscular dysplasia (FMD) as the most common cause, comprises approximately 10% of RAS cases. One study utilizing renal artery duplex sonography within the Cardiovascular Health Study reported that more than 60% stenosis was present in 6.8% of black and white participants. (2) Age-related data showed an increase in atherosclerotic RAS prevalence: 0% in individuals aged 40-49, 2% in those aged 50-59, and 11%, 13%, and 14% in the age groups 60-69, 70-79, and 80+ years, respectively. Additional studies indicate that RAS may be responsible for 1-5% of hypertension cases in unselected patients and 5-22% in patients aged 50 and above with end-stage renal disease. Kuroda et al. found that 10.4% of stroke patients over 40 years of age had atherosclerotic RAS (≥75% luminal narrowing) in an autopsy study [18].
Furthermore, they reported RAS in 14.7%, 28.6%, and 23.9% of patients with hypertension, renal insufficiency, and aortic aneurysm, respectively [18]. Another study in Japanese patients with peripheral artery disease (PAD) showed a prevalence of 22.9% for RAS >50% and 11.0% for RAS >75% [19]. In patients with atherosclerosis elsewhere, particularly those with abdominal aortic and aortoiliac disease, the occurrence of RAS can be as high as 39% [20]. Kalra et al. followed a random sample of the US Medicare population over two years, reporting an incidence rate of renovascular atherosclerotic disease at 3.7 per 1000 patient-years [21]. A study assessing renal artery disease in 14,152 patients undergoing cardiac catheterization found insignificant disease (<50% stenosis) in 5.1% and significant stenosis in 6.3% of cases [22]. Uzu et al. studied 297 myocardial infarction (MI) patients over 40 years old and found a 12% prevalence of atherosclerotic RAS, with higher rates in those with hypertension (19%), proteinuria (39%), and renal insufficiency (39%) [23]. Additionally, renal artery stenosis develops in 1-12% of transplanted kidneys [24]. Our narrative review emphasizes the prevalence of RAS varies significantly across different populations and conditions, influenced by factors such as age, presence of hypertension, renal insufficiency, and coexisting atherosclerotic diseases.
The risk factors for Renal Artery Stenosis (RAS) are closely aligned with those for generalized atherosclerosis. The conditions of dyslipidemia, hypertension, cigarette smoking, diabetes mellitus, viral infections, immunological damage, and elevated homocysteine levels are significant causes of endothelial dysfunction, which comes before atherosclerosis [24]. For those with arterial atherosclerotic disease in other areas of their bodies, the chance of developing atherosclerotic renal artery stenosis (ARAS) ranges from 26% to 50% [17]. According to a research by Harding et al., there are five main risk factors predictive for RAS: getting older, having a history of congestive heart failure, having a severe case of coronary artery disease, being a woman, and having peripheral vascular disease. Furthermore, it was discovered that renal insufficiency and proteinuria were independent predictors of RAS [20]. Notably, no association was discovered between ethnicity and RAS [17].
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Clinical Presentation
RAS has an insidious onset, and its diagnosis remains a challenge to clinicians. It is often ignored due to other confounding and mimicking conditions, necessitating comprehensive and invasive diagnostic procedures [25]. RAS may be asymptomatic or can manifest as active cardiovascular symptoms, including renovascular hypertension (RVH), described as uncontrolled hypertension in a patient on maximum doses of at least three different antihypertensive medications. Patients can present with confusion, shortness of breath, nausea and vomiting, generalized edema, fatigue, muscle cramps, dry and itchy skin, and weight loss [26]. RAS is also associated with the onset of hypertension (HTN) in patients 50 years or older as well as in patients younger than 30 years due to fibromuscular dysplasia [25-27]. Malignant hypertension, worsening of prior well-controlled HTN, lack of family history of hypertension, and sudden onset of hypertension are all associated with RAS [25,27].
Other presenting symptoms of RAS include frequent pulmonary edema without history of congestive heart failure, decline in renal function, unilateral small kidney on imaging, acute kidney injury (AKI), and critical elevation of creatinine after administration of angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II type 1 receptor blocker (ARBs), abdominal or flank bruit on auscultation, hypokalemia, and ischemic nephropathy [25,27]. RAS patients can also present with vascular diseases involving carotid and coronary arteries and retinopathy. A history of cigarette smoking may be present [25,27]. Coronary artery disease is a primary determinant of RAS [25]. As mentioned above, diagnosing renal artery stenosis can be challenging and, therefore, requires thorough work to eliminate other conditions with similar presentations as RAS. These conditions may include hypertensive nephrosclerosis, atheroembolic renal disease, AKI, and malignant hypertension [25-29].
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Diagnostic Approaches
Renal artery stenosis (RAS) is primarily caused by atherosclerosis, with fibromuscular dysplasia being less common and other rare causes [30]. Atherosclerotic RAS prevalence increases with age and is higher among patients with diabetes, aortoiliac occlusive disease, coronary artery disease, or hypertension. Clinically evident atherosclerotic RAS prevalence is 0.5% overall and 5.5% among chronic kidney disease patients [31]. Patients with RAS often have comorbidities like chronic kidney disease, coronary artery disease, stroke, and peripheral vascular disease [30].
Diagnosis of RAS involves various non-invasive methods, including ultrasound, CT angiography (CTA), and magnetic resonance angiography (MRA) [32]. Doppler ultrasound, though adequate for severe stenosis detection, has limitations in detecting moderate stenosis and accessory renal arteries. Criteria for diagnosing RAS via Doppler ultrasound include peak systolic velocity increase, renal-to-aortic peak systolic velocity ratio, post-stenotic turbulence, and visualization of the renal artery. CTA offers detailed images but has limitations in evaluating small arteries and may overstate stenosis [32-36]. MRA, especially contrast-enhanced MRA, provides anatomical and functional information without radiation but may have limitations in detecting distal stenosis [37-39].
Invasive methods like digital subtraction angiography (DSA) remain crucial for RAS diagnosis, offering detailed images while minimizing radiation exposure [32]. Intra-arterial DSA is the standard technique, providing clear images of the vessel lumen. Intravenous DSA offers a less invasive alternative but may miss some cases, especially fibromuscular dysplasia [32]. DSA effectively identifies RAS, including cases missed by other modalities like CTA and MRA [36]. Diagnosis should integrate clinical and laboratory criteria, including serum creatinine concentrations, proteinuria levels, and serologic testing for conditions like systemic lupus erythematosus or vasculitis [32]. A comprehensive approach combining non-invasive imaging, invasive methods, and clinical and laboratory criteria is essential for accurate RAS diagnosis and management.
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Management Strategies
Pharmacological management of renal artery stenosis (RAS) focuses on controlling hypertension and mitigating cardiovascular risks. Medications such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), calcium-channel blockers, and beta-blockers are essential in blood pressure control for unilateral RAS-associated hypertension. However, caution is warranted with RAAS inhibitors due to the risk of acute renal failure, especially in severe bilateral RAS or advanced chronic kidney disease cases. Additionally, the CORAL trial underscores the importance of comprehensive medical management, including LDL cholesterol reduction with high-intensity statins, smoking cessation, glycemic control in diabetes, and antiplatelet therapy to reduce cardiovascular morbidity and mortality [40-43].
Interventional procedures like percutaneous transluminal angioplasty (PTA) and stenting are primary options for RAS. PTA involves balloon catheter inflation to dilate the stenotic artery, while stenting provides structural support. These interventions are indicated for hemodynamically significant stenosis refractory to medical therapy or associated with target organ damage. PTA is preferred for fibromuscular dysplasia, while stenting is recommended for atherosclerotic lesions meeting clinical criteria for intervention [40,44,45]. Percutaneous revascularization may be considered for various clinical scenarios, including asymptomatic bilateral or solitary viable kidney with significant RAS, chronic renal insufficiency with unilateral RAS, and cases of accelerated or resistant hypertension. Surgical revascularization techniques are reserved for complex cases of fibromuscular dysplasia or extensive atherosclerotic disease. Vascular surgical reconstruction aims to restore blood flow while minimizing perioperative risks, especially for patients with complex disease extending into segmental arteries or multiple small renal arteries [46-48]. The choice of management strategy depends on patient characteristics, disease severity, and treatment goals. While medical management offers broad applicability, interventional procedures provide immediate relief but carry procedural risks and require long-term surveillance. Surgical revascularization, though invasive, may be necessary for complex cases that are not amenable to less invasive approaches. Each approach should be carefully tailored to individual patient needs.
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Recent Advances and Research
Recent advances in renal artery stenosis have brought forth innovative techniques that revolutionize diagnosis and treatment approaches [49-50]. Cutting-edge technologies, such as advanced imaging modalities like contrast-enhanced magnetic resonance angiography (CE-MRA) and phase-contrast magnetic resonance angiography (PC-MRA), offer enhanced anatomical and functional insights into RAS without the need for invasive procedures or ionizing radiation [49-51]. These non-invasive methods provide valuable information for accurate diagnosis and treatment planning, improving patient outcomes while minimizing risks. Additionally, novel interventional techniques, including drug-eluting stents and minimally invasive surgical approaches, show promising results in addressing complex RAS cases, highlighting the continual evolution of treatment strategies in the field [52-55]. Recent clinical trials have shed light on the efficacy and safety of various management approaches for RAS, providing crucial insights for optimizing patient care [49,52]. Studies like the CORAL trial have emphasized the importance of comprehensive medical management, while others have explored the role of percutaneous revascularization and surgical interventions in different patient populations [49,53,55]. These trials contribute to evidence-based practices, guiding clinicians in making informed decisions tailored to individual patient needs. Future directions in RAS research may involve further refinement of imaging techniques, exploration of personalized medicine approaches, and the development of targeted therapies to address underlying pathophysiological mechanisms [50]. Collaborative efforts between clinicians, researchers, and industry partners are essential in driving innovation and advancing the field toward improved outcomes and quality of life for patients with RAS.
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Prognosis and Outcomes
Short-term outcomes for patients with renal artery stenosis (RAS) who undergo treatment such as stenting or angioplasty are generally positive. However, results can vary based on patient characteristics and disease severity. Procedural success and complications are key metrics in assessing short-term outcomes. In a study focusing on high-risk patients with RAS, stenting procedures were generally successful, achieving complete revascularization in nearly half of the patients. However, complications such as contrast-induced nephropathy (CIN) occurred in approximately 33% of patients, particularly those with pre-existing diabetes and high baseline creatinine levels. Fortunately, none of the patients required hemodialysis during their initial hospital stay [56]. This finding is consistent with other studies indicating that procedural complications are a significant concern, particularly in patients with high-risk profiles [57]. Renal function improvement is another crucial outcome. Interventional procedures often yield immediate clinical benefits, with significant improvements in blood pressure control observed in most patients. For instance, one study reported that 69% of patients experienced an immediate clinical benefit in hypertension management post-procedure, with some achieving normalization of blood pressure without medication [57]. This aligns with findings from multiple studies that demonstrate the effectiveness of stenting in stabilizing or improving renal function [58].
The impact of stenosis severity and location on outcomes is also significant. The degree and position of stenosis play crucial roles in determining clinical outcomes. Moderate stenosis (50-70%) can still lead to substantial hemodynamic changes and affect renal perfusion, potentially necessitating prompt intervention. The hemodynamic environment near the stenosis can contribute to long-term risks like thrombosis and inflammation, highlighting the importance of considering both short-term and long-term outcomes in treatment planning [58]. Computational studies further support these findings by illustrating how varying degrees of stenosis and their positions can influence renal perfusion and subsequent risks [59]. Short-term outcomes following interventions for renal artery stenosis are generally favorable, with improvements in hypertension and stabilization of renal function. However, the risk of complications such as CIN and the impact of stenosis characteristics on long-term risks should be carefully considered in clinical decision-making.
Long-Term Prognosis for RAS leads to a decrease in blood supply to the affected kidney and an increase to the contralateral one, with a worsening disparity as the stenosis increases. This leads to abnormal perfusion in the resting state, with a resultant impaired renal function [60-62]. Although the perfusion pressure increases in the normal kidney as a compensatory mechanism, it burdens it more, potentially leading to damage [63]. The degree of renal artery stenosis is correlated to systemic blood pressure and the risk of renal atrophy [64]. Invasive lesion management is one of the main treatment options for RAS. Although it has been shown to result in a significant decrease in BP, it is also at risk of recurrent restenosis, like all endovascular procedures [65,66]. The estimated incidence rate of this restenosis is between 6.5% and 40% [67]. These patients tend to present with recurrent symptoms, including recurrent hypertension and deterioration in renal function [68]. The diameter of the index vessel is a significant predictor of restenosis, with smaller vessels being more at risk [65-66,68].
Identifying factors that predict better outcomes in treating renal artery stenosis (RAS) is crucial for optimizing patient selection and improving overall treatment efficacy. Several key predictors have been identified through clinical research. First baseline Renal Function Baseline renal function is a significant predictor of successful outcomes in RAS treatment. Patients with better renal function before intervention typically experience more favorable results. Studies have demonstrated that lower baseline serum creatinine levels are associated with improved renal recovery following procedures such as angioplasty and stenting [56,57]. Second, the severity and anatomical location of the stenosis are critical factors influencing treatment success. Moderate stenosis (50-70%) can still lead to significant hemodynamic changes affecting renal perfusion, necessitating timely intervention. Lesions proximal to the aorta often have better outcomes due to superior perfusion than distal lesions, which are linked with poorer outcomes due to reduced renal perfusion [56-58]. Third, the presence of diabetes mellitus significantly impacts treatment outcomes. Diabetic patients are at a higher risk of developing complications such as contrast-induced nephropathy (CIN). Effective management of blood glucose levels before and after the procedure can substantially improve outcomes [58]. Fourth, post-intervention blood pressure control is a strong predictor of positive outcomes. Patients who achieve effective blood pressure management tend to experience better renal function recovery and overall success. Additionally, pre-procedural management of hypertension is crucial for predicting post-treatment success [59]. Fifth, the choice of procedural technique and the operator's experience significantly influence outcomes. Studies indicate that complete revascularization and advanced techniques lead to better results. Minimizing procedural complications through skilled and experienced intervention is essential for improving success rates [57].
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
Conclusion
Renal artery stenosis presents a complex pathophysiology and clinical spectrum, necessitating a multifaceted approach to diagnosis and management. Recent advances in diagnostic imaging modalities, interventional techniques, and pharmacological therapies have transformed the landscape of RAS management, offering patients personalized and effective treatment options. Innovative technologies such as contrast-enhanced magnetic resonance angiography (CE-MRA) and drug-eluting stents have revolutionized diagnosis and treatment approaches, improving patient outcomes while minimizing procedural risks. Clinical trials like the CORAL trial have provided crucial insights into the efficacy and safety of various management strategies, guiding evidence-based practices. Despite these advancements, challenges remain in predicting long-term outcomes and optimizing treatment selection for individual patients. Future directions in RAS research may involve further refinement of imaging techniques, exploration of personalized medicine approaches, and the development of targeted therapies to address underlying pathophysiological mechanisms. Collaborative efforts between clinicians, researchers, and industry partners are essential in driving innovation and advancing the field toward improved outcomes and quality of life for patients with RAS. Through continued research and innovation, the prognosis for patients with RAS promises enhanced management strategies and improved long-term outcomes.
- Review Article
- Abstract
- Introduction
- Pathophysiology
- Unveiling Origins: Distinguishing Atherosclerotic from Fibromuscular Dysplasia Causes
- Renal Dynamics Unveiled: RAS Influence on Kidney Perfusion and Function
- Epidemiology
- Clinical Presentation
- Clinical Presentation
- Management Strategies
- Recent Advances and Research
- Prognosis and Outcomes
- Conclusion
- References
References
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- Bokhari MR, Bokhari SRA (2023) Renal Artery Stenosis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.
- Colyer WR, Cooper CJ (2009) Cardiovascular morbidity and mortality and renal artery stenosis. Prog Cardiovasc Dis 52(3): 238-242.
- Conlon PJ, Athirakul K, Kovalik E, Schwab SJ, Crowley J, et al. (1998) Survival in renal vascular disease. J Am Soc Nephrol 9(2): 252-256.
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