eMedicine Specialties > Nephrology > Hypertension and the Kidney

Renal Artery Stenosis

Author: Bruce S Spinowitz, MD, FACP, Clinical Professor of Medicine, Weill Medical College of Cornell University; School of Medicine; Associate Chairman, Associate Director and Attending Physician, Department of Medicine, Division of Nephrology, New York Hospital Medical Center Queens; Associate, Nephrology Associates, PC
Coauthor(s): Joanna Rodriguez, MD, Fellow, Department of Internal Medicine, Division of Nephrology, New York Hospital-Queens
Contributor Information and Disclosures

Updated: Jul 15, 2009

Introduction

Background

Specialists have known for a long time that renal artery stenosis (RAS) is the major cause of renovascular hypertension and that it may account for 1-10% of the 50 million people in the United States who have hypertension.

Apart from its role in the pathogenesis of hypertension, renal artery stenosis is also being increasingly recognized as an important cause of chronic renal insufficiency and end-stage renal disease. In older individuals, atherosclerosis (ATH) is by far the most common etiology of renal artery stenosis. As the renal artery lumen progressively narrows, renal blood flow decreases and eventually compromises renal function and structure.

With the increase in the elderly population and the possible increase in the prevalence of renal artery stenosis and ischemic nephropathy, clinicians dealing with renovascular disease (RVD) need noninvasive diagnostic tools and effective therapeutic measures to resolve the problem successfully. This article explores the natural history of this disorder, the value of a variety of invasive and noninvasive diagnostic procedures, and the consequence of allowing the artery to remain obstructed versus reversing renal artery occlusion.

Pathophysiology

In patients with ATH, the initiator of endothelial injury is not clear; however, dyslipidemia, hypertension, cigarette smoking, diabetes mellitus, viral infection, immune injury, and increased homocysteine levels may contribute to endothelial injury. In the atherosclerotic lesion site, endothelium permeability to plasma macromolecules (eg, low-density lipoprotein [LDL]) increases, turnover of endothelial cells and smooth muscle cells increases, and intimal macrophages increase. When atherogenic lipoproteins exceed certain critical levels, the mechanical forces may enhance lipoprotein insudation in these regions, leading to early atheromatous lesions.

Renal blood flow is 3- to 5-fold greater than the perfusion to other organs because it drives glomerular capillary filtration. Both glomerular capillary hydrostatic pressure and renal blood flow are important determinants of the glomerular filtration rate (GFR).

In patients with renal artery stenosis, the chronic ischemia produced by the obstruction of renal blood flow produces adaptive changes in the kidney that are more pronounced in the tubular tissue. These changes include atrophy with decreased tubular cell size, patchy inflammation and fibrosis, tubulosclerosis, atrophy of the glomerular capillary tuft, thickening and duplication of the Bowman capsule, and intrarenal arterial medial thickening. In patients with renal artery stenosis, the GFR is dependent on angiotensin II and other modulators that maintain the autoregulation system between the afferent and efferent arteries and can fail to maintain the GFR when renal perfusion pressure drops below 70-85 mm Hg. Significant functional impairment of autoregulation, leading to a decrease in the GFR, is not likely to be observed until arterial luminal narrowing exceeds 50%.

The degree of renal artery stenosis that would justify any attempt at either surgical intervention or radiologic intervention is not known. A recent study suggested that a ratio of pressure, measured distal to renal artery stenosis, less than 90% relative to aortic pressure, was found to be associated with significant renin release from the affected kidney, renin being measured in the ipsilateral renal vein.1 This might be useful as a functional measurement of significant renovascular stenosis leading to hypertension and, thus, a marker of those individuals more likely to benefit from angioplasty and stenting.1

Frequency

United States

Studies suggest that ischemic nephropathy may be responsible for 5-22% of advanced renal disease in all patients older than 50 years.

Mortality/Morbidity

  • The consequences of renal artery stenosis are hypertension, which may be particularly difficult to control or may require multiple antihypertensive agents (with increased adverse effects), and progressive loss of renal function (ischemic nephropathy).
  • In addition, the discovery of atherosclerotic RVD frequently occurs in the setting of generalized vascular disease (ie, cerebral, cardiac, peripheral), with the co-morbidity associated with disease in those vascular beds. Thus, any therapeutic intervention for renal artery stenosis should logically take into account the underlying prognosis associated with these co-morbidities.

Race

  • RVD is less common in African American patients. The incidence rate in 2 studies of patients with severe hypertension was 27-45% in white persons compared to 8-19% in African American persons.

Sex

  • While the incidence of atherosclerotic RVD is independent of sex, Crowley et al showed that female sex (as well as older age, elevated serum creatinine level, coronary artery disease, peripheral vascular disease, hypertension, and cerebrovascular disease) is an independent predictor of RVD progression.2

Age

  • In 1964, Holley et al reported data from 295 consecutive autopsies performed in their institution during a 10-month period.3 The mean age at death was 61 years. The prevalence rate of renal artery stenosis was 27% of 256 cases identified as having history of hypertension, while 56% showed significant stenosis (>50% luminal narrowing), and, among normotensive patients, 17% had severe renal artery stenosis (>80% luminal narrowing). Among those older than 70 years, 62% had severe renal artery stenosis.
  • Another similar autopsy study reported similar results, with 5% of patients older than 64 years showing severe stenosis; this figure increased to 18% for patients aged 65-74 years and 42% for patients older than 75 years.

Clinical

History

Patients with documented or possible renovascular hypertension may experience progressive azotemia as a consequence of the renal ischemia and/or the persistence of significant hypertension. Refractory hypertension (ie, poor control of blood pressure despite treatment with 3 or more antihypertensive agents) may occur.

Physical

The strong association of RVD with generalized ATH indicates that any typical findings associated with cerebrovascular (eg, carotid bruits, old cerebrovascular accident, transient ischemic attack), cardiovascular, or peripheral vascular disease occur frequently in patients with RVD. Abdominal bruits are highly specific for RVD when heard over the flank and are back-and-forth in nature (ie, present during both systole and diastole).

Patients with ischemic RVD present with one or more of the following clinical, historical, or diagnostic scenarios:

  • Azotemia occurs in patients with peripheral vascular occlusive disease, carotid or coronary artery disease, and other signs of ATH.
  • Sudden worsening of hypertension or renal function may occur.
  • Acute renal failure or decreased renal function after antihypertensive therapy, especially with ACE inhibitors or angiotensin receptor blockers, may occur; an increase in serum creatinine levels of more than 15% in this setting is strongly suggestive of a high incidence of RVD.
  • Unexplained renal insufficiency may develop in elderly patients.
  • Congestive heart failure may occur with poor control of hypertension and renal insufficiency in the absence of a significant decrease in ejection fraction (the so-called flash pulmonary edema).

Causes

Risk factors associated with ischemic renal disease (IRD) are as follows:

  • Hypertension: Of patients with IRD, 35% can be normotensive.
  • Advanced age: Numerous cases occur in persons aged 60-69 years. Incidence increases in persons older than 70 years.
  • Renal insufficiency
  • Extrarenal ATH
  • Diabetes mellitus
  • Smoking

More on Renal Artery Stenosis

Overview: Renal Artery Stenosis
Differential Diagnoses & Workup: Renal Artery Stenosis
Treatment & Medication: Renal Artery Stenosis
Follow-up: Renal Artery Stenosis
References
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References

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Further Reading

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Keywords

renal artery stenosis, RAS, renovascular disease, ischemic nephropathy, atherosclerotic renovascular disease, renovascular hypertension, chronic renal insufficiency, end-stage renal disease, ESRD, atherosclerosis, ATH, RVD, renal artery occlusion, renal disease, kidney disease, ischemic renal disease, renal artery lesions

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Contributor Information and Disclosures

Author

Bruce S Spinowitz, MD, FACP, Clinical Professor of Medicine, Weill Medical College of Cornell University; School of Medicine; Associate Chairman, Associate Director and Attending Physician, Department of Medicine, Division of Nephrology, New York Hospital Medical Center Queens; Associate, Nephrology Associates, PC
Bruce S Spinowitz, MD, FACP is a member of the following medical societies: American College of Physicians, American Society of Nephrology, International Society for Peritoneal Dialysis, International Society of Nephrology, and Renal Physicians Association
Disclosure: AMAG Pharmaceuticals Grant/research funds Independent contractor; Roche Grant/research funds Independent contractor; Amgen Grant/research funds Independent contractor; Affymax Grant/research funds Independent contractor; Ortho Biotech Grant/research funds Independent contractor

Coauthor(s)

Joanna Rodriguez, MD, Fellow, Department of Internal Medicine, Division of Nephrology, New York Hospital-Queens
Disclosure: Nothing to disclose.

Medical Editor

Donald A Feinfeld, MD, FACP, FASN, Consulting Staff, Division of Nephrology & Hypertension, Beth Israel Medical Center
Donald A Feinfeld, MD, FACP, FASN is a member of the following medical societies: American Academy of Clinical Toxicology, American Society of Hypertension, American Society of Nephrology, and National Kidney Foundation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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