Celeste
Unregistered User
(12/17/02 11:23 pm)
Reply
|
Renovascular Hypertension
Renovascular Hypertension
Last Updated: October 3, 2002 Rate this Article
Email to a Colleague
Synonyms and related keywords: renovascular occlusive disease, atherosclerotic renal artery disease, atherosclerotic renovascular disease, renal artery stenosis, renal artery occlusive disease, RVHT, Goldblatt
AUTHOR INFORMATION Section 1 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
Author: Rebecca J Schmidt, DO, FACP, Section Chief, Associate Professor, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine and Medical Center
Coauthor(s): Sandeep S Soman, MD, MBBS, DNB, Assistant Professor, Department of Medicine, University of North Dakota at Fargo; Consulting Staff, Department of Internal Medicine, Division of Nephrology and Hypertension, Veterans Affairs Medical Center
Rebecca J Schmidt, DO, FACP, is a member of the following medical societies: American Society of Nephrology, International Society for Peritoneal Dialysis, International Society of Nephrology, and National Kidney Foundation
Editor(s): L Michael Prisant, MD, FACC, Director of Cardiology Fellowship Training Program, Director of Hypertension Unit, Professor, Department of Internal Medicine, Medical College of Georgia; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; George R Aronoff, MD, Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine; Michael E Zevitz, MD, Consulting Faculty, Clinical Assistant Professor, Department of Medicine, Finch University of Health Science, Chicago Medical School; and Vecihi Batuman, MD, FACP, Chief of Renal-Hypertension, New Orleans VA Medical Center, Professor, Department of Internal Medicine, Section of Nephrology, Tulane University School of Medicine
INTRODUCTION Section 2 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
Background: Renovascular hypertension (RVHT) denotes the causal relationship between anatomically evident arterial occlusive disease and elevated blood pressure. The coexistence of renal arterial vascular (ie, renovascular) disease and hypertension roughly defines this type of nonessential hypertension. More specific diagnoses are made retrospectively when hypertension is improved after intravascular intervention.
Since Goldblatt's seminal experiment in 1934, RVHT has become increasingly recognized as an important cause of clinically atypical hypertension and chronic renal failure, the latter by virtue of renal ischemia. RVHT is the clinical consequence of renin-angiotensin-aldosterone activation. As demonstrated by Goldblatt, renal artery occlusion creates ischemia, which triggers the release of renin and a secondary elevation in blood pressure. Hyperreninemia promotes conversion of angiotensin I to angiotensin II, causing severe vasoconstriction and aldosterone release. The ensuing cascade of events varies depending on the presence of a functioning contralateral kidney.
Aldosterone-mediated sodium and water retention is handled properly by the nonstenotic kidney, precluding volume from contributing to the angiotensin II–mediated hypertension. A solitary ischemic kidney has little or no capacity for sodium and water excretion; hence, volume plays an additive role in the hypertension.
Pathophysiology: The chief pathophysiologic mechanism underlying RVHT involves activation of both limbs of the renin-angiotensin-aldosterone system and depends on the presence or absence of a contralateral kidney. Unilateral renal ischemia initiates hypersecretion of renin, which accelerates conversion of angiotensin I to angiotensin II and enhances adrenal release of aldosterone. The result is profound angiotensin-mediated vasoconstriction and aldosterone-induced sodium and water retention. In the 2-kidney 1-clip model, where the clinical correlate is unilateral renal artery disease, sodium and water handling via pressure diuresis of the contralateral kidney may be sufficient to prevent a volume component to the hypertension. In the setting of a solitary kidney (experimentally, the 1-kidney 1-clip model), sodium and water handling is compromised, sodium and water retention ensues, and volume-mediated hypertension occurs.
In unilateral renal artery stenosis (RAS), renin production is increased by the ischemic kidney but suppressed in the unaffected nonstenotic kidney, which lacks the same ischemic stimulus. Consequently, when 2 kidneys are present with a unilateral stenosis (2-kidney 1-clip model), hyperreninemia persists and blood pressure remains elevated because of an angiotensin II–induced vasoconstrictive effect. Renin production decreases in the contralateral kidney, a pressure diuresis (ie, of excess sodium and water) ensues, and hypertension is maintained by high levels of angiotensin II.
A solitary kidney rendered ischemic by RAS is unable to achieve the pressure diuresis required to handle the aldosterone-induced sodium and water retention. The resultant volume expansion contributes to the elevation in blood pressure and also suppresses the production of renin by the stenotic kidney.
The pathophysiologic scheme for RVHT is presented in Picture 1.
The sympathetic nervous system does not appear to play a role in perpetuating elevated blood pressure in the 2-kidney 1-clip model of RVHT. Evidence for a role in the 1-kidney 1-clip model of RVHT has been presented but is not clear or definitive.
Stages in the development of renovascular hypertension
The evolution of RVHT has been described as having 3 stages. The immediate rise in blood pressure is a direct consequence of hyperreninemia. Over days to weeks, blood pressure remains elevated, but the course and presence of hyperreninemia vary with the presence and function of the contralateral kidney. The mechanism by which hypertension is produced in patients with renovascular disease thus changes over time and varies with the state of sodium balance.
When the contralateral kidney is functional, volume expansion is avoided and renin levels remain high. The 2 kidneys are in opposition; the stenotic kidney avidly retains sodium and produces excess renin in response to renal ischemia, and the nonstenotic kidney continues to excrete sodium and water to maintain euvolemia. The end result is systemic hypertension that is renin mediated and angiotensin mediated.
In the setting of an ischemic solitary kidney, sodium and water retention, together with the vasopressor effects of angiotensin II, act to maintain renal perfusion pressure. The stimulus to produce renin is stifled, and renin levels fall. Hypertension becomes less angiotensin II dependent but instead results from volume expansion. Thus, perfusion pressure is restored at the expense of systemic hypertension and volume overload.
If blood flow is restored during the first 2 phases and renal perfusion is reinstated, blood pressure soon returns to a normal level. Once phase 3 is reached, restoration of renal blood flow may not normalize blood pressure, presumably because of secondary irreversible vascular or renal parenchymal disease.
In the third stage, hypertension often is unremitting, persisting well after the removal of the stenosis. Recalcitrant hypertension in this setting likely represents the presence of ischemic nephropathy in either or both kidneys; patients in whom stenoses were not hemodynamically significant initially also may have persistent hypertension.
The renin-angiotensin system and control of intrarenal hemodynamics in renovascular hypertension
Angiotensin II exerts a vasoconstrictive effect on both afferent and efferent arterioles, with a preferential effect on the efferent side. In the healthy kidney, efferent tone is integral to the maintenance of intraglomerular pressure. Angiotensin blockade increases efferent renal arterial blood flow such that intraglomerular pressure is increased and glomerular filtration is optimized.
In the ischemic kidney with reduced afferent blood flow, intraglomerular pressure and glomerular filtration are maintained by angiotensin II–mediated efferent vasoconstriction. Removal of the efferent vasoconstrictive effect using angiotensin blockade in the ischemic kidney may reduce the glomerular filtration rate (GFR).
Angiotensin-converting enzyme (ACE) inhibitors cause a deterioration of renal function in some patients with renovascular disease—in particular, bilateral RAS. Because angiotensin exerts its predominant vasoconstrictive effect on the efferent renal arteriole, the decrease in renal blood flow caused by afferent vasoconstriction is less than the decrease in the GFR caused by efferent vasoconstriction. The end result is a decrease in the filtration fraction. Inhibition of angiotensin, as achieved by ACE inhibitors, eliminates efferent vasoconstriction and causes a decrease in intraglomerular pressure and the GFR.
Classification
In adults, renovascular disease tends to appear at different times and affects the sexes differently. Atherosclerotic disease affects mainly the proximal third of the main renal artery and is most common among older men. Fibromuscular dysplasia involves the distal two thirds and branches of the renal arteries and is most common among younger women.
Frequency:
In the US: RVHT is the most common type of secondary hypertension, accounting for less than 1% of cases in unselected populations and as many as 30% of cases in selected populations.
Internationally: The prevalence of RVHT internationally is not clear, but it likely accounts for the sole etiology in a similarly small percentage (<1% in the United States) of unselected patients with hypertension.
Mortality/Morbidity: In patients with hypertension, the presence of atherosclerotic renal artery disease is a strong predictor of increased mortality relative to the general population. RVHT in the setting of renal dysfunction is associated with the greatest mortality.
Race: RVHT is less common among the black population than the white population.
Sex: RVHT is most common in younger women and older men. Younger women develop RVHT most commonly from fibromuscular dysplasia affecting the distal two thirds and branches of the renal arteries. Older men develop RVHT most often from atherosclerotic disease affecting mainly the proximal third of the main renal artery.
Age: The onset of RVHT tends to occur in patients younger than 30 years or older than 50 years. CLINICAL Section 3 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
History: Clinical risk factors include a history of hypertension with azotemia or progressive renal insufficiency, accelerated or malignant hypertension, severe hypertension (diastolic blood pressure >120 mm Hg), hypertension with an asymmetric kidney, paradoxical worsening of hypertension with diuretic therapy, and hypertension refractory to standard therapy.
Onset of hypertension occurring in patients younger than 30 years or older than 50 years (may be abrupt)
Abrupt onset of hypertension
Severe or resistant hypertension
Symptoms of atherosclerotic disease elsewhere
Negative family history for hypertension
Smoking tobacco products
Azotemia with ACE inhibition
Recurrent pulmonary edema
Physical: Findings suggestive of long-standing hypertension may or may not be evident upon physical examination.
Recurrent flash pulmonary edema or unexplained episodes of congestive heart failure
Advanced funduscopic changes
Abdominal bruit
A clear abdominal bruit is heard in 46% of patients with RVHT.
It also is heard in 9% of patients with essential hypertension; however, innocent bruits are common in younger individuals.
Systolic-diastolic bruits in combination with hypertension are suggestive of RVHT.
Causes:
Overall, approximately two thirds of RVHT cases are caused by atherosclerotic disease and one third are caused by fibromuscular dysplasia or other congenital disorders.
Other clinical entities that may be associated with RVHT include cholesterol embolic disease, acute arterial thrombosis or embolism, aortic dissection, renal arterial trauma, arterial aneurysm, arteriovenous malformation of the renal artery, and polyarteritis nodosa.
|
Email This To a Friend
Topic Commands
Click to receive email notification of replies 
Click to stop receiving email notification of replies 
