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Table of Contents
Year : 2021  |  Volume : 7  |  Issue : 2  |  Page : 55-57

Renovascular hypertension

Ayush Nephrology Centre, Padley Ganj Gorakhpur, India

Date of Submission04-Mar-2021
Date of Decision05-Mar-2021
Date of Acceptance16-Mar-2021
Date of Web Publication25-Feb-2022

Correspondence Address:
Dr. Anand Banka
Ayush Nephrology Centre, Padley Ganj Gorakhpur - 411 019
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrnm.jrnm_20_21

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Understanding the mechanisms and implications of renovascular disease remains an important challenge for clinicians caring for patients with hypertension. Renovascular hypertension is suspected when the onset of hypertension occurs before the age of 30 or after the age of 50, or when previously stable hypertension becomes more difficult to control. This article briefly reviews pathophysiology of Renovascular Hypertension, clincal pointers diagnostic tests and management of renovascular hypertension.

Keywords: Ischemic nephropathy, renovascular hypertension, secondary hypertension

How to cite this article:
Banka A. Renovascular hypertension. J Renal Nutr Metab 2021;7:55-7

How to cite this URL:
Banka A. Renovascular hypertension. J Renal Nutr Metab [serial online] 2021 [cited 2023 Oct 4];7:55-7. Available from: http://www.jrnm.in/text.asp?2021/7/2/55/338552

  Introduction Top

Renovascular hypertension, the most common form of secondary hypertension, seems simple in theory but is fairly complicated in clinical practice.

Understanding the mechanisms and implications of renovascular disease remains an important challenge for clinicians caring for patients with hypertension. “Renovascular hypertension” is defined as systemic hypertension resulting from renal arterial compromise, often due to occlusive lesions of the main renal arteries.

The major issues in approaching patients with renal artery stenosis relate to the role of renal artery stenosis in the management of hypertension, i.e., “renovascular hypertension,” and to the potential for vascular compromise of renal function, i.e., “ischemic nephropathy.” Hemodynamically significant renal artery stenosis, when bilateral or affecting the artery to a solitary functioning kidney, can also lead to a reduction in kidney function (ischemic nephropathy). This untoward observation may be reversed by interventive maneuvers, e.g., surgical renal revascularization, Percutaneous transluminal renal angioplasty (PTRA), or renal artery stenting.

  Pathophysiology of Renovascular Hypertension Top

Studies demonstrating that vascular occlusion to the kidneys produces a rise in systemic arterial pressure remain among the seminal observations regarding pathogenic mechanisms for hypertension.[1]

The seminal studies of Goldblatt et al.[2] in the 1930s demonstrate that reduction of perfusion to the kidney can produce sustained elevation of arterial pressure.

Later work identified activation of the renin–angiotensin–aldosterone system as a central component of this process.[3],[4]

  Clinical Clues for Renovascular Hypertension Top

Renovascular hypertension is suspected when the onset of hypertension occurs before the age of 30 or after the age of 50, or when previously stable hypertension becomes more difficult to control. A predilection for hypokalemia, an absent family history of hypertension, and several other features favor renovascular hypertension, but these differences are small and have low predictive value. Recent studies in patients referred for “resistant hypertension” indicate that a clinical score comprising the presence of clinical vascular disease, abdominal bruits, body weight, smoking, and several other elements is nearly as predictive of renovascular disease (50%) as findings on nuclear renography.[5]

Perhaps, the most common presentation of renovascular hypertension is “resistant hypertension.” Recent consensus statements define this condition as failure to achieve goal blood pressures (usually considered <140/90 mmHg or lower for high-risk conditions), despite optimal doses of three or more antihypertensive agents, including a diuretic. Common features to such patients include older age, systolic hypertension, obesity, obstructive sleep apnea, and other manifestations of renal dysfunction.[6] The fact that most such patients have multiple comorbidities makes it more difficult to assign a causative role for any specific condition, including renovascular disease.

  Diagnostic Tests and Imaging Top

Numerous studies in the 1970s and 1980s focused on functional measurement of activation of the renin–angiotensin system as a diagnostic clue to renovascular hypertension. These included stimulation (with diuretics, administration of ACE inhibitors) and blockade with angiotensin receptor blockers. Sometimes, they combined with functional or radionuclide imaging.[7],[8],[9] Although these provide insight into the dynamics of blood pressure control and effects on the kidney, they generally fail as diagnostic studies because of the broad overlap with other causes of hypertension and the confusion presented by the changing conditions of study.

Renal artery duplex (Doppler) ultrasound

Stenotic lesions can be detected by comparing the systolic flow velocity in the renal artery to that in the aorta, since the velocity of flow increases as an artery narrows; end-diastolic velocity also may be increased distal to a stenotic lesion.

Duplex Doppler ultrasonography can detect both unilateral and bilateral diseases. It is relatively inexpensive and suitable for serial measurements to determine disease progression. This modality can also be used to detect recurrent stenosis in patients previously treated with angioplasty or surgery.

Spiral computed tomography scan with computed tomography angiography

A spiral (helical) computed tomography (CT) scan with intravenous contrast injection (called CT angiography, or CTA) is a highly accurate noninvasive diagnostic test for imaging renovascular disease due to atherosclerosis but less so for fibromuscular disease.

Magnetic resonance angiography

Although relatively expensive, magnetic resonance (MR) imaging has become a major imaging tool to reliably evaluate size, structure, and vascular anatomy. Gadolinium-enhanced imaging is now less commonly employed due to concerns about nephrogenic systemic fibrosis. Newer technologies promise to allow high-resolution imaging of the major renal vessels without contrast, however, and allow definition of vascular patterns without radiation exposure.

Both MR and CTA (see below) can reliably define “normal” major vessels, thereby assuring the patient that bilateral disease is not present. This fact can be critically important in planning long-term medical therapy.

  Management of Renovascular Hypertension Top

It should be emphasized that therapy must be highly individualized, depending on the circumstances of the patient. Most patients will be treated with intensive medical intervention both before and after renal revascularization. Hence, clinicians face the responsibility mainly of establishing timing and risk-to-benefit ratios of both follow-up medical therapy and vascular intervention.


ACE inhibitors are widely accepted as being superior to other antihypertensive drugs in controlling renovascular hypertension.[10],[11]

Furthermore, ACE inhibitors have been associated with improved survival of these patients, many of whom carry a heavy burden of generalized atherosclerotic disease.

The major concern about ACE inhibitors is their potential to precipitate acute renal failure in patients with renovascular hypertension.[12] Optimal clinical management calls for close follow-up of kidney function and potassium levels when starting an ACE inhibitor in patients with known renal artery stenosis.

At particularly high risk are patients with global renal ischemia due to either bilateral stenosis or stenosis to a solitary kidney; a rise in the serum creatinine has been reported in one third of these patients treated with captopril.[13] However, serum creatinine concentrations returned to baseline levels within 7 days of captopril withdrawal. Most experts agree that with long-term therapy, a rise in creatinine during the first 2 months by 30% over baseline and elevation of potassium up to 5.5 mmol/L are acceptable and do not require stopping ACE inhibitors.[14],[15]

In the current practice, the emphasis is on early recognition of potential risk factors for ACE inhibitor–induced renal side effects and close monitoring of this group of patients. In high-risk patients, particularly those with heart failure, diuretics should be withheld before initiation of ACE inhibition.

Some patients with elevated creatinine can be treated with discontinuation of diuretics rather than ACE inhibitors.

  Role of Renal Revascularization Top

At first glance, restoring the renal circulation in the presence of occlusive vascular disease ought to provide obvious therapeutic benefit. Many patients with intractable renovascular hypertension, and some with renal insufficiency experience major recovery. In practice, however, both endovascular and surgical procedures continue to introduce costs and risks that limit their universal application.

Patients with atherosclerotic renal artery stenosis are at a particularly high risk for small-vessel disease of the kidneys, i.e., nephrosclerosis, as both diseases share a common risk factor profile consisting of diabetes, hyperlipidemia, and smoking. If advanced nephrosclerosis is present, revascularization of the affected renal artery will not improve blood pressure control or renal function because the small-vessel changes are irreversible.

Studies of renal outcomes after PTRA have not been particularly promising.

Subgroup analyses in several studies, irrespective of design, have reported measurable and clinically significant improvement in 25%–30% of patients, no significant change in 45%–50%, and a steady decline in renal function in the remaining 20%–25%.[16]

Patients least likely to benefit are those with decreased kidney size, longer duration of renal insufficiency, advanced renal insufficiency with serum creatinine levels above 3.0 mg/dL,[17] and a baseline renal resistive index of more than 80 (this index is a marker of renal small-vessel disease, measured by ultrasonography).

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Garovic VD, Textor SC. Renovascular hypertension and ischemic nephropathy. Circulation 2005;112:1362-74.  Back to cited text no. 1
Goldblatt H, Lynch J, Hanzal RF, Summerville WW. Studies on experimental hypertension: I. The production of persistent elevation of systolic blood pressure by means of renal ischemia. J Exp Med 1934;59:347-79.  Back to cited text no. 2
DeForrest JM, Knappenberger RC, Antonaccio MJ, Ferrone RA, Creekmore JS. Angiotensin II is a necessary component for the development of hypertension in the two kidney, one clip rat. Am J Cardiol 1982;49:1515-7.  Back to cited text no. 3
Basso N, Terragno NA. History about the discovery of the renin-angiotensin system. Hypertension 2001;38:1246-9.  Back to cited text no. 4
Krijnen P, van Jaarsveld BC, Steyerberg EW, Man in 't Veld AJ, Schalekamp MA, Habbema JD. A clinical prediction rule for renal artery stenosis. Ann Intern Med 1998;129:705-11.  Back to cited text no. 5
Taler SJ, Textor SC, Augustine JE. Resistant hypertension: Comparing hemodynamic management to specialist care. Hypertension 2002;39:982-8.  Back to cited text no. 6
Wilcox CS. Use of angiotensin-converting-enzyme inhibitors for diagnosing renovascular hypertension. Kidney Int 1993;44:1379-90.  Back to cited text no. 7
Sfakianakis GN, Bourgoignie JJ. Renographic diagnosis of renovascular hypertension with angiotensin converting enzyme inhibition and furosemide. Am J Hypertens 1991;4:706S-10S.  Back to cited text no. 8
Novick AC, Fouad FM, Textor SC, Bravo EL, Tarazi RC, Gifford RW, et al. Predictive value of angiotensin II blockade with (sarcosine-1, threonine-8) angiotensin II in renovascular hypertension. J Urol 1983;129:7-10.  Back to cited text no. 9
Franklin SS, Smith RD. Comparison of effects of enalapril plus hydrochlorothiazide versus standard triple therapy on renal func-tion in renovascular hypertension. Am J Med 1985;79:14-23.  Back to cited text no. 10
Hollenberg NK. Medical therapy for renovascular hypertension: A review. Am J Hypertens 1988;1:338S-43S.  Back to cited text no. 11
Hricik DE, Browning PJ, Kopelman R, Goorno WE, Madias NE, Dzau VJ. Captopril-induced functional renal insufficiency in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney. N Engl J Med 1983;308:373-6.  Back to cited text no. 12
Jackson B, Matthews PG, McGrath BP, Johnston CI. Angiotensin converting enzyme inhibition in renovascular hypertension: Frequency of reversible renal failure. Lancet 1984;1:225-6.  Back to cited text no. 13
Ahmed A. Use of angiotensin-converting enzyme inhibitors in patients with heart failure and renal insufficiency: How concerned should we be by the rise in serum creatinine? J Am Geriatr Soc 2002;50:1297-300.  Back to cited text no. 14
Palmer BF. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: What to do if the serum creatinine and/or serum potassium concentration rises. Nephrol Dial Transplant 2003;18:1973-5.  Back to cited text no. 15
Isles CG, Robertson S, Hill D. Management of renovascular disease: A review of renal artery stenting in ten studies. QJM 1999;92:159-67.  Back to cited text no. 16
Cambria RP, Brewster DC, L'Italien GJ, Gertler JP, Abbott WM, LaMuraglia GM, et al. Renal artery reconstruction for the preservation of renal function. J Vasc Surg 1996;24:371-80.  Back to cited text no. 17


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