eMedicine Specialties > Nephrology > Hypertension and the Kidney
Renovascular Hypertension: Treatment & Medication
Updated: Sep 4, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
- Antihypertensive drug therapy is indicated.
- Optimal blood pressure control plays an essential role in the therapeutic management of RVHT; however, aggressive control of other risk factors for atherosclerosis also is key.
- Cessation of smoking is important for its positive impact on the cardiovascular risk profile in patients with hypertension. Similarly, antidyslipidemic therapy for those patients with hyperlipidemia likely provides benefit in atherosclerotic RVHT.
- Progression of atherosclerotic stenosis may occur in as many as one third of patients, and the sequelae of ongoing ischemia to the stenotic kidney are a theoretical concern. Furthermore, normalization of blood pressure may be associated with reduced renal perfusion pressures, and renal function may deteriorate despite good blood pressure control.
- Definitive therapy for the underlying cause must be considered in order to avoid the development of ischemic nephropathy. Intervention of hemodynamically significant stenoses has been presumed to offer clinical benefit; however, trials comparing renal artery revascularization with medical management do not unequivocally favor surgical over medical intervention.3 Thus, the superiority of surgical intervention versus medical intervention (or vice versa) remains unproven.
- Percutaneous transluminal renal angioplasty
- Percutaneous transluminal angioplasty (PTRA) is a nonsurgical procedure used to open stenotic renal arteries, the most amenable lesions being those without total occlusion. Outcomes in patients with lesions resulting from fibromuscular dysplasia appear to be significantly better than they are in persons whose lesions are associated with atherosclerotic stenosis, with cure reported in 50-85% of patients in the former group, and in 8-20% of persons in the latter group.
Restenosis requiring repeat angioplasty was reported in fewer than 10% of patients with fibromuscular disease and in 8-30% of those with atherosclerotic stenosis. Improvement in blood pressure control with fewer antihypertensive medications was achieved in 30-35% and 50-60% of patients with fibromuscular or atherosclerotic lesions, respectively. - A Swedish study of 105 patients treated with PTRA reported a 5-year survival rate of 83% for patients with arteriosclerotic renovascular disease.4 The rate for patients with fibromuscular vascular disease was even higher, reaching 100%.
- The poor results observed in patients with bilateral renal artery disease suggest that surgical intervention should be a strong consideration in this setting.
- Intravascular stents placed during angioplasty may be helpful in the prevention of restenosis and the management of RVHT. Current data suggest that stenting may prove useful in patients with ostial disease, those who develop restenosis after PTRA, or those with complications resulting from PTRA, such as dissection (see images below and Images 4-6). Primary renal artery stenting in patients with atherosclerotic RAS has a high technical success rate and a low complication rate.5,6
- In patients with diffuse atherosclerosis, the complication rate with either surgery or angioplasty is relatively high. Medical therapy may be preferred.
- Percutaneous transluminal angioplasty (PTRA) is a nonsurgical procedure used to open stenotic renal arteries, the most amenable lesions being those without total occlusion. Outcomes in patients with lesions resulting from fibromuscular dysplasia appear to be significantly better than they are in persons whose lesions are associated with atherosclerotic stenosis, with cure reported in 50-85% of patients in the former group, and in 8-20% of persons in the latter group.
Angiogram showing bilateral renal artery stenosis. Courtesy of Department of Radiology, Henry Ford Hospital.
After percutaneous transluminal angioplasty (right renal artery). Courtesy of Department of Radiology, Henry Ford Hospital.
After percutaneous transluminal angioplasty and stent placement (left renal artery). Courtesy of Department of Radiology, Henry Ford Hospital.
Surgical Care
- Surgical revascularization
- The underlying diagnosis is the major determinant of the results of this surgery. As more patients with advanced atherosclerosis in multiple vessels are brought to surgery, performing various bypass procedures may become less feasible because of the following: (1) the certainty that the RAS is the cause of the hypertension is less, and (2) the prognosis may be determined by the extent of atherosclerosis elsewhere in the body.
- Another potential problem is the release of cholesterol emboli during the operation; however, 80-90% of patients undergoing operation for atherosclerotic RVHT benefit (cure or improvement), with a perioperative mortality rate of less than 5%.
- In patients with fibromuscular dysplasia, the cure rate is as high as 80% and morbidity is low; however, these results are not significantly better than what can be achieved with renal angioplasty, at less morbidity, mortality, cost, and inconvenience.
- In patients with diffuse atherosclerosis, the complication rate with both surgery and angioplasty is relatively high.
Medication
All classes of antihypertensive medications are used to treat RVHT; however, the most effective therapy is with an ACE inhibitor, which minimizes the ischemia-induced rise in angiotensin production. Because hypertension may be dependent on angiotensin II, antihypertensives that inhibit renin or angiotensin II are used widely. An ACE inhibitor markedly decreases blood flow through the stenotic kidney; thus, in patients with a solitary kidney or bilateral renovascular disease, blood pressure may fall rapidly, with an ensuing deterioration in renal function. This usually is reversible upon discontinuation of the medication.
Although less clinical experience exists with newer angiotensin receptor blockers (ARBs), they appear to be as effective as ACE inhibitors in experimental models. In patients without hemodynamically significant renal artery disease, an increase in serum creatinine level of up to 35% above baseline with an ACE or ARB is considered acceptable and is not a reason to withhold treatment unless hyperkalemia develops. Both beta-blockers and diuretics also are used, the latter often in conjunction with ACE inhibitors. Diuretics enhance sodium and water diuresis, thereby eliminating the volume-mediated component of RVHT. Calcium channel blockers (CCBs) may provide equally good control of hypertension, with presumably less impairment in function of the ischemic kidney than ACE inhibitors.
A selective aldosterone inhibitor, eplerenone (INSPRA) is now available for the treatment of hypertension. It selectively blocks aldosterone at the mineralocorticoid receptors in epithelial (eg, kidney) and nonepithelial (eg, heart, blood vessels, brain) tissues, thus decreasing blood pressure and sodium reabsorption. The adult dose is 50 mg PO qd and it may be increased after 4 wk, not to exceed 100 mg/d. Contraindications include documented hypersensitivity, hyperkalemia, coadministration with drugs causing increased potassium, type 2 diabetes with microalbuminuria, and moderate-to-severe renal insufficiency (ie, CrCl <50 mL/min or serum creatinine >2 mg/dL [males] or >1.8 mg/dL [females]). Eplerenone is a CYP450 3A4 substrate, thus potent CYP3A4 inhibitors (eg, ketoconazole) increase serum levels about 5-fold, whereas less potent CYP3A4 inhibitors (eg, erythromycin, saquinavir, verapamil, fluconazole) increase serum levels about 2-fold. Grapefruit juice increases serum levels about 25%.
Coadministration with potassium supplements, salt substitutes, or drugs known to increase serum potassium (eg, amiloride, spironolactone, triamterene, ACE inhibitors, angiotensin II inhibitors) increases risk of hyperkalemia. Eplerenone may cause hyperkalemia, headache, or dizziness. Caution is advised with hepatic insufficiency.
Angiotensin-converting enzyme inhibitors
These agents minimize an ischemia-induced rise in angiotensin production. Because hypertension may be dependent on angiotensin II, antihypertensives that inhibit renin or angiotensin II are used widely. All drugs in this class have similar action and adverse effects.
Captopril (Capoten)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. Excreted primarily by the kidney.
Adult
25-75 mg PO tid
Pediatric
Not established
NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics
Documented hypersensitivity; previous history of angioedema or anaphylaxis with ACE inhibitors; hyperkalemia; bilateral RAS; solitary kidney with RAS; pregnancy, due to risk of fetal hypotension; anuria; renal failure
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal impairment, valvular stenosis, or severe congestive heart failure (CHF); adverse effects include severe hypotension, acute renal failure (especially in bilateral RAS), hyperkalemia, dry cough sometimes accompanied by wheezing, and angioedema; cough and angioedema are believed to be mediated by bradykinin
Enalapril (Vasotec)
Competitive inhibitor of ACE. Reduces angiotensin II levels and decreases aldosterone secretion.
Adult
10-20 mg PO qd or divided bid
Pediatric
Not established
NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal impairment, valvular stenosis, or severe CHF
Lisinopril (Zestril, Prinivil)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Adult
10-80 mg PO qd
Pediatric
Not established
May increase digoxin, lithium, and allopurinol levels; probenecid may increase levels; coadministration with diuretics increases hypotensive effects; hypotensive effects may be enhanced when administered concurrently with diuretics and NSAIDs
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal impairment, valvular stenosis, or severe CHF
Angiotensin receptor blockers
Angiotensin II is the primary vasoactive hormone of the renin-angiotensin system and plays an important role in the pathophysiology of hypertension. Besides being a potent vasoconstrictor, angiotensin II stimulates aldosterone secretion by the adrenal gland; thus, ARBs decrease systemic vascular resistance without a marked change in heart rate by blocking the effects of angiotensin II. Type 1 angiotensin receptors are found in many tissues, including vascular smooth muscle and the adrenal gland. Type II angiotensin receptors also are found in many tissues, although their relationship to cardiovascular hemostasis is not known. The affinity of ARBs is approximately 1000-fold greater for the type I angiotensin receptor than for the type II angiotensin receptor.
In general, ARBs do not inhibit ACE, other hormone receptors, or ion channels. ARBs interfere with the binding of formed angiotensin II to its endogenous receptor. Experience in the treatment of RVHT with this group of drugs still is limited. Losartan and valsartan are specific and selective nonpeptide angiotensin II receptor antagonists that block the vasoconstricting and aldosterone-secreting effects of angiotensin II.
Other ARBs have been approved by the FDA, including olmesartan (Benicar). Olmesartan is initiated at 20 mg PO qd and may be increased to 40 mg/d after 2 wk if further BP reduction is required.
Losartan (Cozaar)
For patients unable to tolerate ACE inhibitors. May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Compared to the ACE inhibitors (eg, captopril, enalapril), losartan is associated with lower incidence of drug-induced cough, rash, and taste disturbances.
Adult
Initial: 50 mg/d PO
Maintenance: 25-100 mg/d PO
Pediatric
Not established
Enhances hypotensive effects of antihypertensive agents or diuretics if administered concomitantly; use with potassium-sparing diuretics, potassium salts, or salt substitutes containing potassium may lead to increases in serum potassium; ketoconazole, sulfaphenazole, and phenobarbital may decrease effects; cimetidine and monoxidine may increase effects
Documented hypersensitivity; do not use during second or third trimester of pregnancy (pregnancy category D); bilateral RAS or solitary kidney with unilateral RAS; breastfeeding not recommended during ARB therapy because of potential adverse effects in the infant
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hyperkalemia, suspected bilateral RAS, or solitary kidney with unilateral RAS
Valsartan (Diovan)
For patients unable to tolerate ACE inhibitors. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors. Does not affect response to bradykinin and is less likely to be associated with cough and angioedema. Compared with ACE inhibitors (eg, captopril, enalapril), it is associated with lower incidence of drug-induced cough, rash, and taste disturbances.
Adult
Initial: 80 mg PO qd unless volume depleted
Maintenance: 80-320 mg PO qd
Pediatric
Not established
Ketoconazole, troleandomycin, sulfaphenazole, and phenobarbital may decrease effects; cimetidine and monoxidine may increase effects
Documented hypersensitivity; severe hepatic insufficiency; biliary cirrhosis or obstruction; primary hyperaldosteronism; bilateral RAS
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hyperkalemia, suspected bilateral RAS, or solitary kidney with unilateral RAS
Beta-adrenergic blocking agents
Compete with adrenergic neurotransmitters (eg, catecholamines) for binding at sympathetic receptor sites. Atenolol and metoprolol, in low doses, selectively block beta1-adrenergic receptors in the heart and vascular smooth muscle. Pharmacodynamic consequences of beta1-receptor blockade include a decrease in both resting and exercise heart rate and cardiac output and a decrease in both systolic and diastolic blood pressure. As with all selective adrenergic antagonists, selectivity for the beta1-receptor is lost at higher doses, and they can competitively block beta2-adrenergic receptors in the bronchial and vascular smooth muscles, potentially causing bronchospasm.
Actions that generally make beta-blockers useful in treating hypertension include a negative chronotropic effect that decreases the heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output, a reduction of sympathetic outflow from the CNS, and suppression of renin release from the kidneys. Thus, beta-blockers affect blood pressure via multiple mechanisms.
Metoprolol (Lopressor)
Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG.
Adult
100-400 mg/d PO divided bid
Pediatric
Not established
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; toxicity may increase with coadministration of sparfloxacin, phenothiazines, astemizole, CCBs, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Documented hypersensitivity; uncompensated CHF; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patient closely and withdraw the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG
Atenolol (Tenormin)
Selectively blocks beta1-receptors with little or no effect on beta2 types.
Adult
50 mg PO qd; increase to 100 mg/d if necessary
Pediatric
50-100 mg/d PO qd
Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity
Documented hypersensitivity; CHF; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during IV administration, carefully monitor BP, heart rate, and ECG; relatively contraindicated in severe hepatic disease; caution in poorly controlled diabetes mellitus, particularly brittle diabetes; can prolong or enhance hypoglycemia by interfering with glycogenolysis; can mask signs of hypoglycemia, especially tachycardia, palpitations, and tremors; can occasionally cause hyperglycemia, thought to be due to blockade of beta2-receptors on pancreatic islet cells, which would inhibit insulin secretion
Propranolol (Inderal, Betachron)
Although beta1 selective beta-blockers (eg, metoprolol) are preferred over nonselective agents in patients with asthma or pulmonary conditions in which acute bronchospasm would put them at risk (eg, COPD, emphysema, or bronchitis), all beta-blockers should be used with caution in these patients, particularly with high-dose therapy. Has membrane-stabilizing activity and decreases automaticity of contractions. Not suitable for emergency treatment of hypertension. Do not administer IV in hypertensive emergencies.
Adult
40-80 mg PO bid initial; increase to 160-320 mg/d (some patients require up to 640 mg/d)
Pediatric
Not established
Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; CCBs, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase
Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt discontinuation can result in development of myocardial ischemia, infarction, ventricular arrhythmias, or severe hypertension, particularly in patients with preexisting cardiac disease; caution in hyperthyroidism or thyrotoxicosis because drug can mask tachycardia resulting from this condition; abrupt withdrawal in a patient with hyperthyroidism can precipitate a thyroid storm; patients with severe bradycardia or advanced AV block; do not use in patients with cardiogenic shock or systolic CHF, particularly in those with severely compromised left ventricular dysfunction, because the negative inotropic effect of these drugs can further depress cardiac output; relatively contraindicated in patients with Raynaud disease or peripheral vascular disease because reduced cardiac output and relative increase in alpha stimulation can exacerbate symptoms
Calcium channel blockers
These agents provide control of hypertension associated with less impairment of function of the ischemic kidney. Suggested that they may have beneficial long-term effects, but this remains uncertain.
Diltiazem (Cardizem CD, Dilacor)
CCBs inhibit influx of extracellular calcium across both myocardial and vascular smooth muscle cell membranes. Serum calcium levels remain unchanged.
Resultant decrease in intracellular calcium inhibits contractile processes of myocardial smooth muscle cells, resulting in dilation of coronary and systemic arteries and improved oxygen delivery to myocardial tissue. In addition, total peripheral resistance, systemic blood pressure, and afterload are decreased.
Similar to verapamil in that it inhibits the influx of extracellular calcium across both the myocardial and vascular smooth muscle cell membranes.
Adult
30-80 mg PO q6h (qd if using long-acting form)
Pediatric
Not established
May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone may cause bradycardia and a decrease in cardiac output; when administered with beta-blockers may increase cardiac depression; cimetidine may increase levels
Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in ventricular dysfunction, severe bradycardia, cardiogenic shock, CHF, and patients taking beta-adrenergic blocking agents (can precipitate or exacerbate heart failure or cause excessive bradycardia or cardiac conduction abnormalities); do not use in acute MI and associated left ventricular dysfunction; decreases peripheral resistance and can worsen hypotension; due to inhibitory effects on AV node conduction, do not use in patients with preexisting second-degree or third-degree AV block or previous conduction abnormalities; can worsen abnormal pressure gradient associated with advanced aortic stenosis; caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur; caution in patients with sinoatrial nodal dysfunction (eg, sick sinus syndrome)
Verapamil (Calan)
During depolarization, inhibits calcium ion from entering slow channels or voltage-sensitive areas of the vascular smooth muscle and myocardium.
Adult
80-160 mg PO q8h
75-150 mcg/kg IV
Pediatric
Not established
May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels
Documented hypersensitivity; severe CHF; sick sinus syndrome or second-degree or third-degree AV block; hypotension (<90 mm Hg systolic)
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued treatment); monitor liver function periodically
Nifedipine (Adalat, Procardia)
Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Sublingual administration generally is safe, despite theoretical concerns.
Adult
20-40 mg PO q8h
Pediatric
Not established
Caution with coadministration of any agent that can lower BP, including beta-blockers and opioids; H2 blockers (eg, cimetidine) may increase toxicity
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause lower extremity edema; allergic hepatitis has occurred but is rare
Diuretics
Used only as an adjunct to other medications for RVHT, especially during acute hypertensive crisis. Furosemide is especially effective in managing pulmonary edema associated with hypertensive crises and may be particularly useful in patients unresponsive to other diuretics or those who have severe renal impairment.
Furosemide (Lasix)
Primarily appears to inhibit reabsorption of sodium and chloride in the ascending limb of the loop of Henle. These effects increase urinary excretion of sodium, chloride, and water, resulting in profound diuresis.
Renal vasodilation occurs following administration of furosemide. Renal vascular resistance decreases and renal blood flow is enhanced.
Adult
20-80 mg PO qd/tid
Pediatric
Not established
Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently
Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter
Hydrochlorothiazide (Esidrix, Microzide, HydroDIURIL)
Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water and potassium and hydrogen ions.
Adult
25-100 mg PO qd
Pediatric
Not established
Thiazides may decrease effects of anticoagulants, antigout agents, and sulfonylureas; thiazides may increase toxicity of allopurinol, anesthetics, antineoplastics, calcium salts, loop diuretics, lithium, diazoxide, digitalis, amphotericin B, and nondepolarizing muscle relaxants
Documented hypersensitivity; anuria; renal decompensation
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal disease, hepatic disease, gout, diabetes mellitus, and erythematosus
Bumetanide (Bumex)
Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle. Does not appear to act in the distal renal tubule.
Adult
0.5-2 mg PO qd or divided bid
Pediatric
Not established
Decreases effects of indomethacin and probenecid; may increase lithium toxicity
Documented hypersensitivity; anuria; increasing azotemia
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Profound diuresis with fluid and electrolyte loss may occur; caution in hepatic failure
Vasodilators
These agents are effective in reducing hypertension.
Nitroprusside (Nitropress)
Mainly used when patient presents with a hypertensive emergency secondary to RVHT. See Hypertension and Hypertensive Emergencies.
Adult
0.5-10 mcg/kg/min IV
Pediatric
Not established
None reported
Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic; atrial fibrillation or flutter
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Most serious toxicity is related to accumulation of cyanide, metabolic acidosis, arrhythmias, and excessive hypotension, which may, in turn, cause death; patients with congenital optic atrophy (Leber disease) or toxic amblyopia are deficient in enzyme rhodanese, crucial for metabolism of nitroprusside (patients are at increased risk of developing cyanide toxicity while receiving nitroprusside therapy); watch for thiocyanate toxicity, especially with renal impairment; caution in pulmonary disease (may aggravate preexisting hypoxemia); administer only in setting where adequate equipment and personnel are available to monitor blood pressure closely (may cause severe hypotension); can cause increase in intracranial pressure (relatively contraindicated in preexisting increased intracranial pressure, including encephalopathy)
Renin inhibitor
Newest class of antihypertensive drugs. Acts by disrupting the renin-angiotensin-aldosterone system feedback loop.
Aliskiren (Tekturna)
Direct renin inhibitor. Decreases plasma renin activity and inhibits conversion of angiotensinogen to angiotensin I (as a result, also decreasing angiotensin II) and, thereby, disrupts the renin-angiotensin-aldosterone system (RAAS) feedback loop. Indicated for hypertension as monotherapy or in combination with other antihypertensive drugs.
Adult
150 mg PO qd initially; if needed, may increase to 300 mg/d
Pediatric
<18 years: Not established
Coadministration with irbesartan decreases Cmax by 50%; coadministration with atorvastatin increases Cmax and AUC by 50%; ketoconazole increases plasma levels by about 80%; does not inhibit CYP450 isoenzymes or induce CYP3A4; coadministration with furosemide decreases furosemide Cmax and AUC by 30% and 50%, respectively; high-fat meals substantially decrease absorption; use with maximal dose of ACE inhibitors has not been studied
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Discontinue use in pregnancy as soon as possible because use of drugs affecting the renin-angiotensin system during second and third trimesters has been associated with fetal and neonatal injury, including hypotension, neonatal skull hypoplasia, anuria, renal failure, and fetal death; may cause angioedema; dose-related GI adverse effects may occur
More on Renovascular Hypertension |
| Overview: Renovascular Hypertension |
| Differential Diagnoses & Workup: Renovascular Hypertension |
 Treatment & Medication: Renovascular Hypertension |
| Follow-up: Renovascular Hypertension |
| Multimedia: Renovascular Hypertension |
| References |
| Further Reading |
| « Previous Page | Next Page » |
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Further Reading
Related eMedicine topics:
Angioplasty, Renal Artery
Fibromuscular Dysplasia
Hyperaldosteronism
Hypertension [Nephrology]
Hypertension [Ophthalmology]
Hypertension, Malignant
Renal Artery Stenosis
Renal Artery Stenosis/Renovascular Hypertension
Renovascular Hypertension, Surgical Treatment
Clinical guidelines:
ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease). American College of Cardiology Foundation - Medical Specialty Society
American Heart Association - Professional Association
Society for Cardiovascular Angiography and Interventions - Medical Specialty Society
Society for Vascular Medicine and Biology - Medical Specialty Society
Society for Vascular Surgery - Medical Specialty Society
Society of Interventional Radiology - Medical Specialty Society. 2005. 191 pages. NGC:004740
ACR Appropriateness Criteria® renovascular hypertension. American College of Radiology - Medical Specialty Society. 1995 (revised 2007). 9 pages. NGC:006003
The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. National Heart, Lung, and Blood Institute (U.S.) - Federal Government Agency [U.S.]. 2004 Aug. 22 pages. NGC:003761
VHA/DoD clinical practice guideline for the diagnosis and management of hypertension in the primary care setting. Department of Defense - Federal Government Agency [U.S.]
Department of Veterans Affairs - Federal Government Agency [U.S.]
Veterans Health Administration - Federal Government Agency [U.S.]. 1999 May (revised 2004). 99 pages. NGC:004198
Clinical trials:
Benefits of Medical Therapy Plus Stenting for Renal Atherosclerotic Lesions (CORAL)
Comparison of Best Medical Treatment Versus Best Medical Treatment Plus Renal Artery Stenting (RADAR)
Keywords
renovascular hypertension, renal artery stenosis, renin-angiotensin-aldosterone, renin-angiotensin-aldosterone system, renin, angiotensin, aldosterone, renin angiotensin, fibromuscular dysplasia, renovascular occlusive disease, atherosclerotic renal artery disease, atherosclerotic renovascular disease, renal artery occlusive disease, RVHT, renal artery occlusion, renal arterial vascular disease, hyperreninemia, arterial occlusive disease, renal ischemia, angiotensin I, angiotensin II, secondary hypertension
