Session 1: Hypertension 2013: What To Do While We Wait For the New JNC Guidelines Learning Objectives 1. Understand the importance of proper technique for diagnosing hypertension

and monitoring treatment effectiveness. 2. Apply insights about the complexities and causes of hypertension to

individualize therapy, especially for high-risk patient groups.

Session 1 Hypertension 2013: What to Do While We Wait for the New JNC Guidelines Faculty

Dr Townsend directs the hypertension program at Penn. His research interests are in vascular compliance and CKD progression and CKD complications. His clinical practice includes drug-resistant hypertension, secondary hypertension, and in particular adrenal disorders. He is an empaneled member of JNC 2013 and a co-chair of the American Heart Association’s 2013 Hypertension Summer School. Faculty Financial Disclosure Statement The presenting faculty reports the following: Dr Townsend has no financial relationships to disclose.

Raymond Townsend, MD Professor of Medicine Associate Director General Clinical Research Center/CTSA University of Pennsylvania Philadelphia, Pennsylvania

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Hypertension 2013: What To Do While We Wait for

the New JNC Guidelines

Raymond Townsend, MD

Session 1: 7:45 AM - 9:00 AM

Faculty Disclosure

• Dr Townsend has no financial relationships to disclose.

Learning Objectives

• Understand the importance of proper technique for diagnosing hypertension and monitoring treatment effectiveness

• Apply insights about the complexities and causes of hypertension to individualize therapy, especially for high-risk patient groups

Demographic Question

How many patients with hypertension do you see each week?

1. None

2. 1 - 5

3. 6 - 15

4. 16 - 25

5. 26 - 40

6. Over 40

?

Outcomes Question #1

Which of the following is TRUE?

1. Women tend to run higher home BP readings than men

2. Home and clinic BP readings tend to vary even in normotensive patients

3. Differences in home and clinic BP increase with age

4. The “white coat” effect is typically an increase in SBP of 5 -10 mmHg

5. All of the above

? Outcomes Question #2

In the treatment of hypertension, which is generally TRUE?

1. HCTZ and chlorthalidone are equally effective

2. Furosemide needs to be dosed twice daily

3. Edema seen with amlodipine is due to volume expansion

4. Ethacrynic acid should not be used in patients with sulfa allergy

?

2

Outcomes Question #3

Which of the following may be suggestive of renovasculardisease as the cause of hypertension?

1. Reduced serum creatinine with ACE-I or ARB

2. Elevated plasma renin

3. Slow, steady increase in blood pressure over time

4. Strong family history of hypertension

5. All of the above

?

Case 1

Case 1: Jerry

• 39 y/o WM who presents to your office for wellness check

– No complaints

• Exam

– BP 162/100 mmHg (single reading)

– Pulse 72 RR-20

– No evidence of target organ damage (TOD)

– Height: 5’10’’ Wgt: 205 lbs (BMI-29.4)

• Family history: hypertension-father age 74

• Social history: non-smoker, occasional beers

Jerry: Next Steps?

1. Order home BP monitoring

2. Initiate treatment with HTN medication

3. Restrict salt intake to 2000 mg/day

4. Any of the above would be appropriate next steps

5. None of the above

?

Blood Pressure Measurement

How many errors of BP measurement do you see?

1. One

2. Two

3. Three

4. Four

5. Five

6. Six

? BP Measurement

• Early 1900s BP measured by palpation

• By 1914 life insurance industry recognized that in asymptomatic men, their BP (after their age) was the best way to predict premature death and disability1

• Population-based studies of standardized BP measurement began in 1948 with Framingham

• Large-scale studies required training in BP measurement2

1. Fisher JAMA 1914;63:1752-17542. Curb et al Hypertension 1983;5:610-614

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Question

In an observational study of BP measurement in various settings (office, hospital, skilled nursing facility, home health) what percentage of BP measurements were done according to the guidelines?

1. 60%

2. 30%

3. 10%

4. 0%

Grim et al. Can J Cardiol 1995;11 (suppl H):38H-42H.

? BP Measurement: Common Errors

Error Potential Impact on BP

Improper cuff size (small) Highly variable

Improper arm placement 2.5 mmHg for every inch

Improper positioning (ie, examination table)

5 mmHg DBP seated>supine5 mmHg DBP sitting without back support5 mmHg SBP sitting with legs crossed

Talking 10 mmHg SBP talking5 mmHg SBP listening

Non-validated device Highly variable

Marks LA et al Blood Press Monit 2005;5:153-158. Pickering et al Hypertension 2005;45:142-161. Peters et al Blood Press Monit 1999; 4 97-101.

BP Measurement: Common Errors

• At least a one-time BP should be checked in both arms

– Use the higher arm

– Large difference may be stenosis in subclavian artery or coarctation

• Multiple readings should be recorded- at least 3

– Typically the first is the highest

– Treatment not determined by single readings!

• Observer digit bias (ending in “0”, ie, 140/90 mmHg)

Grim C et al in Hypertension: A Companion to Braunwald’s Heart Disease 2012.

Back to Jerry

• Multiple BP readings were recorded

– 145/95 mmHg average reading

• He was begun on the DASH diet and provided with resources for exercise and weight loss programs

• He was told to monitor his BP and follow-up in office in 2-3 months

DASH = Dietary Approaches to Stop Hypertension

http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf

BP Measurements Outside the Office

What do you recommend to your patients?

1. Purchase a device and take readings at home

2. Take BP at the pharmacy at least once a week

3. Ambulatory BP monitoring (ABPM)

4. Any of the above

5. None of the above

? BP Measurement Devices

Ensure that device is validated

• Manual

– Mercury is still gold standard but disappearing

– Aneroid- ease of calibration

– Non-mercury manual- new device

www.dableducational.org

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BP Measurement Devices

Ambulatory blood pressure monitoring (ABPM) devices• Placed on non-dominant arm• Pre-set readings-typically every 15-

20 min during the day and 30 min at night

• Usually oscillatory measurement

Automated• Finger devices worthless• Wrist devices difficult to use satisfactorily• Most have not undergone validation process

• None that are used widely in community (drugstores)

“White Coat” Effect

• The elevation of BP that occurs with a clinic visit (usually compared to daytime ABPM)

• ABPM probably better than home readings

• BUT… home BP correlate better with ABPM than clinic2

White Coat Effect1

HBPM 14.4/5.0 mmHg

ABPM 18.9/11.4 mmHg

1. Little et al BMJ 2002;325:254.2. Pickering Am J Hypertens 1996;9:1-11.

24-Hour ABPM

• Most effective method to diagnose white coat hypertension and white coat effect

• Both can be diagnosed if mean 24 hr BP is <135/85

– White coat hypertension elevated BP in office in absence of diagnosis or treatment of BP

– White coat effect is presence of elevated BP in office while normal outside in a patient on HTN drug therapy

Acelajado et al Curr Opin Cardiol 2009;24(4):340-344.

Back to Jerry

Three in-office BP readings: mean 145/95 mmHg

How would you evaluate Jerry for cardiovascular risk?

1. Complete metabolic profile

2. ECG

3. Lipid profile

4. Echocardiogram

5. All of the above

6. 1, 2, and 3 only

?

Evaluation of Hypertension JNC-7Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

• Assess lifestyle and identify other cardiovascular risk factors

• Reveal identifiable causes of high BP

• Assess target organ damage

• Laboratory

– Complete blood count (CBC)

– Blood chemistry (including creatinine, potassium, calcium and fasting blood sugar)

– Lipids (total cholesterol, HDL)

– Urinalysis

– ElectrocardiogramJNC-7 2003. Available at http://www.nhlbi.nih.gov/guidelines/hypertension/jncintro.htm

Jerry: Laboratory Results

CBC WNL

CMET

- K+ 4.5 mEq/mL

- Creatinine 1.1 mg/dL

- FBS 88 mg/dL

U/A WNL

Lipids TC -298 mg/dL; LDL 218 mg/dL

HDL 48 mg/dL; TG 175 mg/dL

EKG NSR; Rate 74; no LVH

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Schema for Treatment of Hypertension

Pickering in Black HR, Elliott WJ eds. Hypertension: A Companion to Braunwald's Heart Disease.2nd ed. Elsevier.Saunders 2007

Raised Clinic BPRaised Clinic BP

Target Organ DamageTarget Organ Damage

Raised Home BPRaised Home BP

Raised ABPMRaised ABPM

Continue to Monitor

Continue to Monitor

Start Treatment

Start Treatment

No

No

Yes

Yes

YesNo

Jerry: Follow Up

Returns 8 months later

• Mean office BP:156/98 mmHg HR 88

• HBP- mean:150/94 mmHg

• Weight is unchanged; admits difficulty with DASH diet and keeping exercise regimen

• He’s begun on treatment with lisinopril 40 mg qd

– Considered combination treatment, but deferred

Follow-up 3 months later

• BP still elevated (155/96) and needs additional agent

Hypertension Treatment Algorithim

JNC-7 2003.

Lifestyle Modification

Not at Goal Blood Pressure (<140/90 mmHg)(<130/80 mmHg for patients with diabetes or chronic kidney disease

Initial Drug Choice

Without Compelling Indications With Compelling Indications

Stage 1 Hypertension(SBP 140-159 or DBP 90-99 mmHgThiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination (?)

Stage 1 Hypertension(SBP 140-159 or DBP 90-99 mmHgThiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination (?)

Stage 2 Hypertension(SBP ≥160 or DBP ≥100 mmHgTwo-drug combination for most: thiazide-type diuretic +ACEI, or ARB, or BB, or CCB (?)

Stage 2 Hypertension(SBP ≥160 or DBP ≥100 mmHgTwo-drug combination for most: thiazide-type diuretic +ACEI, or ARB, or BB, or CCB (?)

Drug(s) for the compelling indicationsOther drugs: diuretics, ACEI, ARB, BB, CCB, as needed

Drug(s) for the compelling indicationsOther drugs: diuretics, ACEI, ARB, BB, CCB, as needed

Not at Goal Blood Pressure

Optimize dosages or add additional drugs until goal blood pressure is achieved. Consider consultation with hypertension

specialist.

Optimize dosages or add additional drugs until goal blood pressure is achieved. Consider consultation with hypertension

specialist.

Compelling Indications for Drug Classes

JNC 7. 2003. http://www.nhlbi.nih.gov/guidelines/hypertension/jncintro.htm

Recommended Drugs†

COMPELLING INDICATION* Diuretic BB ACEI ARBI CCBALDOST ANTAG

Heart failure • • • • •

Postmyocardial infarction • • •

High coronary disease risk

• • • •

Diabetes • • • • •

Chronic kidney disease • •

Recurrent stroke prevention

• •

A HTN Treatment ToolBirmingham Square

A: ACE/ARB

B: BB

C: CCB

D: Diuretic

A

BC

D

Lip et al J Hum Hypertens 1998 Nov;12(11):761-763.

Diuretics

• Thiazide and thiazide-like: effective until GFR <35-40 mL/min/1.73m2

• Hypokalemia with usual dose may be evidence of high sodium intake and/or Conn’s syndrome (primary aldosteronism)

• Chlorthalidone: more potent (longer half-life) with similar metabolic effects of HCTZ

• Loop diuretics for hypertension: furosemide should be dosed at least BID

Elliott WJ et al J Clin Hypertens 2008;10:856-862. Germino FW Curr Cardiol Rep 2012 Dec;14(6):673-677.Sica DA et al J Clin Hypertens 2011;13:639-643.

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Beta Blockers

• Selective BB lose selectivity at higher doses, even commonly used doses

• Many of the troublesome side effects are often dose dependent

• Non–duel action beta blockers (in particular tenolol) lower central aortic BP less than brachial BP

Calcium Channel Blockers

• Edema seen is not volume overload, but rather shift in fluid

– Edema especially with amlodipine, felodipine, is dose dependent

– Diuretics will not alleviate the edema in most patients

– ACE inhibitors and ARBs (in appropriate doses) when combined with CCB may improve edema

• Avoid combining verapamil with beta-blockers

Epstein et al Calcium Antagonists in Clinical Practice 2002;713-730.

RAS Inhibitors

ACE Inhibitors

• Most common and troublesome side effect is cough

– Occasionally early effect - for most late onset

– Usually resolves within days of discontinuation

– May not recur with rechallenge months later

• Hyperkalemia - greater risk if comorbid diabetes, CKD

• Up to 25% increase in SCr is acceptable; look for other causes if further increase

• Use therapeutic doses

ARBs

• An alternative to ACE inhibitors, but more expensive

• Angioedema is rare

• Do not use in combination with ACE inhibitors

Sica in Hypertension Black HR, Elliott WJ eds. Hypertension: A Companion to Braunwald's Heart Disease 2007 254-267

Obesity and HypertensionPotential Mechanisms

• Obese patients have higher BP levels- night and day

• Visceral obesity stimulates the RAAS system

• Fat may serve as a storage depot for aldosterone

• Increases risk of non-dipping (also in sleep apnea)

– Esp in high sodium/low potassium intake

• High Na+ intake salt-sensitive phenotype emerges

• Afferent arteriole dilates even if BP high- further injury ensues.

Hall et al Adv Ren Replace Ther 2004;11:41-54.

Hypertension and Diet

• Increased sodium intake mitigates BP response to virtually all antihypertensive medications1

– Especially those that influence RAS

– Impact is greatest in those at lower socieoeconomiclevel

• Dietary potassium supplementation can lower BP and restore normal nocturnal decline in BP2

1. Milan et al J Nephrol 2002;15:1-6.2. Wilson et al Hypertension 1999;34:181-86.

Lifestyle Modifications to Manage Hypertension

Modification Recommendation Approx. SBP

Weight reduction Maintain normal body weight (body mass index 18.5-24.9 kg/m2).

5-20 mmHg/10 kg weight loss

Adopt DASH eating plan

Consume a diet rich in fruits, vegetables, and low-fat dairy products with a reduced content of saturated and total fat.

8-14 mmHg

Dietary sodiumreduction

Reduce dietary sodium intake to no more than 100 mmol per day (2.4 g sodium or 6 g sodium chloride.

2-8 mmHg

Physical activity Engage in regular aerobic physical activity such as brisk walking (at least 30 min per day, most days of the week).

4-9 mmHg

Moderation of alcohol consumption

Limit consumption to no more than 2 drinks (1 oz. or 30 mL ethanol; eg, 24 oz. beer, 10 oz. wine, or 3 oz. 80-proof whiskey) per day in most men and to no more than 1 drink per day in women and lighter weight persons.

2-4 mmHg

JNC7 2003

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Case 2

Case 2: Margaret

• 42-year-old African American female presents with complaint of high blood pressure and elevated blood glucose picked up on screening at her church

• Family History

– Parents and 4/6 siblings with history of hypertension

– 2 older siblings have type 2 diabetes

– Additional history of stroke in family

• Social History

– No alcohol, no smoking, “not good with her diet”

Margaret

• Examination

– BMI- 35.2

• VS

– BP

• 168/94 mmHg(mean)-left

• 162/94 mmHg right

• P-78

– Fundus - AV narrowing

– Neck- no bruit

– Heart- PMI not displaced

– Abdomen- no bruit, obese

– Extremities – edema 1+ bilaterally

Racial Differences in Hypertension and Stroke Risk

• Stroke is 2-3 x more common in blacks than in whites aged 45-65

– REasons for Geographic And Racial Differences in Stroke (REGARDS) study

• 27,748 black and white participants (normotensive, prehypertension, or stage 1 hypertension) followed 4.5 years

• 10 mmHg difference associated with

8% increased stroke risk in whites

24% increased stroke risk in blacks

• These racial differences, coupled with higher prevalence, poorer control of hypertension in blacks, may account for much of the racial disparity in stroke risk

Howard G et al. JAMA Intern Med. 2013 Jan 14;173(1):46-51

Margaret: Next Steps

How would you treat her hypertension?

1. Lifestyle management only

2. ACE inhibitor monotherapy

3. Beta blocker monotherapy

4. Diuretic monotherapy

5. Combination therapy that includes a diuretic

? Effective Approaches in Selected Populations: The Role of RAS Blockers• As monotherapy, ACEIs, ARBs, and conventional beta-blockers are not

as effective in black patients compared with white patients

• However, ACEIs and ARBs should be used in black populations where there is compelling evidence for their effectiveness in whites

Populations Who May Benefit From ACEIs and/or ARBs

Patients with renal disease

Patients with left ventricular hypertrophy (LVH) without diabetes

Patients with LVH with diabetes

Patients with diabetic nephropathy

Patients with heart failure

Patients with diabetes without nephropathy (based on clinical practice) ?

• Additionally, the ACEI ramipril reduces the risk of fatal/nonfatal serious arrhythmic events in high-risk patients without clinical heart failure or overt left ventricular systolic dysfunction

JAMA. 2002;288:2981–2197. JAMA. 2002;288:2421–2431. J Clin Hypertens. 1999;1:141–147. Arch Intern Med. 2003;163:525–541. Med Suisse. 2009;5:25–28.

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Hypertension in African-Americans Slowing GFR Decline

AASK (African-American Study of Kidney Disease and Hypertension)

• Amlodipine vs ramipril

– Major benefit of RAS blockade is in pts with heavy proteinuria (regardless of race)

– AA with non-DM CKD should have ACE inhibitor

– <2 mmHg difference in SBP between CCB vs ACEI

• Add-on therapy included diuretic (attenuated racial difference)

• There is no evidenced-based advantage of lowering BP to less than 140/90 mmHg

Wright JT et al JAMA 2002.;288(19):2421-2431.

Hypertension in African Americans

• Population not homogenous and any broad group recommendations are not predictive of individual response.

– TOMHS-education and income related to urinary sodium excretion rates- not race per se1

• “No particular drug class or therapeutic approach can be reliably extrapolated and applied to AA hypertensive patients with the expectation of uniformly predictable BP responses.”2

1.Ganguli et al Am j Hypertens 1999; 12:69-722. Flack et al in Hypertension in African Americans, Black HR, Elliott WJ eds. Hypertension: A Companion to Braunwald's Heart Disease. Elsevier.Saunders 2007

Hypertension Treatment in African Americans

• Traditionally, CCBs and diuretics are preferred to BB, ACE-Is and ARBs (RAS agents)

• Most patients will require additional therapy- especially those patients with co-existing morbidities

• Home monitoring improved control greater than usual care (MAP-dec 9.6 mmHg versus inc in 5.2 mmHg in usual care)

Rogers et al Ann Int Med 2001;134:1024-1032.

Back to Jerry

Jerry - 10 Years Later

• He is now 50 years old

• His SBP has been creeping up over the last year

– mean HBPM: 154/78 mmHg

• Current meds

• Lisinopril 40 mg daily

• Chlorthalidone 25 mg daily

• Amlodipine 10 mg daily

• Atenolol 25 mg bid

• Atorvastatin 40 mg daily

Jerry

• Examination 5’9” 242 pounds BMI- 35.7

• Mean office BP 166/92 mmHg P=74

– Central obesity-circumference 45 inches

– Neck-without carotid bruit

– Heart-soft 1/6 systolic murmur no S3

– Good distal pulses

• Labs

– Creatinine 1.4 mg/dL

– Electrolytes and other labs WNL

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Question

Resistant hypertension is defined by:

1. Uncontrolled BP despite a regimen of 3 or more drugs including a diuretic

2. Controlled BP achieved on at least 4 drugs

3. Controlled BP achieved only with IV therapy

4. All of the above

5. 1 and 2 only

? Resistant Hypertension

• Uncontrolled blood pressure in hypertensive patients despite treatment with optimal doses of 3 or more anti-hypertensive medications, of which one is a diuretic

• Also includes patients who are controlled on 4 medications

• Must exclude conditions that mimic resistant hypertension

• Prevalence: ~20% in patients with HTN (2005-2008) and increasing

– More frequent in older, obese, male, AA, nonblack Hispanic

Chobanian et al Hypertension 2003;42:1206-1252.Acelajado et al Curr Opin Cardiol 2009;24(4):340-344.Roberie DR et al Curr Opin Cardiol 2012 Jul;27(4):386-391.

Mimics of Resistant Hypertension

• Poorly controlled hypertension

– Inadequately treated or nonadherent

• Pseudo-resistant hypertension

– Improper measurement technique

– Confounding medications (NSAIDs), illicit drugs

– Excessive alcohol consumption

– Pain

– White-coat effect

• Pseudo-hypertension in the elderly

Acelajado et al Curr Opin Cardiol 2009;24(4):340-344.

Spironolactone in Resistant Hypertension

• The addition of spironolactone has been shown to be very effective in patients with resistant hypertension

• The average decrease in BP from multiple studies is 22/10 mmHg

• Adverse events include hyperkalemia, elevated creatinine and gynecomastia

Marrs JC et al. Ann Pharmacother. 2010 44:1762-9..

Secondary HypertensionPrimary Aldosteronism

• Hypokalemia is important clue, however K+ can be normal in 40% of cases1

• Plasma renin <1 ng/mL/hr and elevated plasma aldosterone makes diagnosis in most cases

• Optional confirmatory testing - salt loading with 24 hr collection of urine aldosterone (>14 ug/24 hrs) confirms2

• Patients need be off aldosterone antagonists for at least 3 weeks prior to testing

1. George et al Am J Med 1970;48:343-356.2. Bravo et al Am J Med 1983;74:641-651.

Secondary HypertensionPheochromocytoma

• Most patients have symptoms - although extremely variable - but stereotypical:

– Sustained or paroxysmal symptoms of forceful heart beat, pallor, tremor or diaphoresis

• However, most patients with these symptoms do not have pheochromocytoma

• Some controversy regarding single best test

– Some institutions recommend 24-hour urine collection for metanephrines

– Others utilize fractionated free plasma metanephrines

Young WF et al Mayo Clin Proc 1996;70:757-765.Sawka et al J Clin Endocrinol Metab 2003;88:553-558.Lenders et al Ann Intern Med 1995;123:101-109.

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Secondary HypertensionSleep Apnea

• May be responsible for 15% of resistant hypertension

• Diagnosis with an AHI of >5 with symptoms

• Extent of clinical features may vary

Increased CV risk (36.7% OSAS vs 6.6% none)

Daytime Night-time

Excessive daytime sleepiness Snoring

Impaired concentration Unrefreshing sleep

Irritability/personality change Choking episodes during sleep

Decreased libido Witnessed apneas

Restless sleep

Nocturia

Taler et al Hypertension 2002;39:982-88. American Academy of Sleep Medicine Task Force Sleep 1999;22:667-89Peker et al AmJ Resp Crit Care Med 2002;166:159-65.

Secondary HypertensionRenovascular Disease

• Most common remedial cause of hypertension1

• Can only be diagnosed after an intervention2

• Renal artery stenosis (RAS) is NOT renovascularhypertension (RVH)2

– 32% normotensives: 56% over age 60 have advanced renal artery disease on angiogram but not RVH3

– Procedure on artery only impacted 25% of pts4

1. JNC-7 Hypertension 2003;42:1206-1252.2. Maxwell et al JAMA 1972;220:1195-1204.3. Eyler et al Radiology 1962;78:879-892.4. Smith HW J Urol 1956;76:685-701.

Secondary HypertensionRenovascular Clinical Clues

Characteristic ARR

Abdominal Bruit 5

Recent loss of BP control (or onset) 2

Unilateral small kidney 2

History of accelerated hypertension 2

Unprovoked hypokalemia (<3.4 mEq/L) 2

Increased serum Cr with ACEI or ARB 1.8

No family history of hypertension 1.8

Atherosclerosis in another vascular bed 1.8

Elevated plasma renin 1.8

ARR – Approximate relative risk

Elliott WJ in Black HR, Elliott WJ eds. Hypertension: A Companion to Braunwald's Heart Disease. Elsevier.Saunders 2007

Summary

• The diagnosis of hypertension requires proper measurement of BP and multiple readings

• Include out-of-office measurements in decision-making

• Use appropriate meds and dosing in treatment

• Recommendations for special populations are not patient specific

• Work-up resistant hypertension when appropriate

• Recognize the mimics of resistant hypertension and after excluding evaluate for resistant and secondary hypertension

Outcomes Question #1

Which of the following is TRUE?

1. Women tend to run higher home BP readings than men

2. Home and clinic BP readings tend to vary even in normotensive patients

3. Differences in home and clinic BP increase with age

4. The “white coat” effect is typically an increase in SBP of 5 -10 mmHg

5. All of the above

? Outcomes Question #2

In the treatment of hypertension, which is generally TRUE?

1. HCTZ and chlorthalidone are equally effective

2. Furosemide needs to be dosed twice daily

3. Edema seen with amlodipine is due to volume expansion

4. Ethacrynic acid should not be used in patients with sulfa allergy

?

11

Outcomes Question #3

Which of the following may be suggestive of renovasculardisease as the cause of hypertension?

1. Reduced serum creatinine with ACE-I or ARB

2. Elevated plasma renin

3. Slow, steady increase in blood pressure over time

4. Strong family history of hypertension

5. All of the above

?

Questions?