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Nephrology Boards: HTN > SECONDARY CAUSES OF HYPERTENSION > Flashcards

SECONDARY CAUSES OF HYPERTENSION Flashcards

1
Q

Indications for Evaluation of Secondary HTN

A

Drug-resistant HTN

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2
Q

Indications for Evaluation of Secondary HTN

A

Refractory HTN:

Failure to achieve goal blood pressure (i.e., <140/90 mm Hg), despite being treated by a HTN specialist over at least three visits over a 6-month period or longer

Refractory HTN patients tend to have higher heart rate (81 vs. 70) compared to those who are controlled, despite being on more β-blocker use. Sympathetic dysregulation is thought to play a role.

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3
Q

Specific Causes of Secondary HTN

A

Top three causes: renal parenchymal disease, aldosteronism, renal artery disease.

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4
Q

Specific Causes of Secondary HTN

Obesity

A

Proposed contributing factors: hyperleptinemia, hyperinsulinemia, endothelial dysfunction, sympathetic nervous system (SNS) activation, kidney injury, fructose ingestion, hyperaldosteronism driven by circulating oxidized fatty acids (linoleic acid) or uric acid, concurrent obstructive sleep apnea (OSA)

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5
Q

Specific Causes of Secondary HTN

Obesity

A

Fructose gets phosphorylated rapidly intracellularly leading to → local adenosine triphosphate depletion and uric acid generation → uric acid–induced endothelial dysfunction, SNS activation.

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6
Q

Specific Causes of Secondary HTN
Obesity
OSA:

A

OSA occurs in 30% of patients with HTN and up to 70% to 90% of patients with drug resistant HTN.

The association between OSA and HTN is dependent on OSA severity and presence of obesity. Association is not significant in individuals with BMI < 25 kg/m2 (National health and Evaluation Survey).

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7
Q

Specific Causes of Secondary HTN
Obesity
OSA:

A

Signs and symptoms to consider OSA in hypertensive patients: snoring, gasping/choking, daytime somnolence particularly with associated functional impairment (e.g., “sleeping on the job”).

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8
Q

Specific Causes of Secondary HTN
Obesity
OSA:

A

Physical risks: older men (>50 years old), “crowded” oropharynx, large neck circumference (>50 cm or >20 inches)

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9
Q

Specific Causes of Secondary HTN
Obesity
OSA:

A

Treatment with continuous positive airway pressure (CPAP) ventilation:

Improves BP control with use >4 hours in young patients (2 to 5 mm Hg reduction)

Recommended for symptomatic patients

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10
Q

Specific Causes of Secondary HTN
Obesity
OSA:

A

β-blockers are most effective antihypertensive agent in OSA due to sympathetic overactivity.

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11
Q

Specific Causes of Secondary HTN
Obesity
OSA:

A

Renal denervation improves office BP (average reduction of 34/13 mm Hg), but no significant effect on ambulatory BP (average reduction of 8 mm Hg) in small case series involving 10 patients.

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12
Q

Bariatric surgery versus lifestyle modifications/medical therapy

A

greater weight loss, greater BP reduction, lower antihypertensive drug requirement with bariatric surgery compared with lifestyle modifications/medical therapy alone, even in patients without morbid obesity

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13
Q

Neurogenic HTN

A

Cerebral blood flow = cerebral perfusion pressure/cerebrovascular resistance, where

Cerebral perfusion pressure = MAP − ICP and should be >60 mm Hg.

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14
Q

Neurogenic HTN

HTN after stroke:

A

Contributing factors: cushing reflex, catecholamine and cortisol release, lesion involving brain stem or hypothalamus, nonspecific response, acute stress.

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15
Q

Neurogenic HTN

HTN after stroke:

A

BP management per American Heart/American Stroke Associations:

For stroke patients receiving thrombolytic therapy:

Before thrombolytics: lower BP if SBP > 185 mm Hg or DBP > 110 mm Hg.

After thrombolytics: lower BP if SBP > 180 mm Hg or DBP > 105 mm Hg.

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16
Q

Neurogenic HTN

HTN after stroke:

A

Nonthrombolytic therapy stroke patients:

Antihypertensive medications should be withheld unless SBP > 220 mm Hg or DBP > 120 mm Hg.

When indicated, lowering BP by ~15% is reasonable.

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17
Q

Neurogenic HTN

HTN after stroke:

A

For acute cerebral hemorrhage:

If SBP > 200 mm Hg or MAP > 150 mm Hg, consider aggressive BP reduction (goal MAP 130 mm Hg if increased ICP, otherwise MAP 110 mm Hg).

If SBP > 180 mm Hg or MAP > 130 mm Hg plus evidence of or suspicion for elevated ICP, consider monitoring of ICP and reducing BP to keep cerebral perfusion pressure > 60 mm Hg.

If SBP > 180 mm Hg or MAP > 130 mm Hg and no evidence of or suspicion of elevated ICP, consider modest reduction of BP (e.g., MAP of 110 mm Hg or target BP of 160/90 mm Hg).

Most common agents used: IV labetalol and nicardipine

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18
Q

Antihypertensive agent selection in acute cerebrovascular hypertension
LABETALOL

A

Effect on Cerebral Blood Flow: Neutral
Effect on Intracranial Pressure: Neutral
Comments: Do not affect Cerebral Autoregulation

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19
Q

Antihypertensive agent selection in acute cerebrovascular hypertension
ESMOLOL

A

Effect on Cerebral Blood Flow: Neutral
Effect on Intracranial Pressure: Neutral
Comments: Concensus guidelines suggest IV Labetalol and Nicardipine as first line agents in acute hypertensive phase of stroke. This one is Contraindicated if bradycardic. May be used in the setting of cerebral ischemia or increased ICP.

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20
Q

Antihypertensive agent selection in acute cerebrovascular hypertension
NICARDIPINE

A

Effect on Cerebral Blood Flow: Neutral
Effect on Intracranial Pressure: May Increase
Comments: Long duration of action. Variabe effect on Cerebral Autoregulation. May be used in patients with acute ICH and SAH. Nimodipine is routinely used in patients with SAH, has been shown to improve outcome, presumably from a neuroprotective effect. Nifedipine is not recommended due to potential for hypotension.

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21
Q

Antihypertensive agent selection in acute cerebrovascular hypertension
HYDRALAZINE

A

Effect on Cerebral Blood Flow: May cause both Cerebral and arterial venodilation.
Effect on Intracranial Pressure: May increase ICP. May be used in patients with small to moderate-sized ICH or SAH if no ICP.
Comments: May be used when Beta-Blockers are contraindicated (e.g., bradycardia)

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22
Q

Antihypertensive agent selection in acute cerebrovascular hypertension
SODIUM NITROPRUSSIDE

A

Effect on Cerebral Blood Flow: May cause both Cerebral and arterial venodilation.
Effect on Intracranial Pressure: May increase ICP. May be used in patients with small to moderate-sized ICH or SAH if no ICP.
Comments: There is a concern for cyanide toxicity, reduced platelet aggregation. Cerebral steal possible in pts with cerebral ischemia

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23
Q

Antihypertensive agent selection in acute cerebrovascular hypertension
NITROGLYCERIN

A

Effect on Cerebral Blood Flow: May cause both Cerebral and arterial venodilation.
Effect on Intracranial Pressure: May increase ICP. May be used in patients with small to moderate-sized ICH or SAH if no ICP.
Comments: There is a concern for cyanide toxicity, reduced platelet aggregation. Cerebral steal possible in pts with cerebral ischemia

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24
Q

Antihypertensive agent selection in acute cerebrovascular hypertension
ENALAPRILAT

A

Effect on Cerebral Blood Flow: Neutral
Effect on Intracranial Pressure: —
Comments: Long duration of action.

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25
Q

Neurogenic HTN

HTN after carotid endarterectomy and endovascular procedures (e.g., angioplasty, stenting

A

Contributing factors: carotid baroreceptor impairment after surgical manipulation, elevated catecholamine levels, activation of trigeminovascular axon reflex

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26
Q

Neurogenic HTN

HTN after carotid endarterectomy and endovascular procedures (e.g., angioplasty, stenting

A

Carotid hyperperfusion syndrome following carotid endarterectomy:

Occurs during first week after surgery

Cerebral hyperperfusion is defined as having a postoperative increase in cerebral flow of >100% compared with preoperative flow on the ipsilateral side.

Ipsilateral symptoms: pulsatile headaches, seizures, intracranial hemorrhage, cerebral edema

Contralateral symptoms: neurological deficits

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27
Q

Neurogenic HTN

HTN after carotid endarterectomy and endovascular procedures (e.g., angioplasty, stenting

A

Management:

Continuous intra- and postoperative BP monitoring

Strict BP control with SBP < 120 mm Hg

Preferred agents: intravenous labetalol or clonidine

AVOID: vasodilators such as nitroglycerin, sodium nitroprusside

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28
Q

Neurogenic HTN

HTN after spinal cord injury affecting the sixth or above the sixth thoracic spinal nerve (autonomic dysreflexia):

A

Defined as SBP > 20% from baseline with associated change in heart rate (brady- to tachycardia), and at least one of the following: headache, facial flushing, blurry vision, stuffy nose, sweating, piloerection. Flush sweaty skin above lesion levels is due to brain stem parasympathetic activation.

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29
Q

Neurogenic HTN

HTN after spinal cord injury affecting the sixth or above the sixth thoracic spinal nerve (autonomic dysreflexia):

A

Occurs in up to 70% of patients with spinal injury affecting the sixth thoracic spinal nerve or higher level

Occurs in up to 90% of pregnant women during labor and delivery. Use of epidural or spinal anesthesia may reduce risk.

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30
Q

Neurogenic HTN

HTN after spinal cord injury affecting the sixth or above the sixth thoracic spinal nerve (autonomic dysreflexia):

A

Pathophysiology:

Immediately following spinal injury: loss of supraspinal sympathetic control leading to initial period of muscle flaccidity and “spinal shock,” clinically evident as bradycardia and hypotension

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31
Q

Neurogenic HTN

HTN after spinal cord injury affecting the sixth or above the sixth thoracic spinal nerve (autonomic dysreflexia):

A

Pathophysiology:

Weeks to months following injury: extrajunctional sprouting of α-receptors, denervation hypersensitivity, impaired presynaptic uptake of norepinephrine, and derangement of spinal glutamatergic neurons

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32
Q

Neurogenic HTN

HTN after spinal cord injury affecting the sixth or above the sixth thoracic spinal nerve (autonomic dysreflexia):

A

Pathophysiology:

Noxious stimuli below neurologic level of the lesion triggers a spinal reflex arc that results in increased sympathetic tone and HTN.

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33
Q

Neurogenic HTN

HTN after spinal cord injury affecting the sixth or above the sixth thoracic spinal nerve (autonomic dysreflexia):

A

Pathophysiology:

Common noxious stimuli are from urinary overdistention and fecal impaction. Others: sympathomimetic medications and sildenafil citrate used for sperm retrieval

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34
Q

Neurogenic HTN

HTN after spinal cord injury affecting the sixth or above the sixth thoracic spinal nerve (autonomic dysreflexia):

A

Management:

Preventive measures: good bowel, bladder, and skin care

Treatment:

Position patient upright to precipitate orthostatic BP.

Remove noxious stimuli (e.g., tight clothing, devices, fecal disimpaction, bladder catheterization as applicable).

Medications: select fast-acting, short-lived agents for persistent SBP elevation > 150 mm Hg. Consider other noxious stimuli, hospitalization if no resolution.

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35
Q

Parenchymal kidney disease

A

is the most common cause of secondary HTN

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36
Q

Simple renal cysts and HTN

A

Association thought to be due to cyst compression on adjacent renal parenchyma resulting in focal ischemia and activation of the renin–angiotensin–aldosterone system.

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37
Q

Simple renal cysts and HTN

A

Association with HTN is strengthened with increased number of cysts (≥2) and increased cystic size > 1.4 to 2.0 cm.

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38
Q

Simple renal cysts and HTN

A

Management:

Cyst decompression anecdotal reports of reducing BP.

Use of RAAS blockers may be beneficial.

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39
Q

Proteinuria and HTN

A

Proteinuria with loss of plasminogen in urine, leads to the formation of plasmin by tubular urokinase-like plasminogen activator. Plasmin directly stimulates the distal tubular sodium epithelial channel ENaC and sodium reabsorption (thus HTN) via the proteolytic cleavage of ENaC extracellular α- and γ-subunits.

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40
Q

Proteinuria and HTN

A

Potential role of amiloride or triamterene as preferred agent in the management of edema and salt sensitivity in patients with proteinuria and HTN.

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41
Q

Renovascular HTN

Clinical manifestations:

A

Clinical manifestations:

Activation of renin–angiotensin–aldosterone system: seen in early phase in bilateral renal artery stenosis, but sustained in unilateral disease

Paroxysmal symptoms due to SNS activation

Loss of nocturnal BP dipping

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42
Q

Renovascular HTN

Clinical manifestations:

A

Accelerated end-organ damage: left ventricular hypertrophy, microvascular disease, renal fibrosis

Abdominal systolic–diastolic bruits, sensitivity 39% to 63%, specificity 90% to 99%

Slow progression of renovascular HTN is thought to be associated with an adaptive response to tissue hypoxia thereby minimizing structural damage.

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43
Q

Renovascular HTN

A

Diagnostic studies:

Contrast angiography: gold standard: provides both structural and functional information; Risks: procedure-related vascular injury, contrast-induced AKI (CI-AKI).

Spiral computed tomographic angiography: good images of vessels; Risks: CI-AKI

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44
Q

Renovascular HTN

A

Magnetic resonance angiography with gadolinium: good structural and functional images of vessels; Risks: nephrogenic systemic fibrosis if gadolinium is used in patients with eGFR < 30 mL/min/1.73 m2; Other disadvantages: high interobserver variability; limited sensitivity for mid and distal vascular lesions associated with FMD. A lternative MRI contrast in patients with eGFR < 30 mL/min/1.73 m2: Feraheme

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45
Q

Renovascular HTN

A

Captopril renography (renal nuclear scan): provides information on renal blood flow (uptake/appearance of isotope [MAG3] phase) and filtration (excretory phase), hence information on size and excretory capacity of kidney. Delayed excretory phase following captopril administration suggests significant role of AII in maintaining GFR. Advantage: high negative predictive value, that is negative test essentially rules out clinically significant renal artery stenosis.

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46
Q

Renovascular HTN

A

Renal arterial Doppler (ultrasonography): most effective for detection of lesions in proximal main renal artery (thus likely not great study for fibromuscular dysplasia [FMD] where lesions are typically more distal). Advantages: inexpensive, readily available; Disadvantages: no functional information.

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47
Q

Renovascular HTN

A

Renal vein renin measurements: used to predict BP response to renal revascularization: a ratio > 1.5 (stenotic kidney):1.0 (nonstenotic kidney), predicts good BP response in > 90% of patients. However, nonlateralization may also have good response in ~50%.

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48
Q

Renovascular HTN

A

HTN occurs in the presence of a critical stenosis (e.g., >70% to 80%); Stenotic lesions < 60 % typically do not lead to clinically significant reduction in renal arterial flow to induce systemic activation of vasopressors to cause HTN.

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49
Q

Renovascular HTN

Unilateral stenosis

A

Unilateral stenosis (one-clip, two-kidney HTN model): one stenosed (experimental clipping of one renal artery) + one normal kidney

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50
Q

Renovascular HTN

Unilateral stenosis

A

Stenosed “clipped” kidney has reduced renal perfusion pressure → stimulation of neuronal NO synthase and cyclooxygenase 2 in macula densa → release of renin from juxtaglomerular apparatus → activation of RAAS, (i.e., increased angiotensin II (AII) and aldosterone) → systemic BP increases to restore renal perfusion pressure, increased sodium retention.

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51
Q

Renovascular HTN

Unilateral stenosis

A

Normal contralateral kidney undergoes pressure natriuresis to restore sodium and volume balance, thus counteracts the stenosed kidney’s attempt to improve its own perfusion → continued RAAS activation by stenosed kidney → angiotensin II-dependent HTN; aldosterone-induced renal K+ and H+ secretion in the contralateral kidney, hence hypokalemia and metabolic alkalosis.

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52
Q

Renovascular HTN

Unilateral stenosis

A

Long-term HTN also attributes to activation of SNS, impairment of NO generation, endothelin release, and hypertensive microvascular injury in the normal contralateral kidney.

53
Q

Renovascular HTN

Unilateral stenosis

A

Clinical implication of RAAS activation in unilateral renal artery stenosis:

RAAS inhibition: reduces BP, enhances lateralization of diagnostic testing, reduces GFR in stenotic kidney.

54
Q

Renovascular HTN

Unilateral stenosis

A

Common clinical conditions equivalent to one-clip, two-kidney HTN (unilateral stenosis):

Unilateral FMD

Unilateral renal atherosclerotic disease

Unilateral renal artery aneurysm, dissection, embolism, thrombosis, traumatic occlusion, vasospasm

Unilateral renal arteriovenous fistula

Aortic dissection affecting renal ostium

“Page” kidney (perinephric compression, i.e., large capsular hematoma, perinephric fibrosis)

Extrinsic compression (e.g., tumor) on one renal artery

Aortic stent occluding origin of renal artery

55
Q

Renovascular HTN

Bilateral renal artery stenosis

A

Bilateral renal artery stenosis (one-clip, one-kidney HTN) or (two-clip, two-kidney HTN model):

Entire kidney mass is exposed to reduced pressures from site of stenosis.

There is no “normal nonstenotic kidney.”

56
Q

Renovascular HTN

Bilateral renal artery stenosis

A

Initial activation of SNS, RAAS leads to sodium and water retention. Since there is no “normal kidney” to excrete the sodium and volume retained, volume overload eventually develops which leads to inhibition of RAAS.

HTN is not RAAS-dependent, but volume-dependent.

57
Q

Renovascular HTN

Bilateral renal artery stenosis

A

Clinical implications:

Patients can be salt-sensitive → easy development of “flash pulmonary edema,” following a high dietary salt load

Diuretics may be effective in lowering BP.

58
Q

Renovascular HTN

Bilateral renal artery stenosis

A

Use of RAAS inhibition:

Only lowers BP after euvolemia has been achieved (i.e., RAAS activation only occurs after negative feedback from volume expansion has been removed).

May significantly lower GFR and cause kidney failure.

59
Q

Renovascular HTN

Bilateral renal artery stenosis

A

Since RAAS is inhibited due to volume expansion, patients with bilateral renal stenosis or equivalent (see conditions below), typically do not develop hypokalemia and metabolic alkalosis. In fact, the opposite, hyperkalemia and metabolic acidosis, may be present.

60
Q

Renovascular HTN

Bilateral renal artery stenosis

A

Clinical conditions equivalent to one-clip, one-kidney HTN model:

Bilateral arterial stenosis or stenosis of solitary kidney

Significant coarctation of aorta or any flow-limiting lesions (e.g., atheroembolic disease, aneurysms, extrinsic mass compression) of suprarenal abdominal aorta

Renal artery vasculitis

Congenital vascular anomalies

61
Q

Renovascular HTN

Fibromuscular dysplasia

A

Nonatherosclerotic arteriopathy affecting large and medium-sized arteries, typically mid to distal renal artery beyond the first 2 cm from aorta.

62
Q

Renovascular HTN

Fibromuscular dysplasia

A

Epidemiology:

Prevalence of clinically significant renovascular FMD is 4/1,000, cerebrovascular involvement 1/1,000 (may present with carotid flow abnormalities, stroke); may be up to 3% to 6% in normotensive individual.

Familial presentation in 10%, thought to be autosomal dominant.

63
Q

Renovascular HTN

Fibromuscular dysplasia

A

Clinical manifestations:

Commonly seen in young (15 to 50 years old) females with early-onset HTN.

64
Q

Renovascular HTN

Fibromuscular dysplasia

A

Associated conditions: Marfan and Ehlers–Danlos syndromes, tuberous sclerosis, cystic medial necrosis, coarctation of aorta, Alport syndrome, renal agenesis or dysgenesis, α1-antitrypsin deficiency, medullary sponge kidney, PHEO, infantile myofibromatosis, ergotamine preparation, methysergide, cigarette smoking, collagen III glomerulopathy, atherosclerotic renovascular disease.

65
Q

Renovascular HTN

Fibromuscular dysplasia

A

Lesions are characterized by disruptions of vascular wall components with abnormal collagen deposition in bands, ± disruption of elastic membrane.

66
Q

Renovascular HTN

Fibromuscular dysplasia

A

FMD typically occurs in the middle or distal portions of renal artery or branch vessels and may present with aneurysms, occlusion, dissection, arteriovenous fistulas, or thrombosis.

67
Q

Renovascular HTN

Fibromuscular dysplasia

A

FMD types:

Medial (85% to 100%) > intimal (<10%) > adventitial (<1%)

Media and perimedial fibroplasia classically have “string of beads” appearance. Medial hyperplasia may only present as smooth stenosis of artery.

Initimal and adventitial fibroplasia present as smooth stenotic segments or diffuse attenuation of vessel lumen.

68
Q

Renovascular HTN

Fibromuscular dysplasia

A

Natural history:

Progression of disease slows down with age.

Rarely causes ischemic kidney failure, but associated thrombosis or dissection of affected renal vessel may lead to renal infarction.

69
Q

Renovascular HTN

Fibromuscular dysplasia

A

Management of FMD + HTN: percutaneous transluminal renal angioplasty (PTRA) versus surgical revascularization:

PTRA:

Higher chance of BP lowering following PTRA in younger patients or those with lower pre-PTRA BP, shorter duration of HTN, and positive captopril test.

If restenosis occurs, repeat PTRA may be performed as needed.

70
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Surgical revascularization:

If aneurysmal dilations > 1.5 cm in diameter

Covered stent grafts may also be used in renal artery aneurysms.

71
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Atherosclerotic plaque formed from the first 1 to 2 cm of renal artery or from aorta extending into renal ostium (more proximal involvement compared with FMD).

72
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Epidemiology:

Seen in 10% to 40% of patients undergoing coronary angiography

Similar prevalence in African Americans and Caucasians in one study cohort involving 870 patients > 65 years old

Autopsy series: prevalence of 4% to 20%; 25% to 30% in those >60 years old, 40% to 60% in those >75 years old

Estimated to contribute to decline in kidney function in 15% to 22% of patients with end-stage kidney disease

73
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Clues to presence of ischemic renal disease due to atherosclerosis:

Asymmetry of kidney size

Recent kidney function deterioration

AKI following use of ACEI or ARB due to acute reduction in intraglomerular filtration pressure (due to loss of AII-dependent efferent vasoconstriction to maintain intraglomerular filtration pressure)

74
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Clues to presence of ischemic renal disease due to atherosclerosis cont’d:
AKI following acute systemic BP reduction with any other hypertensive agents

Presence of flash pulmonary edema, more common in bilateral compared with unilateral stenosis

Consider renal stenosis in patients with known or at increased risks for atherosclerotic disease and unexplained kidney injury

75
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

NOTE: Most patients with renovascular HTN do not develop AKI with ACEI/ARB because

In unilateral renal artery stenosis, the normal contralateral kidney may still have adequate function to mask any reduced filtration pressure in the affected kidney by ACEI/ARB.

76
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Most patients with renovascular HTN do not develop AKI with ACEI/ARB because:
In bilateral RAS, AII is suppressed due to sodium retention. Hence, ACEI/ARB does not directly reduce glomerular filtration pressure.

Those with AKI with ACEI/ARB tend to have other additional source(s) contributing to reduced renal perfusion, for example, volume depletion, cardiac decompensation.

77
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Management of atherosclerotic renal artery stenosis:

Medical therapy:

RAAS inhibition as safely tolerated (SCr increases less than 20% to 30% from baseline is acceptable).

Use of other agents as needed to control BP: CCB, diuretics, etc.

Daily aspirin

Statin as tolerated particularly if hyperlipidemia and/or CKD and >50 years old

Smoking cessation if applicable

78
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Invasive therapy:

No evidence of renal or cardiovascular benefits with invasive therapy if stable kidney function and BP

79
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Cardiovascular outcomes of renal atherosclerotic lesions (CORAL) trial: comparative trial for renal artery stenting versus best medical therapy involving 947 patients with uncontrolled HTN and atherosclerotic renal artery stenosis, BP > 155 mm Hg while on >2 BP medications

Average SBP was 2.3 mm Hg lower in the stent group throughout the trial (median follow-up 3.6 years).

No difference in incidence of cardiovascular or renal death, myocardial infarction, hospitalization for congestive heart failure, stroke, progressive CKD, or need for renal replacement therapy

80
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Meta-analysis of five RCT involving 1,159 patients comparing percutaneous renal artery revascularization (with or without stenting) versus medical therapy on future occurrence of nonfatal myocardial infarction: Renal revascularization did not affect risk of nonfatal MI.

81
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

However, invasive therapy may be considered in younger viable (low comorbidities) patients with:

Rapidly progressive disease (i.e., AKI with RAAS inhibition or achievement of BP control)

Failure to appropriate medical therapy

Unexplained acute heart failure, “flash pulmonary edema”

82
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Renal artery stenting versus surgical revascularization:

Surgical revascularization is reserved for patients with technically challenging vascular lesions or associated aortic disease.

83
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Intervention being considered: concurrent renal revascularization and use of anti-inflammatory therapies or agents that can alter mitochondrial function to reduce the generation of reactive oxygen species and/or ATP depletion during reperfusion.

84
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Contraindications to invasive therapy: advanced kidney disease (e.g. SCr > 3 to 4 mg/dL, kidney length < 8 cm), poor surgical candidate, or low life-expectancy.

85
Q

Renovascular HTN

Atherosclerotic renal artery stenosis

A

Atherosclerotic renal artery stenosis typically affects the proximal 1 to 2 cm of the renal artery from aorta, FMD involves the distal 1/2 to 1/3 of the renal artery, and polyarteritis nodosa involves multiple aneurysmal dilatations within the kidneys

86
Q

Endocrine causes of HTN

A

Endocrine causes of HTN: from pituitary → thyroid → parathyroid → adrenals

87
Q

Endocrine causes of HTN

A

Pituitary: acromegaly

Pituitary tumor producing excessive circulating growth hormone (GH). Other GH-producing tumors: pancreatic, hypothalamic, breast, bronchial malignancies

More common in women and older patients

88
Q

Endocrine causes of HTN

acromegaly

A

Pathogenesis:

Sodium retention with inappropriately normal to only minimally low renin and aldosterone levels and normal atrial natriuretic peptide.

Others: GH–induced vascular hypertrophy with decreased vascular compliance, increased SNS, associated hyperthyroidism.

89
Q

Endocrine causes of HTN

acromegaly

A

Clinical manifestations: skull, hands, feet enlargement, excessive sweating, carpal tunnel syndrome, sexual dysfunction, diabetes mellitus, thyromegaly, thyrotoxicosis, headaches, visual field defects

90
Q

Endocrine causes of HTN

acromegaly

A

Diagnosis:

Elevated plasma GH, especially in response to an oral glucose tolerance test

Others: plasma insulin-like growth factor I, lateral skull X-ray (thickened skull vault, enlarged frontal sinuses), MRI of pituitary fossa

91
Q

Endocrine causes of HTN

acromegaly

A

Management:

Tumor-specific:

Transphenoidal adenomectomy is treatment of choice if no contraindication

Tumor radiation

Dopaminergic agents: bromocriptine and cabergoline, octreotide

HTN: diuretics as primary agent, addition of others as needed

92
Q

Endocrine causes of HTN

Pituitary: Cushing syndrome

A

Pituitary: Cushing syndrome (pituitary adenoma producing excess adrenocorticotropic hormone (ACTH); other sources of excess ACTH secretion: adrenal tumors, bronchogenic carcinoma.

93
Q

Endocrine causes of HTN

Pituitary: Cushing syndrome

A

Pathogenesis:

Increased cardiac output and peripheral vascular resistance

Concurrent production of mineralocorticoids

Cortisol inhibition of NO

Increased sensitivity to catecholamines, AII, and β-adrenergic stimulation

Blunted response to atrial natriuretic peptide

94
Q

Endocrine causes of HTN

Pituitary: Cushing syndrome

A

Diagnosis:

24-hour urine free cortisol

Dexamethasone suppression test

Low dose (1 mg) at midnight

High dose (partially suppresses ACTH from pituitary tumors but not with ectopic ACTH)

Corticotropin-releasing hormone test.

Imaging studies: CT or MRI of pituitary, adrenals, thorax/abdomen/pelvis

Simultaneous bilateral inferior petrosal sinus sampling for ACTH measurements

95
Q

Endocrine causes of HTN

Pituitary: Cushing syndrome

A

Management:

Cushing disease: resection of pituitary adenoma

Cushing syndrome:

Unilateral adrenalectomy if adrenal adenoma

Adrenal carcinoma is associated with poor survival

Antihypertensive medications: consider potassium-sparing diuretics

96
Q

Endocrine causes of HTN

Thyroid

A

Hypothyroidism-associated HTN:

Sodium retention

Increased peripheral vascular resistance; 30% of patients have diastolic HTN

Underdamping of swings in SNS activity

97
Q

Endocrine causes of HTN

Thyroid

A

Hyperthyroidism-induced HTN:

Pathogenesis:

Increased cardiac output, heart rate, myocardium contractility. (Peripheral vascular resistance tends to be reduced.)

Expanded blood volume

Increased RAS activity but not SNS

Classic presentation: high pulse pressure HTN, ISH

98
Q

Endocrine causes of HTN

Parathyroid

A

Parathyroid: Hyperparathyroidism-induced HTN is thought to be due to increased peripheral vascular resistance, presumably due to hypercalcemia

99
Q

Endocrine causes of HTN
Adrenals
PHEO

A

PHEO:

90% arise from adrenals, 10% extra-adrenal (paraganglioma, PGL).

Most are benign; 10% metastasize to regional lymph nodes

Common hormones produced: norepinephrine, epinephrine, dopamine

Malignant disease or large tumor mass may have very high dopamine levels.

100
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Sporadic disease:

Often focal, unilateral involvement

Up to 14% have somatic mutations

101
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Familial disease:

Typically multifocal, bilateral, extra-adrenal disease, age < 50 years old, may be associated with germ line mutations (most are autosomal dominant)

102
Q

Endocrine causes of HTN
Adrenals
PHEO

A

RET gene: multiple endocrine neoplasia type 2 (MEN 2):

MEN 2a: medullary thyroid carcinoma, hyperparathyroidism, cutaneous lichen amyloid

MEN 2b: medullary thyroid carcinoma, multiple neuromas, marfanoid habitus

Mostly epinephrine secretion

Paroxysmal symptoms

103
Q

Endocrine causes of HTN
Adrenals
PHEO

A

von Hippel–Lindau gene: von Hippel–Lindau syndrome

Syndrome with retinal and CNS hemangioblastomas, renal cell carcinoma, pancreatic, endolymphatic sac, epididymal tumors

Predominant noradrenergic secretory pattern

Can present primarily with asymptomatic HTN due to downregulation of α-adrenoceptors

104
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Neurofibromatosis type 1 gene:

Neurofibromatosis type 1 (a.k.a. von Recklinghausen disease): neurofibromas, café-au-lait spots

Mostly epinephrine secretion

Paroxysmal symptoms

105
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Genes encoding the B and D subunits of mitochondrial succinate dehydrogenase (SDHB, SDHB): familial PGLs (head and neck) and PHEOs; no secretory activity; no symptoms related to catecholamines, but space-occupying effect

106
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Hypoxia induced factor -2α (HIF-2α), somatic mutation: multiple duodenal somatostatinomas, polycythemia

107
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Common clinical manifestations of PHEOs:

Classic: paroxysmal HTN, headaches, diaphoresis, palpitations, anxiety, chest/abdominal pain, nausea/vomiting, dyspnea, pallor

Severe HTN with trauma, delivery, or sudden onset

Subclinical

108
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Physical examination: 2/3 labile HTN, 1/3 persistent HTN; reciprocal changes in BP and heart rate may occur with predominantly norepinephrine secreting tumors; postural hypotension; low-grade fevers, tachycardia, skin may be cool, mottled appearing.

109
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Diagnosis:

Plasma free metanephrines and normetanephrines greater than four- to fivefold of normal → positive test. High sensitivity

If positive plasma study, obtain urine metanephrines and normetanephrines. High sensitivity and high specificity

110
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Glucagon stimulation:

Indicated if equivocal plasma study

Administer 2 mg glucagon IV bolus. Positive test: greater than threefold increase in baseline levels of catecholamines within 1 to 2 minutes

111
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Clonidine suppression test:

Indicated if equivocal plasma study

Administer 0.3 mg clonidine. Positive test: failure to reduce plasma catecholamines to >50% from baseline

112
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Imaging studies:

MRI or CT: abdomen/pelvis if no family history; neck to pelvis if family history or suspicion for genetic disease

If negative, consider metaiodobenzylguanidine (MIBG) scan, indium In111-labeled octreotide scan, plasma-free metanephrines coupled with vena caval sampling, or positron emission tomography (PET) scan.

MIBG has high sensitivity (83% to 100%) and specificity (95% to 100%) in sporadic PHEO.

MIBG has been suggested to be inferior to PET in the evaluation of PHEO/PGL in familial and metastatic disease.

113
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Management:

BP control:

α-adrenergic blockers (phenoxybenzamine [usually not well tolerated due to orthostatic hypotension]), doxazosin, terazosin

CCB

Add β-blockers if tachycardia or arrhythmias after full α-adrenergic inhibition. Consider agents with both α- and β-inhibition (e.g., carvedilol, labetalol).

114
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Surgical removal:

Preoperative preparation: BP control weeks prior to surgery

Intraoperative BP management options: phentolamine, sodium nitroprusside, and magnesium sulfate

Postoperative management: monitor for hypoglycemia and hypotension

115
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Long-term management:

BP control if persistent HTN

If malignant PHEO, use both α- and β-adrenergic blockers as needed for symptoms, radiation therapy for bone metastatic disease, and chemotherapy (cyclophosphamide, vincristine, and dacarbazine). Median survival ~5 years.

116
Q

Endocrine causes of HTN
Adrenals
PHEO

A

Follow-up (life-long):

Adrenal PHEO < 5 cm and no suspected hereditary syndrome: biochemical screening at 1 year, then every other year thereafter

PHEO > 5 cm or hereditary syndromes, multifocal PGL: biochemical evaluation after 6 months following surgery, then yearly thereafter with periodic imaging study

For patients with biochemically silent disease: periodic imaging study

117
Q

Endocrine causes of HTN

Adrenals

A

Adrenal incidentaloma/hyperplasia/adenoma/carcinoma:

Screening aldosterone/renin ratio (ARR):

ARR > 30 and aldosterone levels > 20 ng/dL

Sensitivity 90%, specificity 91%, positive predictive value 69%

118
Q

Endocrine causes of HTN

Adrenals

A

Factors affecting ratio:

False negative ARR due to increased renin: dietary salt restriction, malignant or renovascular HTN, diuretics (including spironolactone, eplerenone), dihydropyridine calcium channel blockers, ACEI/ARB, selective serotonin reuptake inhibitors

False positive ARR due to suppressed renin: β-blockers, α-methyldopa, clonidine, NSAIDS. False positives may also occur in patients with renal dysfunction and older age.

Optimization of ARR measurements: normalize serum potassium levels prior to measuring ARR.

Avoid use of medications that can affect ARR if clinically safe.

119
Q

Endocrine causes of HTN

Adrenals

A

Prevalence of high ARR is 16% to 20% in patients with HTN.

Prevalence of confirmed primary aldosteronism is 4.5% to 9.5%

120
Q

Endocrine causes of HTN

Adrenals

A

Confirmatory testing following positive ARR:
IV salt loading: 2 L NS over 4 hours (recumbent) → (+) if plasma aldosterone > 10 ng/dL (<6 ng/dL in normal subjects)

Oral salt loading: 2 g NaCl tablets t.i.d. × 3 days and potassium supplement → (+) if 24-hour urine aldosterone > 14 g/24-hour (UNa should also be >200 mEq to assess compliance with Na load)

121
Q

Endocrine causes of HTN

Adrenals

A

Fludrocortisone-suppression test: fludrocortisone acetate 0.1 mg q6h with high salt diet (3 mmol/kg/d) × 4 days and potassium supplement → (+) if plasma aldosterone > 5 ng/dL and PRA < 1.0 ng/mL/h.

122
Q

Endocrine causes of HTN

Adrenals

A

Imaging studies:

CT/MRI imaging with adrenal cuts: Adrenal carcinoma is more likely with increasing size; 2% of masses up to 4 cm, 6% of masses from 4 to 6 cm, 25% of masses > 6 cm are malignant.

123
Q

Endocrine causes of HTN

Adrenals

A

Adrenal venous sampling (AVS) for lateralization of aldosterone levels should be considered in good candidates for adrenalectomy (young, non-obese patients with limited end-organ damage and short duration of HTN and hypokalemia) to confirm the correct side of the hyperfunctioning gland prior to removal. NOTE: AVS for lateralization of aldosteronism should be measured along with a selectivity index (adrenal vein to inferior vena cava cortisol ratio > 5:1) to indicate successful adrenal vein catheterization. A low selectivity index may indicate erroneous blood sampling from a vein other than the adrenal vein, which may give a falsely low aldosterone level, thus falsely negative lateralization test.

124
Q

Endocrine causes of HTN
Adrenals

Long-term effects of hyperaldosteronism:

German registry compared mortality rates of 300 patients with primary aldosteronism (either surgically or medically managed) to 600 hypertensive patients and 600 normotensive controls over a 16-year follow-up revealed:

A

No difference in mortality among the three groups.

Cardiovascular deaths were higher for patients with primary hyperaldosteronism (50%) compared to those with essential (38%) or normotensive controls (35%).

Unadjusted analyses suggested better outcomes with adrenalectomy versus medical therapy, but not on multivariate analyses, thought to be due to healthier patient selection for adrenalectomy.

125
Q

Endocrine causes of HTN
Adrenals

Management:

A

Medical intervention:

MRA: aldosterone antognists spironolactone or eplerenone

Aldosterone synthase activity blocker LC1699 versus eplerenone: eplerenone more effective in reducing BP and improving hypokalemia. LC1699, however, reduces, whereas eplerenone increases aldosterone levels. Long-term effects of elevated aldosterone levels are not known.

126
Q

Endocrine causes of HTN

Adrenals

A

Surgical versus medical intervention:

Better cardiovascular mortality with surgical intervention than MRA is questioned by patient selection for surgery versus MRA.

Nonetheless, adrenalectomy may still be considered in younger patients with short disease duration and minimal or no evidence of end-organ damage.

127
Q

Acute intermittent porphyria:

A

Rare autosomal dominant disorder with deficiency of porphobilinogen deaminase affecting heme production and associated with increased porphobilinogens

128
Q

Acute intermittent porphyria:

Clinical Manifestations

A

Clinical manifestations:

Intermittent severe colicky abdominal pain, constipation, dystonic bladder with urinary retention/incontinence, dark urine, autonomic dysfunction with increased circulating catecholamine levels resulting in HTN, tachycardia, sweating, restless and tremors, peripheral neuropathy, proximal muscle weakness, neuropsychiatric disorders, SIADH with hyponatremia. Skin rash is not a typical manifestation compared to other forms of porphyria.

Attacks may be brought on by infections, hormonal or dietary changes, drugs.

129
Q

Acute intermittent porphyria:

Diagnosis and Management

A

Diagnosis: elevated urinary porphobilinogens (urine spot test)

Management:

Mild attacks: high-dose oral glucose (400 g/d) or intravenous dextrose 10% solution

Severe attacks, severe neurologic symptoms: hematin (hemin) 3 to 4 mg/kg/d for 4 days

Pain control with narcotics as needed

Laxatives, softeners for constipation, particularly if narcotics are used

Gabapentin for seizures

Nephrology Boards: HTN (16 decks)

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