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Emma Sy MoeisDivision of Nephrology & Hypertension
Department of Internal Medicine,
Medical Faculty of Sam Ratulangi University, Manado
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100or> 160Stage 2
90-99or140-159
Stage 1
Hypertension80-89or120-139Prehypertension
18 y.o
Adults on no antihypertensive medications and who arenot acutely ill.
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Hypertension
EssentialSecondary
Causes
Endocrine
Hypertension
Non-Endocrine
Hypertension
Primer (essential) No specific causes that can
be identified
95% of all hypertensioncases
Secondary
Causes can be identified
5% of all hypertensioncases
Kidney disease is the maincause (90%) of all
secondary hypertensioncases
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Renal parenchymal disease:acute nephritis,chronic glomerulonephritis, etc.
Renovascular disease:renal artery stenosis,
atherosclerosis,fibroplasia, etc.
Endocrine causes
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Pheochromocytoma Mineralocorticoid excess (e.g., primary hyperaldosteronism) Glucocorticoid excess (e.g., Cushings syndrome) Acromegaly
Diabetes mellitus
Obesity
Congenital adrenal hyperplasia
Estrogen-induced hypertension Pregnancy-induced hypertension Renin-secreting tumors Hypothyroidism
Hyperthyroidism
Liddle syndrome
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a 47 year old woman referred because ofpoorly controlled hypertension. She has leg
cramps and polyuria, but no episodes ofheadache, sweating or palpitations.There is no family history of hypertension.She is not obese.
HR: 78/min and BP 160/98 mmHg, the examis otherwise normal.
Plasma potassium: 2.5 mM
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1. What symptoms are caused byhypertension? By severe hypokalemia?
2. What are the three major endocrine causesof hypertension (ie, disorder in which themajority of patient has high blood pressure)?How common are they in patient with
hypertension?3. Which endocrine cause of hypertension ismost likely in this patient? What test shouldbe done now?
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Symptoms caused by hypertension:
None
Symptoms caused by severe hypokalemia: Leg cramps
polyuria
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1. What symptoms are caused by hypertension?By severe hypokalemia?
2. What are the three major endocrine causes of
hypertension (ie, disorder in which themajority of patient has high blood pressure)?How common are they in patient withhypertension?
3. Which endocrine cause of hypertension is mostlikely in this patient? What test should be donenow?
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Three major endocrine causes of hypertension: Primary hyperaldosteronism Pheochromocytoma Cushing syndrome
In patient with hypertension, approximately
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1. What symptoms are caused byhypertension? By severe hypokalemia?
2. What are the three major endocrine causesof hypertension (ie, disorder in which themajority of patient has high blood pressure)?How common are they in patient with
hypertension?3. Which endocrine cause of hypertension ismost likely in this patient? What testshould be done now?
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The most likely endocrine causes of hypertension in this
case is Primary Hyperaldosteronism
Test should be done now: Plasma Renin Activity (PRA)
Ratio of Plasma Aldosterone to PRA
Indication for screening for Primary Hyperaldosteronism
1. Hypertension with hypokalemia2. Refractory hypertension (BP >140/90 despite 3 antihypertensives)3. Hypertension with adrenal incidentaloma (incidental adrenal tumor)4. Juvenile patient with hypertension and positive family historyI
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A blood sample is drawn with the patient seatedPlasma Aldosterone: 25 ng/dlPlasma Renin Activity:
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4. Do these result establish a diagnosis? Whywere aldosterone and renin activity
measured simultaneously? Can a diagnosisbe made by measuring either hormonelevel alone?
5. What is the purpose of saline infusion?6. What are the major causes of this syndrome?
Why is it important to distinguish betweenthem, and how can this be done?
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Yes, these result establish diagnosis
of primary hyperaldosteronism
Plasma Aldosterone: 25 ng/dlPlasma Renin Activity:
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Adapted from Young WF Jr, Hogan, MJ. Renin-independent hypermineralocorticoidism. Trends in Endocrinology and Metabolism 1994;5:97106.
Plasma Aldosterone:25 ng/dlPlasma Renin Activity:
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The test should be measured simultaneouslybecause the two hormone may has normal
variation caused by body position, salt intakeand other factor that affected ECF volume, sofor the purpose of having the ratio, it should betaken in the same time
The diagnosis should be performed by both testof hormone level
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4. Do these result establish a diagnosis? Why werealdosterone and renin activity measured
simultaneously? Can a diagnosis be made bymeasuring either hormone level alone?5. What is the purpose of saline infusion?6. What are the major causes of this syndrome?
Why is it important to distinguish betweenthem, and how can this be done?
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The purpose ofNaCl 0.9% iv
infusion is todemonstrating thatplasma aldosteronecannot besuppressed by ECFvolume expansion
Confirmatory test Procedure Interpretation Concerns
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Confirmatory test Procedure Interpretation Concerns
Oral sodium loading test Sodium intake > 200mmol (~6 g) per day,verified by 24-hour
urine sodium. Adequate slow-release
potassium chloridesupplementation.
Urinary aldosterone ismeasured in the 24-
hour urine collectionfrom morning of day 3
to morning day 4.
Unlikely PA :Urinary aldosterone : 12 mcg/24 hr
(>33.3 nmol/d)Cleveland Clinic :
> 14 mcg/24-hr(38.8 noml/d)
Should not be performedin patients with :- Severe uncontrolled
Hpt- renal insufficiency
- cardiac insufficiency- Cardiac arrhytmia
- Severe hypokalemia
Saline infusion test In recumbent positionat least 1 hour before
and during infusion 2 ltrNaCl 0.9% IV over 4
hrs, start at 8:00-
9.30am Blood sample (renin,
aldosterone,cortisol &plasma Kalium) aredrawn at time 0 & after
4 hrs with BP & HRmonitored throughout
the test.
Unlikely PA :aldosterone levels
< 5 ng/dL Very Probably PA :
Aldosterone levels
> 10 ng/dL Indeterminate levels
5 - 10 ng/dL
Should not be performedin patients with :
- Severe uncontrolledHpt
- renal insufficiency
- cardiac insufficiency- Cardiac arrhytmia
- Severe hypokalemia
Confirm Procedure Interpretation Concerns
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Confirmatorytest
Procedure Interpretation Concerns
Fludrocort
isone
suppression test
Fludrocortisone oral : 0.1 mg per
6 hrs for 4 days
Slow-release KCl supplements(per 6 hrs, measured 4 x/d, close
to 4.0 mmol/L)
Slow-release NaCl supplements
(30 mmol 3 x with meals) &
Dietary salt to maintain urinary
sodium excretion rate at least 3
mmol/kgBW Day 4: measured
- plasma aldosterone & PRA at
10 am, in seated posture
- plasma cortisol: measured at 7
am & 10 am
Confirms PA :
- upright plasma
aldosterone > 6 ng/dL(day 4 at 10 am)
- PRA < 1 ng/ml/h
- plasma cortisol : lower
than the value
obtained at 7 am (to
exclude confounding
ACTH effect)
FST is the most sensitive
for confirming PA:
- less likey to provoke non-renin-dependent
alteration of aldosterone
levels
- allows for the potentially
confounding effects of
potassium to be
controlled, for ACTH(viacortisol) to be monitored &
detected
- Safe when performed by
experienced hands
CaptoprilChallenge
test
Captopril 25-50 mg oral aftersitting/standing at least 1 hr.
Measured PRA, plasma
aldosterone, cortisol at time 0, 1
or 2 hrs after challenge with
remaining seated.
PA :- Plasma aldosterone
remain elevated
- PRA remains
suppressed
Difference APA & IHA:
- Some decrease of
aldosterone levels isoccasionall seen in
Reports of substantialnumber of false negative or
equivocal results.
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4. Do these result establish a diagnosis? Whywere aldosterone and renin activity measured
simultaneously? Can a diagnosis be made bymeasuring either hormone level alone?5. What is the purpose of saline infusion?6. What are the major causes of this syndrome?
Why is it important to distinguish betweenthem, and how can this be done?
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The major causing of this syndrome are:
Aldosterone-secreting adrenal adenomas
(2/3 of cases)
Bilateral adrenal hyperplasia
The importance to distinguish between them is due todifferent management. In aldosterone-secretingadrenal adenomas, surgery is an option while in bilateraladrenal hyperplasia medical management is needed
This can be done by CT scan examination
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Abdominal CT scan shows a 2 cm mass in theright adrenal
This finding confirm the diagnosis of Aldosterone-secreting adenomas on right adrenal as the cause of
primary hyperaldosteronism
Answer
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Adapted from Young WF Jr, Hogan, MJ. Renin-independent hypermineralocorticoidism. Trendsin Endocrinology and Metabolism 1994;5:97106.
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DiganosisandTreatment
Algorithmfor PrimaryHyperaldosteronism
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