Download Kidneys and Hypertension

Kidneys and Hypertension
Dr. Shahrzad Shahidi
Nephrologist
Isfahan University of Medical sciences
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Hypertension (HTN)
Persistent elevation of arterial blood
pressure (BP)
 31% of Americans have BP > 140/90
mmHg
 Most patients asymptomatic
 Single most preventable cause of
premature death in developed countries.

Chobanian AV, et al. Hypertension 2003;42(6):1206–1252 2
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Adult Classification
Classification
Normal
Systolic BP
Diastolic BP
(mmHg)
(mmHg)
Less than 120 and Less than 80
PreHTN
120-139
or
80-89
Stage 1 HTN
140-159
or
90-99
Stage 2 HTN
> 160
or
> 100
Chobanian AV, et al. Hypertension 2003;42(6):1206–1252
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Classification for Adults
Classification based on average of > 2
properly measured seated BP
measurements from > 2 clinical
encounters
 If systolic & diastolic BP values give
different classifications, classify by
highest category
 Prehypertension: patients likely to
develop hypertension

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Pathogenesis.
No one gene is responsible.
 Studies shows that several difft genes
may have an effect on BP.

RARE SINGLE GENE CAUSES OF HTN
HAVE BEEN IDENTIFIED.
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Single Gene Causes of
HTN
Glucocorticoid remediable aldosteronism
 Syndrome of minerelocorticoid excess
 Pheochromocytoma - may occur with
MEN type 2, Von Hippel Lindau disease,
Neurofibromatosis type 1
 Liddle’s Syndrome

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Renin angiotensin system
–secreted by the juxtaglomerular
apparatus.
 It converts angiotensinogen (inactive) to
angiotensin 1 .It then converts to
angiotensin 2 by ACE.
 Increased renin – RAS, Renal cell
carcinoma & rarely some renin secreting
tumours.
 Renin
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Actions of angiotensin II
Arteriolar vasoconstriction.
 Efferent arteriolar vasocnstriction.
 Aldosterone secretion.
 Epinephrine release (adrenaline).
 Smooth muscle hypertrophy.
 Inhibit renin release (negative feed
back).
 Myocardial growth.

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Other pathogenesis
stiffness – Aging , DM,
Kidney disease.
 Sympathetic nervous systemActivation associated with sudden
rise in BP.- By increasing stroke
volume, HR , systemic vascular
resistance and activation of RAS.
 Arterial
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Secondary Hypertension
 Renovascular
Disease
 Renal parenchymal disease:
 CKD
 Glomerulonephritis
 ADPKD
 Obstructive
uropathy,…
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Renal artery stenosis
Atherosclerotic or fibromuscular
dysplasia as etiology
 Clinically difficult to control HTN
 Renal dysfuntion
 Resistant fluid retention
 Worsening Cr with ACEI or ARB

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Investigations
 US
Kidneys- assymmetry.
 Doppler of renal arteries.
 Captopril renogram - affected kidney
may show a 30% decline in function.
 MRA.
 Angiogram- secure diagnosis & allow
intervention.
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Treatment - in Atheroslerotic
RAS
 Modify
risk factors.
 Control BP with loop diretics, CCBs,
centrally acting agents, B blockers,
 Treatment by angioplasty & stenting
OR surgery.
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Indications for surgery
 Single
kidney with stenosis.
 Bilateral RAS.
 Uncontrolled BP/ flash pulm edema.
 Rapidly deteriorating kidney
function.
 Meaningful nephron mass in the
kidneys.
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Fibromuscular dysplasia.
Otherwise healthy young women aged
15-50 yrs.
 Angiography with
“string of beads”
pattern
 Angioplasy is the
treatment.

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Fibromuscular Dysplasia, before
& after PTRA
Safian & Textor. NEJM 344:6
Atherosclerotic RAS before &
after stent
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Initial assessment
 Duration
of HTN
 Other CVD risk factors.
 Anything to suggest secondary HTN.
(50<Age <30, sudden onset, presents
as malignant HTN, sudden
deterioration in BP control, resistant
HTN)
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Initial evaluation
contributory factors like –drugs,
overweight, Excess alcohol, excess salt
intake, Lack of exercise, Environmental
stress, smoking.
 Evidence of Complications- stroke, TIA,
Carotid bruit, IHD, CHF, Cardiomegaly,
PVD, Hypertensive retinopathy, Renal
impairment, Proteinuria, Sexual
dysfunction.
 Other
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Initial Evaluation
 Previous
drug treatment and
side effects.
 Contraindication to specific
drugs.
 Family history
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Initial basic investigations
 Hematocrit
 Urinalysis
 FBS
 ECG
 HDL, LDL
(after 9-12 h fast)
 Optional
 TG
tests:
urinary albumin
excretion or ACR
 Cr
K
 Ca
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Target organ damage
Heart- LVH, IHD, LVD,CHF.
 Brain- Stroke, TIA, Vasular dementia.
 Kidney- Chronic Kidney Disease.

 Eyes- Retinopathy.

Peripheral Vasculature - Peripheral
arterial disease.
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Treatment Goals
Reduce morbidity & mortality
 Select drug therapy based on evidence
demonstrating risk reduction

Patient Population
Most patients
DM
CKD
Target BP
< 140/90 mmHg
< 130/80 mmHg
<130/80 mmHg
Chobanian AV, et al. Hypertension 2003;42(6):1206–1252
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Lifestyle Modifications
Modification
Weight loss
DASH-type
diet
Reduced salt
intake
Physical
activity
Moderation of
alcohol intake
Recommendation
Approximate Systolic
BP Reduction (mm Hg)
Maintain normal body weight
2
(BMI 18.5–24.9 kg/m )
Consume a diet rich in fruits,
vegetables, and low-fat dairy products
with a reduced content of fat
Reduce dietary Na intake to no more
than 100 mmol per day
(2.4 g Na or 6 g NaCl)
Regular aerobic physical activity (at
least 30 min/d, most days of the week)
Limit consumption to 2 drinks/d in men
and 1 drink/d in women & lighterweight persons
DASH, Dietary Approaches to Stop Hypertension
5–20 per 10-kg
weight loss
8–14
2–8
4–9
2–4
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What Drug in CKD
 In
all proteinuric renal disease
ACEI & ARB has a beneficial role.
 Dcreases intraglomerular pressure
& thus reduce proteinuria.
 Dual blockade with ACEI & ARB is
a useful combination.
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In CKD
 Expect
the need of 3 meds.
 First life style modification.
 If proteinuria ACEI or ARB.
 If fluid overload diuretics.
 If persistant proteinuria add ARB or
ACEI.
 Last vascular smooth muscle
relaxant: Minoxidil
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Remember side effects
 Hyperkalemia
(ACE, ARB)
 Fluid retension (Amlodipine)
 Bradycardias (B blocker, Clonidine)
 Massive fluid overload & Tachycardia
(Minoxidil)
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Antihypertensives - ACEIs
 No
ACEI shown to be superior to any
other ACEI
 1˚
goal: treat BP to target
 2˚ goal: control proteinuria
 ACEIs
generally more cost-effective
than ARBs
 Adverse effects with an ACEI; switch
to an ARB may be appropriate
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Antihypertensives - ACEIs
Begin at a low dose; increase dose at
4-week intervals to reduce
microalbuminuria (even normotensive
patients)
 Antiproteinuric effects not necessarily
attained at antihypertensive doses
 Increase dose until proteinuria reduced
by 30-50%

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Antihypertensives: ARBs
 ARBs
have similar efficacy to ACEIs
for kidney protection in patients
with several forms of GN
 Proteinuria reduction: 25 to 47%
 Most clinicians use ACEI/ARB
therapy in patients with nondiabetic
CKD & proteinuria
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Antihypertensives: ARBs
 Selection
of ACEIs vs ARBs
 Cost
of therapy
 Patient tolerance
 Clinician preference
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Nondihydropyridine CCBs
 Diltiazem/verapamil
decrease
glomerular injury without negatively
changing renal hemodynamics
 May have beneficial effects on
proteinuria similar to ACEIs
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Nondihydropyridine CCBs
 Studies
suggest efficacy of
combination therapy with ACEIs &
nondihydropyridine CCBs may be
superior in proteinuria reduction than
either agent alone
 Generally 2nd line when ACEIs or
ARBs not tolerated
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Speculations on JNC VIII

Diuretics will remain first line therapy




Chlorthalidone vs. HCTZ
Beta blockers will be dropped to 2nd or 3rd line
therapy
Combination RAAS inhibition may carry more
risk than benefit and will probably not be
recommended (some exceptions)
Strong emphasis on combination therapy
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