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HYPERTENSION AND RENAL DISEASE

FKG UNPAD 2013

AFIATIN
Nephrology and Hypertension Division
Internal Medicine Department
Medical Faculty Padjadjaran University / dr.Hasan
Sadikin Hospital
Bandung

Reference

Kaplans Clinical Hypertension, Norman M.K, 9th


Edition, 2006
2003 World Health Organization International
Society of Hypertension Guidelines for the
Management of Hypertension
Guidelines 20014 (Report of The Eight Report of The
Joint National Committee on Prevention, Detection,
Evaluation and Treatment of High Blood Pressure

Lecture Content

Introduction
Epidemiology
Definition
Pathophysiology
Pathogenesis
Pathophysiology of T.O.D
Measurement of blood pressure
History, Physical examination
Treatment

Epidemiology
2 million new cases of hypertension
diagnosed each year in the U.S.
23% of men and 25% of women over the
age of 18 in the U.S. have HTN
The prevalence of HTN among African
Americans is increased 30-50% in each
age group compared to persons of
European descent

Epidemiology cont.
The prevalence of HTN increases steadily with
age; over 70% of women and 50% of men in the
U.S. over the age of 70 have HTN
Linear relationship between the degree of HTN
and the risk for CV and renal disease
Heart disease and stroke are the 1 st and 3rd
leading causes of death in the U.S.
More than $259 billion in direct and indirect
costs

Hypertension
Hypertension is not a disease
It is an arbitrarily defined disorder to which
both environmental and genetic factors
contribute
Major risk factor for:
cerebrovascular disease
myocardial infarction
heart failure
peripheral vascular disease
renal failure

Blood pressure is a continuous variable


which fluctuates widely during the day
physical stress
mental stress

The definition of hypertension has been


arbitrarily set as:
That blood pressure above which the
benefits of treatment outweigh the risks
in term of morbidity and mortality

At what blood pressure is a patient


hypertensive?
BHS

140/90

JNC-VII

140/90

WHO-ISH

Opt <120/<80

140/90

The current recommendation in the UK is


140/90
However risk is important and in diabetes
130/80

What is the JNC VII?


Seventh Report of the Joint National
Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood
Pressure
Uses evidence-based medicine and consensus
Updates approaches to hypertension control
including diagnosis, evaluation, lifestyle
modification, and drug therapy

Definition
Based on recommendation JNC VII, The Classification of
BP for adult 18 years :
Normal

: systolic lower than 120

diastolic lower than 80


Pre-hypertension

: systolic 120 139

diastolic 80 99
Stage-1 : systolic 140 159 or
diastolic 90 99
Stage-2 : systolic equal to or more than 160 or
diastolic equal to or more than 100

New (2003) WHO-ISH Definitions


and Classification of BP Levels
Category

Systolic BP
(mm Hg)

Diastolic BP
(mm Hg)

Optimal BP
Normal BP
High-Normal

<120
<130
130-139

<80
<85
85-89

Grade 1 Hypertension (mild)


Subgroup: Borderline
Grade 2 Hypertension (moderate)
Grade 3 Hypertension (severe)

140-159
140-149
160-179
>180

90-99
90-94
100-109
>110

Isolated Systolic Hypertension


Subgroup: Borderline

>140
140-149

<90
<90

Guidelines for Measurement of Blood


Pressure
1. Patient conditions
1.1. Posture
Initialy, particularly in patients over age 65,
diabetic, or receiving antihypertensive
therapy, check for postural changes by
taking readings after 5 minutes supine, then
immediately and 2 minutes after they stand
For routine follow-up, sitting pressures are
recommended. The patient should sit quietly
with the back supported for 5 minutes and
the arm supported at the level of the heart.

Guidelines for Measurement of


Blood Pressure (continued)
1.2. Circumstances
No caffeine during the hour preceeding the
reading
No smoking during the 15 minutes precding the
reading
No exogenous adrenergic stimulants (e.g.
phenylephrine in nasal decongestants or eye
drops for pupillary dilation)
A quiet, warm setting.
Home readings taken under varying
circumstances and 24 hours ambulatory
recordings may be preferable and more accurate
in predicting subsequent cardiovascular disease.

Guidelines for Measurement of


Blood Pressure (continued)

2. Equipment :
Cuff size : the bladder should encircle and
cover two - thirds of the length of the arm;
if it does not, place the bladder over the
brachial artery. If bladder is too small, high
readings may result.
Manometer : Aneroid gauges should be
calibrated every 6 months against a
mercury manometer.
For infants, use ultrasound equipment (e.g.
the Doppler method)

Guidelines for Measurement of


Blood Pressure (continued)

3. Technique
3.1. Number of readings
On each occasion, take at least two
readings, separated by as much time as is
practical. If readings vary by more than 5
mmHg, take additional readings until two
are close.
For diagnosis, obtain three sets of
readings at least 1 week apart.
Initially, take pressure in both arms; if the
pressures differ, use arm with the higher
pressure.
If the arm pressure is elevated, take
pressure in one leg, particularly in
patients younger than 30.

Guidelines for Measurement of


Blood Pressure (continued)
3.2. Performance

Inflate the bladder quickly to a pressure 20


mmHg above the systolic pressure, as
recognized by disappearance of the radial
pulse.
Deflate the bladder 3 mmHg every second
Record the Korotkoff phase V
(disappearance), except in children, in whom
ose of phase IV (muffling) may be preferable.
If the Korotkoff sounds are weak, have the
patient raise the arm, open and close the
hand.

4. Recordings

Note the pressure, patient position, the arm,


cuff size ; e.g. 140/90, seated, right arm,

Bladder Length

Centre of
bladder must
be over artery

Children > 5
years

12 cm

Usually supplied
Strongly
recommende
d for routine
use

23 cm

Normal and lean arms


Muscular and Obese arms

35 cm
42 cm

2.
The cuff must be level with
the heart. If Arm
Circumference exceeds 33
cm, a large cuff must be
used. Place stethoscope
diaphragm over brachial
artery
1.
The patient
should be
relaxed and the
arm must be
supported.
Ensure no tight
clothing
constricts the
arm

3.
The column of
mercury must be
vertical. Inflate to
acclude the pulse.
Deflate at 2 to 3
mm/sec. Measure
systolic (first
sound) and
diastolic
(disappearance) to
nearest 2 mmHg.

Pathophysiology
BP=TPR X CO (blood pressure is
the product of total peripheral
resistance and cardiac output)

A schematic to demonstrate the interaction of environmental factors with underlying genetic


predisposing factors to increase blood pressure through the activation of a variety of
pathogenetic mechanisms.

Sever P S , Messerli F H Eur Heart J 2011;eurheartj.ehr177


Published on behalf of the European Society of Cardiology. All rights reserved. The Author
2011. For permissions please email: journals.permissions@oup.com

Autoregulation
BLOOD PRESSURE = CARDIAC OUTPUT X PERIPHERAL RESISTANCE
Hypertension

Preload

Fluid
Volume

Contractility

Increased PR

Functional
Constriction

Structural
Hypertrophy

Volume
Redistribution

Renal
Sodium
retention

Excess
sodium
intake

= Increased CO and/or

Descreased
filtration
surface

Genetic
alteration

Sympathetic
nervous
overactivity

Stress

Reninangiotensin
excess

Cell
membrane
alteration

Hyperinsuli
nemia

Genetic
alteration

Obesity

Endothelium
derived
factors

Causes of Sympathetic
Nervous System (SNS)
Activation Genetic
Diet
Factors
SNS
Activation

Acute
Physical
Stressors

Psychosocial
Stress
Catecholamine levels

Heart
rate

Cardiac
output

Blood
pressure

Platelet
aggregation

ANGIOTENSINOGEN

Macula densa signal


Renal arteriolar pressure
Renal nerve activity

Renin
ANGIOTENSIN I
Converting
enzyme
ANGIOTENSIN II

ANGIOTENSIN III
ANGIOTENSINASE A

Adrenal
cortex

Kidney

Intestine

CNS

Vascular
smooth
muscle

Peripheral nervous
system

Heart

Adrenergic
facilitation
Contractility

Aldosterone
Sympathetic
discharge
Distal
nephron
reabsorption

Sodium and water


reabsorption

Maintain or increase
ECFV

Thirst salt
appetite

Vasopressin
release

Vasoconstriction

Total peripheral
resistance

Cardiac
output

Angiotensinogen
Renin

Angiotensin I
ACE

vasoconstriction

Angiotensin II
aldosterone (inc. reabsorp of Na)

Inc. blood volume

Inc. PVR

Pre
hypertension

Established hypertension
30-50 years

10-30 years
CO

Complicated hypertension
40-60 years
(T. O. D)

HEREDITY - ENVIRONMENT

Age

PRE - HYPERTENSION

0 - 30

Normotension EARLY HYPERTENSION


ESTABLISHED HYPERTENSION
UNCOMPLICATED

30 - 50

COMPLICATED

Accelerate CARDIAC
LARGE CEREBRAL
dHypertroph
VESSEL
Ischemia
malignant
y Failure
Aneurysm Thrombosis
course
Infarction Dissection Hemorrhag
e

RENAL
Nephrosclerosi
s Failure

Causes of Hypertension
Essential or Primary
Underlying pathophysiologic alteration
of unknown cause;
95% of cases of HTN
Secondary-Resulting from a specific cause
such as renal or endocrine disorders;
5% of cases

Primary Hypertension
Is usually of gradual onset
Usually develops between the ages of 30 and 50
Tends to remain asymptomatic for 10 to 20
years
Triggers include obesity, psychological stress,
high-sodium intake, and alcohol intake over 1
ounce per day

Aetiology of essential
hypertension
The aetiology of hypertension is
polyfactorial
polygenic

Likely causes:
Increased reactivity of resistance vessels and
resultant increase in peripheral resistance
as a result of an hereditary defect of the smooth

muscle lining arterioles

A sodium homeostatic effect


In essential hypertension the kidneys are unable

to excrete appropriate amounts of sodium for


any given BP. As a result sodium and fluid are
retained and the BP increases

Other factors
Age : BP tends to rise with age, possibly as a
result of decreased arterial compliance and
should be treated agressively as in the young

Genetics and family history


A history of hypertension tends to run in
families
The closest correlation exists between sibs
rather parent and child

Environment
Mental and physical stress both increase

blood pressure
However removing stress does nor

necessarily return blood pressure to normal


values
True stress responders who have very high BP

when they attend their doctor but low normal


pressures otherwise tend to be highly
resistant to treatment

Sodium Intake
The SALT study and more recently the DASH
study have confirmed a strong relationship
between hypertension, stroke and salt intake
Reducing salt intake in hypertensive
individuals does lower blood pressure
However reducing salt intake in normotensives
appears to have no effect
Reducing salt intake to 60-80mmol/day does
lower BP
However there are real difficulties in achieving
this level of salt restriction (fast food)

Alcohol
The most common cause of hypertension in
the young Scot
Affects 1% of the population
Small amounts of alcohol tend to decrease
BP
Large amounts of alcohol tend to increase BP
If alcohol consumption is reduced BP will fall
over several days to weeks.
Average fall is small 5/3 mmHg

Weight
Obese patients have a higher BP
Up to 30% of hypertension is
attributable in part or wholly to obesity
If a patient loses weight BP will fall
In untreated patients a weight loss of
9Kg has been reported to produce a fall
in BP of 19/18 mmHg
Weight reduction is the most important
non-pharmacological measure available

Race
Caucasians have a lower BP than black
populations living in the same environment
Black populations living in rural Africa have a
lower BP than those living in towns
Reasons are not clear
Possibly black populations are more susceptible
to stress when living in towns
Respond in different ways to changes in diet
Black populations are genetically selected to be
salt retainers and so are more sensitive to an
increase in dietary salt intake

Secondary
Hypertension
5-10% of all hypertension has an identifiable
cause
Removal of the cause does not guarantee that
the hypertension or risk will return to normal
Sustained hypertension produces end-organ
damage to blood vessels, heart and kidney
This type of damage tends to increase BP
further and so a vicious self-propagating cycle
is established

Causes for Secondary


Hypertension

Renal disease

20% of resistant hypertensive patients


chronic pyelonephritis
renal artery stenosis
polycystic kidneys

Drug Induced
NSAIDs
Oral contraceptive
Corticosteroids

Pregnancy
pre-eclampsia

Endocrine
Conns Syndrome
Cushings disease
Phaeochromocytoma
Hypo and hyperthyroidism
Acromegaly

Vascular
Coarctation of the aorta

Sleep Apnea

Hypertension Syndrome
Its More Than Just Blood Pressure

Obesity

Decreased
Arterial
Compliance

Endothelial
Dysfunction

Abnormal
Lipid
Metabolism
Accelerated
Atherogenesi
s

Abnormal
Glucose
Metabolism

HYPERTENSION

LV Hypertrophy
and Dysfunction

Abnormal
Insulin
Metabolism

BloodClotting
Mechanism
Changes

Neurohormo
nal
Dysfunction
RenalFunction
Changes

Kannel WB. JAMA. 1996;275:1571-1576. Weber MA et al. J Hum Hypertens. 1991;5:417423. Dzau VJ et al. J Cardiovasc Pharmacol. 1993;21(suppl 1):S1-S5.

The cardiovascular (CV) continuum

Remodelling
Ventricular dilation/
cognitive dysfunction

Myocardial
infarction &
stroke
Atherosclerosis and
left ventricular
hypertrophy
Endothelial
dysfunction

Risk factors*:
hypertension, diabetes,
obesity, smoking, age

Congestive heart failure/


secondary stroke
Microalbuminuria

Macroproteinuria
Nephrotic
proteinuria

End-stage
renal
disease

End-stage
heart disease,
brain damage
and dementia
Cardio/
cerebrovascular
death

Intervention at any point along the chain of events may modify


cardiovascular disease progression and provide cardioprotection
*An additive effect of risk factors has been shown in the risk for a CV event

Dzau VJ, et al. Circulation 2006;114:28502870; Figure adapted from Dzau V, Braunwald E.
Am Heart J 1991;121:12441263; Yusuf S, et al. Lancet 2004;364:937952

Management
The most essential element in reducing
the morbidity and mortality associated
with hypertension is long term
compliance/adherence
achieved through life style modification
alone or in combination with
pharmacologic therapy (stepped care)

Lifestyle modification
weight reduction
sodium restriction
dietary fat modification
exercise
alcohol restriction
caffeine restriction
relaxation techniques
potassium supplementation

Figure. Algorithm for Treatment of Hypertension


Lifestyle Modification
Not at Goal BP
(<140/90 mm Hg or <130/80 mm Hg for Those With Diabetes
Or Chronic Kidney Disease)

Initial Drug Choices

Hypertension With
Compelling Indications

Hypertension Without
Compelling Indications

Stage 1 Hypertension
(systolic BP 140-159 mm Hg
Or Diastolic BP 90-99 mm Hg)
Thiazide type diuretics for most
may consider ACE inhibitor, ARB,
-blocker, CCB, or Combination

Stage 2 Hypertension
(systolic BP 160 mm Hg
Or Diastolic BP 100 mm Hg)
2-Drug
2-Drug combination for most
(usually thiazide - type diuretic
and ACE inhibitor or ARB or
-blocker, CCB)

Drug(s) for the


Compelling indication
Other antihypertensive drugs
(diuretics, ACE inhibitor, ARB, blocker, CCB) as Needed

Not at Goal BP
Optimize Dosages or Add Additional Drugs Until Goal BP is Achieved
Consider Consultation With HypertensionSpecialist

BP > 180/110 mm Hg
Pospone Op
AHA/JNC 7

Elective Op

Evaluation :
therapy
BP measurement confirmation
Target organ damage ?

BP < 180/110 mm Hg BP >180/110 mm Hg

Performe operation target organ damage

Yes
Pospone op
BP
Optimalizing

No
Performe op

Emergency Op
Performe op

BP Monitoring
ECG monitoring
Admit to ICU pre and post op
Give antiischemia (beta blocker)
Consider spinal/epidural
anesthesia
Avoid increase or decrease of BP
> 20 % baseline
EKG post op dan periksa
troponin

AFIATIN
Bagian/UPF Ilmu Penyakit Dalam
FK. UNPAD / RSUP dr.Hasan Sadikin
Bandung

FENOMENA
GUNUNG
ES

PGK tahap 5

PGK Tahap 4
PGK Tahap 3
PGK Tahap 2
PGK Tahap 1

ANATOMI GINJAL

2 buah
retroperitoneal

FUNGSI GINJAL
EKSKRESI
MENGATUR KESEIMBANGAN
CAIRAN DAN ELEKTROLIT
MENGATUR TEKANAN DARAH
ENDOKRIN :
menghasilkan hormon-hormon :
aldosteron, renin, eritropoetin

PENYAKIT GINJAL DAN


SALURAN KEMIH
INFEKSI
KEGANASAN
BATU GINJAL DAN SALURAN KEMIH
GAGAL GINJAL AKUT
GAGAL GINJAL KRONIS :
Etiologi
Primer : penyakit ginjal sendiri : batu ginjal,
tumor ginjal,infeksi ginjal kronis
Sekunder dari penyakit lain (sistemik) :
diabetes, hipertensi, hiperurisemia,autoimun

Kelompok Masyarakat dengan Penyakit Ginjal Kro


1. Definisi PGK
Tabel 1
Definisi PGK sesuai Rekomendasi NKF - DOQI 2002
1. Kerusakan ginjal > 3 bulan
a. Kelainan struktur anatomi ginjal
b. Penanda kelainan laboratorium
Kelainan urinalisis
Kelainan serum BUN dan kreatinin
Prosedur pencintraan ginjal
2. Penurunan fungsi filtrasi glomerulus

Kelompok Masyarakat dengan Penyakit Ginjal Kron


2. Penyebab PGK
Tabel 2
Penyebab Penyakit Ginjal Kronisa (PGK)
Glomerulonefritis
Perjalanan penyakit cepat dapat
dihambat
Penyakit dasar tidak dapat dihindari
Batu ginjal
Kekambuhan dapat dicegah
Koreksi batu dapat mencegah PGK
Diabetes mellitus

Gout
Lupus

Nefropati dapat dicegah


Terapi rasional dapat memperlambat
kerusakan ginjal
Kerusakan ginjal dapat dicegah
Perjalanan penyakit dapat dihambat
Nefropati lupus dapat dicegah

Kelompok Masyarakat dengan Penyakit Ginjal Kron


3. Keluhan dan Gejala PGK
Tabel 3
Tahapan PGK sesuai rekomendasi NKF - DOQI 2002
Deskripsi Kerusakan
Tahapan
Ginjal
1
2
3
4
5

Kerusakan ginjal, fungsi


ginjal normal atau
meningkat
Kerusakan ginjal, fungsi
ginjal turun ringan
Penurunan sedang fungsi
ginjal
Penurunan berat fungsi
ginjal
Gagal ginjal

LFG
(ml/menit/1.73 m2
90
60 80
30 59
15 29
< 15

Keluhan dan Gejala

Tanpa keluhan dan gejala


Diketahui dari hasil uji
saring
Tanpa keluhan dan gejala
Diketahui dari hasil uji
saring
Tanpa keluhan dan gejala
Diketahui dari hasil uji
saring
Keluhan dan gejala
Multi organ (ringansedang)
Keluhan dan gejala

PGK Tahap 1
R Konservatif
PGK Tahap 5

Cuci Darah

Hemodialisis
CAPD
Gagal

Cangkok
Ginjal

Berhasil

Evaluasi

4. Program Penyuluhan
4.1 Tujuan :
a. Mengenal penyebab PGK :
* Dapat diobati dengan obat/tindakan bedah
* Menghambat perjalanan penyakit sehingga
terhindar dari tahapan 5 PGK
b. Mengenal beberapa prinsip terapi konservatif
(tabel)

Tabel. Prinsip terapi konservatif


1. Mencegah penurunan progresif fungsi ginjal
Hindari konsumsi obat yang merusak ginjal
Hindari penyakit muntah dan diare
Hindari asupan protein hewani yang ketat
Hindari kehamilan
Kendalikan kelainan jantung
2. Program memperlambat penurunan progresif fungsi
ginjal
Kendalikan tekanan darah tinggi
Kendalikan infeksi ginjal
Asupan diet seimbang (proporsional)
Kendalikan hiperfosfatemia
Kendalikan anemia
Kendalikan kelainan jantung
3. Terapi untuk mengatasi keluhan dan gejala
Keluhan gatal
Keluhan mual
Keluhan kejang otot
Keluhan terkait anemia

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