HYPERTENSION IS THE COMMON CAUSED

IN CHRONIC KIDNEY DISEASE

Mohammad Rudiansyah
DIVISION OF NEPHROLOGY & HYPERTENSION
DEPARTEMENT OF INTERNAL MEDICINE
FACULTY OF MEDICINE
UNIVERSITY OF LAMBUNG MANGKURAT / ULIN GENERAL HOSPITAL
BANJARMASIN
 Pendahuluan
WHO (World Health Organization) : HT sbg nomor satu faktor
risiko kematian, 7,5 juta kematian/thn (13% dari seluruh
.
kematian)  penyakit akibat tekanan darah yg tinggi,
terutama penyakit kardiovaskular.

Arahan kelompok hipertensi & kardiovaskuler  pengobatan

HT  menurunkan risiko jangka panjang morbiditas &
mortalitas kardiovaskuler.

Hipertensi  pembunuh diam-diam (silent killer) sering tanpa

gejala.

Sekitar 5jt populasi dewasa di AS & >1 milyar penduduk dunia

 HT.

National Health and Nutrition Examination Survey (NHANES)

 hanya 53% dari penderita hipertensi yg berobat berhasil
mencapai target tekanan darah dibawah 140/90 mmHg.4
 Tekanan darah pada pasien hemodialisis (HD) sulit
dikendalikan.
 Hipertensi terjadi pada 70 – 90% pasien HD
 Tekanan darah terkontrol hanya 30% dari pasien
yg mendapat obat antihipertensi dan hanya 12%
pada pasien hipertensi yang tidak diobati.
 Kematian akibat penyakit jantung iskemik 17x
lebih besar populasi dialisis daripada umum di
Eropa.
 Prevalensi Hipertensi Dunia
Prevalence of hypertension (%)

60 55
49 49
47
42
38 38
40
28

20

0
US Italy Sweden England Spain Finland Japan* Germany

Adults aged 35–64 years (data are age- and sex-adjusted), except* (adults aged ≥ 30 years)
Hypertension defined as BP  140/90 mmHg or on treatment

Wolf-Maier et al. JAMA. 2003;289:23632369; Sekikawa, Hayakawa. J Hum Hypertens. 2004; 2004;18:911–912.
Cardiovascular Mortality Risk Doubles with
Each 20/10 mmHg Increment in
Systolic/Diastolic BP*
Cardiovascular mortality risk
8
8X
risk
6

4
4X
risk
2
2X
1x risk risk
0
115/75 135/85 155/95 175/105
Systolic BP/Diastolic BP (mmHg)

*Individuals aged 40–69 years Lewington et al. Lancet 2002;360:1903–13

Penurunan Tekanan Darah Sistolik 2 mmHg
Menurunkan Risiko Mortalitas 7-10%
• Meta-analysis of 61 prospective, observational studies
• 1 million adults aged 40–69 years with BP > 115/75 mmHg
• 12.7 million person-years 7% reduction in
risk of ischaemic
heart disease
2 mmHg and other
decrease in vascular disease
mean SBP mortality
10% reduction in
risk of stroke
mortality

Lewington et al. Lancet. 2002;360:1903–1913.

Tekanan darah yang sama atau
melebihi 140 mmHg sistolik dan/atau
sama atau melebihi 90 mmHg
diastolik pada sescorang yang tidak
sedang makan obat antihipertensi
 Klasifikasi tekanan darah menurut ASH/ISH
2013, JNC VII (Chobanian,2004) & 2014
Hypertension Guideline (JNC 8)

Tekanan Darah Tekanan Darah

Kategori
Sistolik Diastolik

Normal <120 mmHg <80 mmHg

Pre-hipertensi 120-139 mmHg 80-89 mmHg

Stage 1 140-159 mmHg 90-99 mmHg

Stage 2 >160 mmHg >100 mmHg

 Klasifikasi tekanan darah
menurut ESH/ESC 2013
Kategori Sistolik (mmHg) Diastolik (mmHg)

Optimal < 120 dan < 80

Normal 120 – 129 dan/atau 80 – 84

Normal tinggi 130 – 139 dan/atau 85 – 89

Hipertensi grade 1 140 – 159 dan/atau 90 – 99

Hipertensi grade 2 160 – 179 dan/atau 100 – 109

Hipertensi grade 3 > 180 dan > 110

Hipertensi sistolik terisolasi > 140 < 90

 Prinsip dasar ESH/ESC 2013
 Rekomendasi sesuai penelitian dari ulasan
literatur yang ada.
 Pertimbangan dengan prioritas utama data
random, uji kontrol & meta analisis tapi tidak
melupakan juga aspek diagnostik dari hasil
observasional & penelitian-penelitian lain yang
sesuai keilmuannya.
 Menentukan derajat bukti ilmiah, kekuatan
rekomendasi diagnostik utama & isu pengobatan
penyakit-penyakit lain
 Kelas rekomendasi
Classes of Suggested wording to
Definition
recommendations use
Class I Evidence and/or general agreement Is recommended/is
that a given treatment or procedure indicated
is beneficial, useful, effective.

Class II Conflicting evidence and/or a

divergence of opinion about the
usefulness/efficacy of the given
treatment or procedure.

Class IIa Weight of evidence/opinion is in Should be considered

favour of usefulness/efficacy.
Class IIb Usefulness/efficacy is less well May be considered
established by evidence/opinion.
Class III Evidence or general agreement that Is not recommended
the given treatment or procedure
is not useful/effective, and in some
cases may be harmful.

(Mancia et al, 2013)

 Level of evidence

Level of Data derived from multiple randomized

evidence A clinical trials or meta-analyses.

Data derived from a single randomized

Level of
clinical trial or large non-randomized
evidence B
studies.

Consensus of opinion of the experts

Level of
and/or small studies, retrospective
evidence C
studies, registries.

(Mancia et al, 2013)

 Risiko kardiovaskuler menurut kategori
tekanan darah (ESH/ESC 2007)
Other risk Normal High normal Grade 1 HT Grade 2 HT Grade 3 HT
factors, OD or SBP 120-129 SBP 130-139 or SBP 140-159 or SBP 160-179 or SBP ≥180 or
disease or DBP 80-84 DBP 85-89 DBP 90-99 DBP 100-109 DBP ≥110

No other risk Average Average Low Moderate High added

factors risk risk added risk added risk risk

Low Low Moderate Moderate Very high

1-2 risk factors
added risk added risk added risk added risk added risk

3 or more risk
Moderate High added High added Very high
factors, MS, OD High added risk
added risk risk risk added risk
or diabetes

Established CV Very high Very high Very high Very high Very high
or renal disease added risk added risk added risk added risk added risk

(Mancia-ESH/ESC 2007, 2007)

 Risiko kardiovaskuler menurut klasifikasi
tekanan darah (ESH/ESC 2013)
Other risk factors, Blood Pressure (mmHg)
Asymptomatic organ damage High normal Grade 1 HT Grade 2 HT Grade 3 HT
SBP 130-139 SBP 140-159 SBP 160-179 SBP ≥180
or disease
or DBP 85-89 or DBP 90-99 or DBP 100-109 or DBP ≥110

No other risk factors Low risk Moderate risk High risk

Moderate to
1-2 risk factors Low risk Moderate risk High risk
high risk

Low to Moderate to
> 3 RF High risk High risk
moderate risk high risk

Moderate to High to
OD, CKD stage 3 or diabetes High risk High risk
high risk very high risk

Symptomatic CVD, CKD stage > 4 or

Very high risk Very high risk Very high risk Very high risk
diabetes with OD/RFs
 Gejala Hipertensi
Hipertensi sering TIDAK bergejala

Penderita hipertensi maupun tekanan darah yang normal

 Sakit kepala
 Pusing
 Kelelahan

Hipertensi berat atau menahun dan tidak diobati

 Sakit kepala
 Kelelahan
 Mual, muntah
 Gelisah dan pandangan menjadi kabur
 Apa sajakah gejalanya?
Subyektif, tidak selalu sama pada tiap orang
Apakah penyebab hipertensi?

primer

Terjadi akibat gaya hidup yang

tidak sehat atau adanya faktor
keturunan

sekunder

Disebabkan oleh penyakit lainnya

yang mengganggu tekanan darah
seperti penyakit ginjal atau DM
 Apakah hipertensi dapat disembuhkan?

Tidak
Hipertensi hanya dapat dikendalikan sehingga membutuhkan terapi
dan perbaikan gaya hidup seumur hidup
Terapi hipertensi

OBAT-
OBATAN
PERBAIKI GAYA
HIDUP
ATUR BERAT
BADAN
DIET
Hipertrofi ventrikel kiri
Proteinuria dan gangguan fungsi ginjal
Aterosklerosis pembuluh darah
Retinopati
Stroke atau TIA
Infark miokard
Angina pektoris
Gagal jantung
 Modifikasi Gaya Hidup

Target tekanan darah tidak tercapai (<140/90 mmHg atau <130/80 mmHg pada
pasien dengan DM atau penyakit ginjal kronik

Pilihan obat inisiasi

Hipertensi tanpa
Hipertensi dengan
compelling indications
compelling indications

Hipertensi stage 1 Hipertensi stage 2 Lihat petunjuka pemilihan obat dengan

Gol. diuretik tiazid Kombinasi 2 obat (biasanya gol. compelling indications
Pertimbangkan: diuretik tiazid dan Penghambat ACE Obat antihipertensi lain bila dibutuhkan
penghambat ACE, atau antagonis resptor AII atau (diuretik, antagonis reseptor AII,
penyekat reseptor , penyekat reseptor  atau penghambat ACE, penyekat reseptor ,
penghambat kalsium, atau penghambat kalsium penghambat kalsium
kombinasi

Target tekanan darah tidak tercapai

Optimalisasi dosis atau tambahkan obat lain sampai target tekanan darah tercapai
Pertimbangkan untuk konsultasi kepada spesialis hipertensi
 Initiation of antihypertensive treatment
(ESH/ESC 2007) Back

Other risk Normal High normal Grade 1 HT Grade 2 HT Grade 3 HT

factors, OD or SBP 120-129 or SBP 130-139 or SBP 140-159 or SBP 160-179 or SBP ≥180 or
disease DBP 80-84 DBP 85-89 DBP 90-99 DBP 100-109 DBP ≥110
Lifestyle changes Lifestyle changes Lifestyle
for several for several weeks changes +
No other risk No BP No BP
months then drug then drug immediate
factors intervention intervention
treatment if BP treatment if BP drug
uncontrolled uncontrolled treatment
Lifestyle changes Lifestyle changes Lifestyle
for several weeks for several weeks changes +
1-2 risk factors Lifestyle changes Lifestyle changes then drug then drug immediate
treatment if BP treatment if BP drug
uncontrolled uncontrolled treatment

3 or more risk Lifestyle changes Lifestyle

factors, MS, Lifestyle changes and consider changes +
OD or diabetes drug treatment Lifestyle changes Lifestyle changes
immediate
+ drug treatment + drug treatment
drug
Lifestyle changes
Diabetes Lifestyle changes treatment
+ drug treatment
Lifestyle
Established CV Lifestyle changes Lifestyle changes Lifestyle changes Lifestyle changes changes +
or renal + immediate drug + immediate + immediate drug + immediate drug immediate
disease treatment drug treatment treatment treatment drug
treatment
 Inisiasi modifikasi gaya hidup & pengobatan
antihipertensi (ESH/ESC 2013) Back

BP = blood pressure; CKD = chronic kidney disease; CV = cardiovascular; CVD = cardiovascular disease;
DBP = diastolic blood pressure; HT = hypertension; OD = organ damage; RF = risk factor; SBP = systolic blood pressure.
 Terapi Hipertensi

Terapi nonfarmakologi

 Menerapkan gaya hidup yang sehat

 Modifikasi gaya hidup

DASH (Dietary Approach to Stop Hypertension)
Ukuran keberhasilan modifikasi gaya hidup yg
mampu menurunkan tekanan darah

 Restriksi garam,
 Konsumsi narkoba, alkohol & rokok STOP
 Konsumsi lebih banyak sayuran, buah-buahan,
rendah lemak & tipe diet lainnya,
 Penurunan BB & mempertahankannya.
 Latihan fisik teratur.
Treatment of Adults with Systolic/Diastolic
Hypertension without Other Compelling
Indications
TARGET <140/90 mmHg
INITIAL TREATMENT AND MONOTHERAPY
A combination of 2 first line
Lifestyle modification drugs may be considered as
therapy initial therapy if the blood
pressure is >20 mmHg systolic
or >10 mmHg diastolic above
target

Thiazide ACEI ARB Long-acting Beta-

CCB blocker*

• BBs are not indicated as first line therapy for age 60 and above

ACEI, ARB and direct renin inhibitors are contraindicated in

pregnancy and caution is required in prescribing to women of child
bearing potential

2009 Canadian Hypertension Education Program Recommendations

 ESH/ESC: Antihypertensive Treatment Preferred
Drug
- ACE Aldo-
Diuretic ARB CCB
blocker inhibitor antagonist

• • • • •
Heart failure

Post-MI • • •

Angina pectoris • • • •

• •
Diabetes

Renal • •
dysfunction

Previous stroke
Any blood pressure lowering agent

Mancia G, et al. 2007 ESH/ESC Guidelines for the Management of Arterial Hypertension. J Hypertens 2007;25:1105-1187
 Hypertension
in Chronic Kidney Diseases
 Prevalence of high blood pressure by level
of GFR

GFR (ml/min) %

60 ml/min 78
30 ml/min 87
10 ml/min 97

NKF/CKD,2002
Patient in HD unit RSSA: 76%
hypertension
The Profile of Chronic Hemodialysis Patients Based on Blood Pressure
n = 52
30

28

25

54 %

20
Total

15

12

10

23 %
6 6
5

12 %
12 %

0
<130 / < 80 130-139 / 80-89 140-159 / 90-99 >= 160 / >=100
Blood Presure
Increasing BP is closely associated with increasing risk
of ESRD
25 *
22.1
Adjusted relative risk

20

15 *
11.2
10 *
6.0
*
5 * 3.1
1.0 1.2 1.9
0
<120§ <130 130–139 140–159 160–179 180–209 ≥210
80 85 85–89 90–99 100–109 110–119 120
BP (mmHg)
*p<0.001; ESRD due to any cause in 332,544 men screened for MRFIT
§Men with optimal BP was the reference category

Klag MJ, et al. 1996

 Hypertension and Chronic Renal Disease:
Hemodynamic Abnormalities
Cardiac Total Systemic
Mean BP = Output X Vascular Resistance

Increased Cardiac Output Decreased

Volume Expansion Increased Vasodilation
 Glomerular filtration Vasoconstriction  Prostacyclin
 Adrenergic Stimuli  Nitric oxide
 Sodium retention  Angiotensin II  EDHF*
 Extracellular Fluid  Endothelin
 Symphatetic nerve-  Endothelium-derived
Activity Contracting Factors
 Thromboxane
Myocardial Performance
 Adrenergic Activity
*Endothelium-derived
Hyperpolarizing Factors
Textor SC. Renal Parenchymal Disease and Hypertension. Schrier RW (Editor). Atlas of Diseases of the
Kidney, 2001;Vol3:Chapter2.4
 Angiotensin II

mo infiltration
and activation
Proteinuria  TGF- and ECM  PAI-1  Aldosteron

 Cytokine  PGc  ECM degradation

production

Endothelial and mesangial

cell exposure
shear stress/stretch

Inflamation Direct injury to glomerular cells ECM accumulation

Glomerular and tubulointerstitial fibrosis

The pathogenesis of progressive renal injury and fibrosis following nephron loss
Kidney international, Vol 57 (2000), pp 1803-1817
Volume expansion associated with high blood pressure
Goal of Treatment Hypertension in CKD

 Reduced Cardiovascular morbidity and mortality

 Effective Blood Pressure Control Reduces Cardiovascular
Morbidity and Mortality
Systolic-diastolic hypertension Isolated-systolic hypertension

Fatal and non Fatal and non

Mortality Mortality
10 fatal events fatal events
All All
Stroke CHD Causes CV Non CV Stroke CHD Causes CV Non CV
0
NS NS

-10

<0.01 <0.01 0.02

-20
<0.001 0.01
<0.001
-30
<0.001

-40
<0.001
-50
Event reduction in patients on active antihypertensive treatment versus placebo or no treatment.
CHD: coronary heart disease; CV: cardiovascular

Cifkova et al. J Hypertens 2003; 21: 1779–86

Goal of Treatment Hypertension in CKD

 Slowing progression of Renal Function

 PROGRESSIVE RENAL DAMAGE:
The Final Common Pathway
RENAL INJURY

Reduction in nephron mass

Glomerular capillary hypertension

Increased glomerular permeability

Increased BP
to macromolecules
Increased filtration of plasma proteins Proteinuria

Excessive tubular protein reabsorption

Tubulointerstitial inflammation

RENAL SCARRING
NKF/K-DOQI 2002
Impact of Antihypertensive Therapy on Glomerular
Filtration Rate in a Patient With Diabetic Nephropathy
GFR Before ( ) and During ( ) Antihypertensive Treatment
100

* Start of Treatment
75
GFR mL/min

*
*
50 ** * * * *
* * ** * * * *
* *
* *
*
25

0
0 10 20 30 40 50 60 70 80 90 100 110
Months
Mogensen CE. Pract Cardiol. 1983;9(4):156-179.
Adapted from He and Whelton, J Hypertens,
1999.
Meta Analysis: Lower Mean BP
Results in Slower Rates of Decline in
GFR in Diabetics and Non-Diabetics

MAP (mmHg)
95 98 101 104 107 110 113 116 119
0

-2
GFR (mL/min/year)

r = 0.69; P < 0.05

-4

-6

-8 Untreated
HTN
-10

-12
130/85 140/90
-14
Bakris GL, et al. Am J Kidney Dis.
2000;36(3):646-661.
 MULTIPLE RISK-FACTOR INTERVENTION
STRATEGY TO SLOW PROGRESSION

RECOMMENDATIONS

1. Diet: CHO, Protein (level 1)

2. Control BP (level 1)
3. ACE-I/ARB (level 1)
4. Control hyperglycaemia (level 2)
5. Control lipemia (level 1,2)
6. STOP Smoking (level 1,2).

Hebert et al: KI 2001 59:1211-26

a. renalis dextra a. renalis sinistra
 Brain

Ischemic attack
infarction Hemorhage
Heart

Angina MI Heart Failure

Peripheral
Arteries

PAD
Microalbuminuria
Kidney Proteinuria
Renal failure
Nephrosclerosis Anemia
 Anamnesis
 mual, muntah, sesak nafas,
 pucat, cepat lelah, bengkak tubuh.
 Pemeriksaan fisik
 Tekanan tinggi, respirasi meningkat,
 konjunctiva anemis,
 edema paru : ronkhi basah basal,
 edema ektremitas.
 Pemeriksan penunjang
 Hb di bawah angka normal,
 peningkatan kadar ureum, kreatinin, kalium, asam urat,
 asidosis metabolik.
 Urin terdapat proteinuria dan albuminuria.
 Pemeriksaan rontgen thoraks
 edema paru disertai kardiomegali,
 Pemeriksaan ultrasonografi abdomen
 kelainan struktur ginjal.
 Perubahan Vasokonstriksi
Penyempitan
struktur arteriole aferen &
lumen
mikrovaskuler eferen
Aktivasi
Respon Iskemik
inflamasi glomerular
Aktivasi
Pelepasan

Mediator
Endotelin A II intrarenal
inflamasi

Meningkatkan Akumulasi di
Aktivasi apoptosis
produksi matriks mikrovaskuler glomerulus

SKLEROSIS GLOMERULUS/NEFROSKLEROSIS
Lestariningsih, 2011
 Perubahan
struktur
mikrovaskuler

Akumulasi di
mikrovaskuler glomerulus

Iskemik PGK
glomerular
Kerusakan ginjal akibat Hipertensi esensial
HIPERTENSI HIPERTENSI
ESENSIAL BERAT

BENIGNA MALIGNA

Hialinosis Hialinosis Fenotipe Keruskan Fenotipe Keruskan

Arteriole Arteri Interlobar Glomerulus Akut Vaskuler

Nekrosis Proliferasi Iskemik

Trombosis
Fibrinoid Myointima Glomerulus
Zucchelli & Zuccala, 1994; Hill, 2009; Meyrier & Simon, 1992
 Tekanan Glomerular
 Mean arterial pressure (MAP)
atau tekanan perfusi
 Resistensi arteriole aferen
 Resistensi arteriole eferen
Faktor2 pd patogensis Hipertensi Glomerular

 Mekanisme autoregulasiglomerular yg tidak

adekuat  tidak mampu mempertahankan :
 homeostasis tubuloglomerular feedback
 tekanan intraglomerular
 Iskemik glomerular
 Hemodinamik glomerular
 Peran dari Angiotensin II intraglomerular.
Kidney and Hypertension
DM
Normal
CKD
autoregulation
autoregulation:impaired
CCB
ACEI

Glomerular Glomerular hypertension

pressure: stable Systemic BP dependent

(Kashihara N)
 Aging
Primary Renal Disease
Systemic Hypertension Diabetes Mellitus
Renal Ablation
Dietary Factor

GLOMERULAR HYPERTENSION

ENDOTHELIAL INJURY MESANGIAL INJURY

EPITHELIAL INJURY
Release of vasoactive factors Accumulation of macromolecules
Proteinuria
Vascular lipid deposition Matrix production
Permeability to water
Intracapillary throbosis Cell proliteration

GLOMERULAR SCLEROSIS

Pivotal role of glomerular hypertension in the initiation and

progression of structural injury
Brenner B M
 Hipervolemia
 Eritropoeitin (EPO)
 Disfungsi endotel
 Hiperparatiroidisme
 Kalsifikasi cabang arteri
 Peningkatan aktivitas simpatis
 Hiperaktivitas sistem renin-angiotensin
 Kenaikan curah jantung
 Tingginya resistensi vaskuler sistemik
 Sekresi inhibitor Na-K-ATPase  peningkatan
kalsium
 Peningkatan kalsium intraseluler sel otot polos
 vasokonstriksi.
 Kelebihan cairan meningkatkan kapasitansi
vaskuler, terjadi kenaikan tekanan darah.
 Terapi eriptropoetin (EPO)  TD naik 10
mmHg.
 Hipertensi sering terjadi pd pasien dg anemia
berat diberikan EPO cepat & risiko meningkat
dg hipertensi sebelumnya.
 Mekanisme belum jelas
 Minimalisasi dg
 Mengoptimalkan terapi dialis
 memperhatikan regulasi volume
 memberikan EPO subkutan
 meningkatkan hematokrit secara perlahan-lahan
 Salah satu petanda awal untuk kerusakan target organ1
 Berkontribusi untuk gangguan kardiovaskuler seperti
aterosklerosis,2 hipertensi & gagal jantung3
 Pada Ginjal, menyebabkan fibrosis, proliferasi otot
polos vaskuler & sampai tejadinya disfungsi ginjal4
 Disfungsi ginjal  klirens menurun  peningkatan
konsentrasi endotelin-1  Hipertensi pd PGK.
 Akumulasi inhibitor endogen senyawa NO vasoaktif di
endotel pembuluh darah 1-asymmetric-dimethyl
arginine (1-ADMA) (defisiensi NO  HT)

1. Annuk M, et al. Kidney Int Suppl 2003;84:50-53.

2. Erhart LR. Int J Clin Pract 2003;57:211-218.
3. Vapaataol H, Mervaala E. Med Sci Monit 2001;7:1075-1085.
4. Klahr, Morrissey. Kidney Int Suppl 2000;75:S7–S14
 Gagal ginjal hiperparatiroidisme sekunder yg menyebabkan
peningkatan kalsium intraseluler.
 Kalsium intraseluler hormon paratiroid.
 Hormon paratiroid rerata TD.
 Efek paratiroidektomi  tekanan darah masih
diperdebatkan.
 Peran hiperparatiroidisme pada patogenesis hipertensi pada
dialisis masih belum jelas.
 Uremik gangguan metabolik dan endokrin metabolisme
kalsium dan fosfor :
 progresivitas kalsifikasi vaskuler
 aterosklerosis
• Pasien gagal ginjal
cenderung untuk mengalami
peningkatan tekanan nadi
dan hipertensi sistolik
terisolasi
• Kalsifikasi vaskuler akibat
deposisi pasif kristal
hidroksiapatit ke dalam
dinding arterial karena
peningkatan produk
kalsium-fosfat
• Peningkatan kekakuan
arteri tampaknya
mempunyai peran utama
yang menyebabkan
kehilangan distensibilitas
pembuluh darah besar dan
kecil

FILM
 Akumulasi metabolit uremik
mengaktifkan kemoreseptor di ginjal
dan menimbulkan refleks neural yang
merangsang pusat kardiovaskuler di
batang otak.
 Mekanisme potensial yang mendasari
hiperaktivitas simpatis meliputi
peningkatan Angiotensin II dan ADMA
 penyebabnya belum jelas
 PERANAN SISTEM SARAF SIMPATIS

Stimulasi jantung:
- ↑ kontraktilitas miokard  ↑ Stroke volume

ß-1
Blood Pressure = Cardiac output x Peripheral vascular resistance
Cardiac output = Heart rate x Stroke Volume
Stroke Volume  Venous return & Myocardial Contractility

ᾳ-1
Arteri:
-Vasokonstriksi  ↑ resistensi vaskular
Vena:
- ↑ preload  ↑ Stroke volume
 Hipervolemia  Peningkatan BB > 2 kg intradialitik
 Eritropoeitin (EPO)  kadang diberikan
 Disfungsi endotel  msh mungkin, klirens menurun
 konsentrasi endotelin-1 mungkin meningkat (tdk
ada bukti pemeriksaan)
 Hiperparatiroidisme  blm bisa dipastikan
 Kalsifikasi cabang arteri  sangat jelas lihat vs
banding
 Peningkatan aktivitas simpatis  sangat mungkin
 Hiperaktivitas sistem renin-angiotensin
 sangat mungkin
 TERAPI HIPERTENSI

 Diet lunak 1500 kkal/24 jam, protein 1,2

gr/kgBB/24 jam
 IVFD NaCl 0,9% 1500 cc/24 jam HIPERTENSI
 Captopril 3x25 mg
RESISTEN
 Amlodipin 1x10mg
 Klonidin
 Bisoprolol 1x5mg
 HCT 1-0-0
• Captopril (ACE-I)
 Asam Folat 3x1 • Amlodipin (CCB)
 CaCO3 3x1 • Klonidin (Cental Alfa 2-Agonist)
 Persiapan Denervasi Renal • Bisoprolol (Beta Blocker)
• HCT (Diuretika)
 Intravenous Agents for Hypertensive Emergencies
Agent Onset Duration Advantage Disadvatage
Diltiazem 5-10 min 2-4 hrs CNSprotection, Bradycardia
coronary & renal hypotension
perfusion
Nitroglycerine 2-5 min 3-5 min Coronary Tolerance, variable
perfusion efficacy

Fenoldopan < 5 min 5-10 min Renal perfusion Increase IOP

Hydralazine 10-20 min 3-9 hrs Eclampsia Tachycardia,

headache,ICP î
Nicardipine 5-15 min 1-4 hrs CNS protection Avoid in CHF or
cardiac ischemia

Enalaprilat 15-30 min 6 hrs CHF, acute LV Avoid in MI

failure
Nitroprusside Immediate < 3 min Potent, titratable Cyanide,
thiocyanate,>ICP
Preferred Drugs for Selected Hypertensive
Emergencies
Emergency Preferred Drugs Drugs to Avoid

CVA Diltiazem Diazoxide,hydralazine

Labetalol (increase ICP), nitropruside
Nicardipine
Hypertensive Diltiazem Diazoxide,hydralazine
Encephalopathy Nicardipine (increase ICP)
Labetalol
Nitroprusside
Congestive Heart Nitroglycerine Labetalol and Esmolol
Failure Loop Diuretics (decreased HR),
Nitroprusside nicardipine,diltiazem
Enalaprilate
Myocardial infarct, Diltiazem Diazoxide,hydralazine
Angina Nitroprusside (increase HR,O2 demand
Nitroglyceri
Nicardipinene
Aortic Dissection Nitroprusside Diazoxide,hydralazine,
Labetalol nicardipine
Esmolol
Hypertensive emergencies,Roy Colven,in Emergency Medical Therapy,2000. WB saunders Company
 Management of HTN Urgencies

 No proven benefit of rapid BP reduction in

asymptomatic patients
 Goal BP ≤160/110 mmHg or fall less than
25% MAP within 6 -48 hours
 Oral medications preferred,shortacting
given in repeated doses
 Close monitoring for overshoot hypotension
 Thereafter, a longer acting agent is
prescribed
Hypertensive emergencies: Malignant hypertension and hypertensive encephalopathy .UpToDate.
Norman M Kaplan, MD. Last literature review version 16.3: September 2008
 DENERVASI RENAL
 Menurunkan kadar noradrenalin di seluruh tubuh
 Menurunkan impuls saraf simpatis di vaskular otot
skeletal  aktivitas saraf simpatis otot setelah
denervasi simpatis renal.26
 Menurunkan aktivitas eferen simpatis ginjal 
penurunan kadar noradrenalin ginjal.
 Tidak ada hubungan hilangnya jumlah saraf simpatis dg
kadar norepinefrin & aktivitas plasma renin.30
 Meningkatkan aliran darah ginjal.
 Menurunkan aktivitas renin plasma.
 Penurunan aliran simpatis pusat melalui pengaruh ginjal
sangat penting
 Hasil msh blm cukup memuaskan
 STENT

FILM
 RECOMMENDATIONS FOR
DIALYSIS PATIENTS

 OPTIMAL BP : 135/85 mmHg (Sist 120 – 140)

 Preferred Rx : control ECV

K/DOQI Clinical Practice Guidelines for

Cardiovascular Disease in Dialysis Patients.
Am J Kidney Dis 2005; 45(Suppl 3):S49.
Saad E & Charra B,
Semin Dial, 2004
 Average Number of Antihypertensive
Agents Needed to Achieve BP Goals

ALLHAT (<140/90 mm Hg BP)

UKPDS (<85 mm Hg DBP)

ABCD (<75 mm Hg DBP)

MDRD (<92 mm Hg MAP)

HOT (<80 mm Hg DBP)

AASK (<92 mm Hg MAP)

1.0 1.5 2.0 2.5 3.0 3.5 4.0

Number of antihypertensive agents
MAP, mean arterial pressure.
Bakris GL et al. Am J Kidney Dis.
Dis. 2000;36:646-
2000;36:646-661.
Cushman WC et al. J Clin Hypertens 2002; 4(6):393-
4(6):393-404.
Take messages !
 Prevalence of HT is high in CKD and increase
as stage advances
 The causes of HT in CKD is multifactor, the
main cause is renin system,
hypersympathetic,volume expansion,reduced
vasodilator
 Decreasing blood pressure will reduce
cardiovascular event and slowing progression
of GFR
 Intensive dialysis and achieve dry weight is
importance factors to controll blood pressure
in CKD
 Bahan Makanan Tinggi Garam
 Telur asin
 Ikan asin
 Keju
 Kerupuk
 Kecap
 Mie Instan
 Makanan dalam
kaleng
 Bumbu penyedap
vetcin,
 Kornet
 Tauco, petis,
 Maggi
 Garam dapur
 Hipertensi merupakan awal
terjadinya penyakit lain yang
mematikan.
Kendalikan tekanan darah anda
dengan pola hidup sehat agar hidup
anda lebih sehat dan bahagia

Periksakanlah tekanan
darah anda secara rutin
Bagaimana agar tetap dapat melakukan
aktifitas sampai usia lanjut

Kendalikan Stress

Jangan merokok

Konsumsi makanan sehat

Olah raga teratur

Kurangi konsumsi obat

Olah raga apa yang tepat untuk
Pasien Hipertensi?

Latihan untuk Latihan kekuatan: Latihan

kesehatan -angkat beban kelenturan &
jantung: -senam aerobik keseimbangan
-renang -lari tubuh:
-renang -senam taichi
-berjalan -yoga
-naik tangga -menari
-bersepeda -bersepeda
-tennis
 Kegiatan sehari-hari yang
menyehatkan

• Usahakan berjalan kaki

• Merawat kebun
• Menyapu dan bersih- untuk pergi ke tempat
atau tanaman.
bersih rumah yang berjarak dekat.
• Bermain dengan
• Naik tangga daripada
cucu.
lift untuk lantai yang
rendah
Kegiatan sehari-hari yang dilakukan secara rutin dan teratur sama
dengan berolah raga
 Kegiatan sehari-hari yang
menyehatkan

• Parkirlah kendaraan lebih • Berjalan di setiap lorong

jauh dari tempat yang supermarket pada saat
dituju berbelanja
• Lakukan senam leher saat • Berdiri mengantri, melatih
sedang di lampu merah keseimbangan
 Ingatlah!
 Lakukan kegiatan dengan hati senang.
 Nikmatilah setiap kegiatan yang anda lakukan.
 Jangan memaksakan diri, berkonsultasilah dengan
dokter anda sebelum memilih jenis kegiatan yang tepat.
 Mulailah perlahan lalu tingkatkan sesuai kemampuan.
 Lakukanlah secara rutin.
 Bagaimana menjaga agar tetap SEHAT?
Lakukan! Hindari atau hentikan sama sekali!

Jaga berat Olah raga rutin Minuman

badan tetap Stress beralkohol
normal

Makan makanan Makan cukup Obat2 terlarang

seimbang, rendah calcium, Rokok
(narkoba)
garam &lemak, kalium, &
magnesium
MAU SEHAT?
Website: www.idikalsel.org
FB: IDI Wilayah Kalsel atau
https://www.facebook.com/idikalsel

Website: www.klinikrafisa.co.id
FB: Klinik Spesialis Rafisa Dahlia atau
https://www.facebook.com/klinikrafisa
Twitter: @klinikrafisa
film