SKRIPSI - Universitas Muhammadiyah...

27
ii SKRIPSI DESI IMASTUTI STUDI PENGGUNAAN FUROSEMIDE PADA PASIEN CHRONIC KIDNEY DISEASE (CKD) (Penelitian di Rumah Sakit Umum Daerah Sidoarjo) PROGRAM STUDI FARMASI FAKULTAS ILMU KESEHATAN UNIVERSITAS MUHAMMADIYAH MALANG 2017

Transcript of SKRIPSI - Universitas Muhammadiyah...

Page 1: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

ii

SKRIPSI

DESI IMASTUTI

STUDI PENGGUNAAN FUROSEMIDE PADA

PASIEN CHRONIC KIDNEY DISEASE (CKD)

(Penelitian di Rumah Sakit Umum Daerah Sidoarjo)

PROGRAM STUDI FARMASI

FAKULTAS ILMU KESEHATAN

UNIVERSITAS MUHAMMADIYAH MALANG

2017

Page 2: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,
Page 3: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

ii

Page 4: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

iii

Page 5: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

iv

KATA PENGANTAR

Assalamu’alaikum Warahmatullahiwabarakatuh

Alhamdulillahirabbilalamin, segala puji bagi Allah Tuhan Semesta Alam,

yang menghidupkan dan mematikan, yang memberi hidayah kepada yang

dikehendaki dan mencabut hidayah dari yang dikehendaki. Tuhan yang telah

memberikan nikmat sehat, waktu, kemudahan maupun kesabaran sehingga penulis

dapat menyelesaikan skripsi yang berjudul ”STUDI PENGGUNAAN

FUROSEMIDE PADA PASIEN CHRONIC KIDNEY DISEASE (CKD)

(Penelitian di Rumah Sakit Umum Daerah Sidoarjo)” untuk mencapai gelar

Sarjana Farmasi pada Program Studi Farmasi Fakultas Ilmu Kesehatan

Universitas Muhammadiyah Malang. Dalam penyusunan skripsi ini, penulis tidak

terlepas dari peranan pembimbing dan bantuan dari berbagai pihak. Oleh karena

itu, dengan segala kerendahan hati penulis ingin mengucapkan banyak

terimakasih kepada:

1. Allah SWT, yang mana dengan segala rahmat nikmat pertolongan, petunjuk

dan kekuatan dari-Nyalah, penulis dapat menyelesaikan amanah sebagai

mahasiswa di Universitas Muhammadiyah Malang .

2. Bapak Yoyok Bekti P, M.Kep., Sp. Kom., selaku Dekan Fakultas Ilmu

Kesehatan Universitas Muhammadiyah Malang yang telah memberikan

kesempatan penulis untuk belajar di Fakultas Ilmu Kesehatan Universitas

Muhammadiyah Malang.

3. Ibu Nailis Syifa’ S. Farm., M.Sc., Apt., selaku Ketua Program Studi

Fakultas Ilmu Kesehatan Universitas Muhammadiyah Malang yang telah

memberi motivasi dan kesempatan penulis untuk belajar di Fakultas Ilmu

Kesehatan Universitas Muhammadiyah Malang.

4. dr. Atok Irawan, Sp.p., selaku direktur Rumah Sakit Umum Daerah Sidoarjo

beserta jajarannya khususnya bagian farmasi klinik dan seluruh staf pegawai

bagian rekam medik Rumah Sakit Umum Daerah Sidoarjo yang telah

banyak membantu dalam proses pengambilan data skripsi.

5. Ibu Nailis Syifa’ S. Farm., M.Sc., Apt., selaku dosen pembimbing I, Bapak

Drs. Didik Hasmono, M.S., Apt., selaku dosen pembimbing II, Ibu Hidajah

Page 6: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

v

Rachmawati, S.Si., Apt., Sp.FRS., selaku dosen penguji I, Ibu Prof. Dra.

Lilik Yusetyani, Apt., Sp. FRS., selaku dosen penguji II. Terimakasih atas

kesabaran dan waktunya untuk membimbing dan meberi saran, pengarahan,

serta dukungan kepada penulis selama penyusunan skripsi.

6. Ibu Siti Rofida, S.Si., Apt., M.Farm., selaku dosen wali beserta semua dosen

Program Studi Farmasi Universitas Muhammadiyah Malang, terimakasih

banyak atas arahan, nasehat, dan bimbingannya selama ini.

7. Kedua orang tua, dan adik tercinta yang selalu memberikan dukungan serta

motivasi dalam menyelesaikan skripsi ini.

8. Sahabat dan teman terbaik nur awaliyyah, baiq wafa aulia, lathifah

muyassaroh, tya pratiwi, reza diah prataningtyas, ulifah yulianti, ninik

setyowati terimakasih sudah menjadi teman seperjuangan penelitian skripsi

dalam suka dan duka.

9. Untuk semua pihak yang belum disebutkan namanya dikarenakan

keterbatasan, penulisan mohon maaf dan terimakasih yang sebesar-

besarnya. Semua keberhasilan ini tak luput dari bantuan dan doa yang telah

diberikan.

Penulis tidak mampu membalas jasa yang telah diberikan. Semoga Allah

SWT membalas amal kebaikan semua pihak. Penulis menyadari sepenuhnya

bahwa skripsi ini jauh dari kesmepurnaan, oleh karena itu penulis mengharapkan

kritik dan saran yang membangun untuk memperbaiki kekurangan yang ada.

Semoga skripsi ini dapat memberikan manfaat dan kosntribusi dalam dunia

farmasi dan dunia ilmu pengetahuan pada umumnya, serta berguna bagi penelitian

selanjutnya.

Wassalamu’ alaikumwarahmatullahiwabarakatuh

Malang, 03 Juni 2017

Penyusun,

Desi Imastuti

Page 7: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

vi

RINGKASAN

Chronic Kidney Disease (CKD) didefinisikan sebagai kelainan struktur dan

fungsi ginjal selama tiga bulan atau lebih. Kelainan struktural ginjal meliputi

albuminuria lebih dari 30 mg/hari, terjadinya hematuria atau adanya sel darah

merah dalam sedimen urin, gangguan elektrolit dan kelainan lain akibat gangguan

tubular. Di Indonesia sebanyak 0.2% dari total penduduk di Indonesia menderita

Chronic Kidney Disease (CKD). WHO memperkirakan di Indonesia akan terjadi

peningkatan penderita gagal ginjal pada tahun 1995-2025 sebesar 41,4%. Menurut

data Persatuan Nefrologi Indonesia (PERNEFRI) diperkirakan terdapat 70.000

penduduk Indonesia yang menderita gagal ginjal, dan angka ini akan terus

meningkat sebesar 10% setiap tahunnya.Dilaporkan pada tahun 2007 hingga 2014

jumlah pasien baru yang melakukan hemodialisis setiap tahunnya terus

meningkat, pada tahun 2007 terdapat 4.997 pasien sedangkan tahun 2014 terdapat

17.193 pasien.Penyebab terjadinya CKD dipengaruhi oleh 3 faktor yaitu faktor

susceptibility, faktor inisiasi, dan faktor progression.

Manifestasi dari CKD terkait dengan uremia umumnya tidak memiliki gejala,

dapat diidentifikasi saat Glomerular Filtration Rate (GFR) kurang dari 60 ml/min

per 1.73m2. Ketika GFR menunjukkan 15-30 ml/min per 1.73m

2 maka frekuensi

hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia, dan

asidosis sebesar 20%, hipokalsemia dan serum albumin rendah sebesar 5-10%.

Penurunan fungsi ginjal yang progresif menyebabkan penurunan GFR dan massa

tubular. Penurunan GFR mengakibatkan menurunnya filtrasi Na+

dan ekspansi

volume. Ekspansi volume akan memicu penurunan absorbsi Na pada tubular

ginjal, namun kegagalan dalam menekan reabsosbsi Na akan meningkatkan

volume cairan ekstrasellular. Massa tubular yang berkurang juga akan menekan

reabsorbsi Na pada setiap nefron. Namun penekanan yang tidak tepat pada

reabsorbsi tubular akan lebih meningkatkan volume dan memicu hipertensi

sehingga pasien CKD diberikan furosemide untuk mengatasi edema dan

hipertensi. Furosemide ialah turunan dari asam 5-sulfamoil-2 aminobenzoat yang

memiliki struktur dan aktifitas diuretik optimum. Furosemide tetap menjadi

diuretik pilihan untuk mengontrol tekanan darah dan mengurangi gejala edema

karena furosemide dapat meningkatkan ekskresi fraksinasi Na sebesar 20% dan

efisien tanpa dipengaruhi GFR. Mekanisme aksi dari furosemide terletak di ansa

henle asenden dengan menghambat transport aktif klorida pada channel Na-K-2Cl

yang terletak pada luminal membran sehingga menghalangi reabsorbsi natrium

dan klorida yang menyebabkan terjadinya natriuresis. Penghambatan aktif

transport klorida oleh furosemide menyebabkan terjadinya natriuresis secara cepat

dengan mengurangi gradien filtrasi dan mencegah reabsorbsi pasif air pada nefron

sehingga natrium akan diekskresikan bersama urin dan volume cairan

exstrasellular kembali normal.

Tujuan dari penelitian ini adalah mempelajari dan menganalisa pola

penggunaan furosemide terkait dosis, rute, frekuensi, dan lama pemberian yang

dikaitkan dengan data klinik dan data laboratorium pada pasien Chronic Kidney

Disease (CKD) di Instalasi rawat Inap Rumah Sakit Umum Daerah Sidoarjo.

Penelitian ini dilakukan secara observasional dengan rancangan penelitian

secara deskriptif dan pengumpulan data secara retrospektif dimana data yang

digunakan adalah data primer berupa Rekam Medik Kesehatan (RMK). Kriteria

Page 8: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

vii

inklusi dari penelitian ini meliputi pasien dengan diagnosis CKD dengan data

Rekam Medis Kesehatan (RMK) yang mencakup data terapi obat furosemide dan

obat lain yang menyertai di Instalasi rawat inap Rumah Sakit Umum Daerah

Sidoarjo mulai periode 1 Januari 2016 sampai 31 Agustus 2016, diperoleh

sebanyak 32 data Rekam Medik Kesehatan (RMK) sebagai sampel. Dimana data

tersebut semuanya termasuk kriteria inklusi. Data demografi pasien berdasarkan

jenis kelamin, terdapat 19 pasien laki-laki (59%) dan13 pasien perempuan (41%).

Pada penelitian, diperoleh kelompok usia terbanyak yang menderita CKD adalah

rentang usia 51-60 tahun (40%). Klasifikasi CKD terbanyak adalah GFR <15

ml/mnt/1,73 m2 (72%). Faktor resiko paling banyak ditemukan adalah hipertensi

(68%).

Pola penggunaan furosemide tunggal sebanyak 28 pasien (58%),

penggunaan kombinasi dua sebanyak 10 pasien (21%), dan penggunaan

kombinasi tiga sebanyak 10 pasien (21%). Pola penggunaan furosemide tunggal

paling banyak adalah furosemide (3x20 mg) IV sebanyak 9 pasien (32%).

Penggunaan furosemide kombinasi 2 paling banyak adalah furosemide (2x20 mg)

IV + amlodipin (1x10 mg) PO sebanyak 3 pasien (15%). Penggunaan kombinasi 3

paling banyak adalah furosemide (3x40 mg) IV + amlodipin (1x10 mg) PO +

valsartan (1x160 mg) PO sebanyak 1 pasien (10%). Penggunaan dosis, rute, dan

frekuensi furosemide yang diberikan sudah sesuai dengan guideline yang ada.

Page 9: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

x

DAFTAR ISI

HALAMAN JUDUL .......................................................................................... i

LEMBAR PENGESAHAN ............................................................................... ii

LEMBAR PENGUJIAN ................................................................................... iii

KATA PENGANTAR ....................................................................................... iv

RINGKASAN .................................................................................................... vi

ABSTRACT .......................................................................................................viii

ABSTRAK ......................................................................................................... ix

DAFTAR ISI ....................................................................................................... x

DAFTAR TABEL ............................................................................................ xiv

DAFTAR GAMBAR ......................................................................................... xv

DAFTAR LAMPIRAN .................................................................................... xvi

DAFTAR SINGKATAN .................................................................................. xvii

BAB I PENDAHULUAN ................................................................................... 1

1.1 Latar Belakang .............................................................................................. 1

1.2 Rumusan Masalah ......................................................................................... 4

1.3 Tujuan Penelitian .......................................................................................... 4

1.3.1 Tujuan Umum .......................................................................................... 4

1.3.2 Tujuan Khusus .......................................................................................... 4

1.4 Manfaat Penelitian ........................................................................................ 4

1.4.1 Bagi Peneliti ............................................................................................. 4

1.4.2 Bagi Rumah Sakit ..................................................................................... 5

BAB II TINJAUAN PUSTAKA ........................................................................ 6

2.1 Tinjauan tentang Ginjal ................................................................................. 6

2.1.1 Anatomi dan Struktur Ginjal .................................................................... 6

2.1.2 Pembuluh Darah Ginjal ............................................................................ 7

2.1.3 Fungsi Ginjal ............................................................................................ 8

2.2 Tinjauan tentang Chronic Kidney Disease (CKD) ...................................... 9

2.2.1 Definisi Chronic Kidney Disease (CKD) ................................................ 9

2.2.2 Epidemiologi Chronic Kidney Disease (CKD) ...................................... 10

2.2.3 Etiologi Chronic Kidney Disease (CKD) ............................................... 10

2.2.4 Klasifikasi Chronic Kidney Disease (CKD) .......................................... 14

Page 10: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

xi

2.2.5 Faktor Resiko Chronic Kidney Disease (CKD) ..................................... 14

2.2.6 Patofisiologi Chronic Kidney Disease (CKD) ....................................... 15

2.2.7 Manifestasi Klinis Chronic Kidney Disease (CKD) .............................. 17

2.2.7.1 Edema ............................................................................................... 17

2.2.7.2 Anemia ............................................................................................. 20

2.2.7.3 Mineral Bone Disease ...................................................................... 20

2.2.7.4 Hiperkalemia .................................................................................... 20

2.2.7.5 Asidosis Metabolik ........................................................................... 21

2.2.8 Diagnosa Chronic Kidney Disease (CKD) ............................................. 21

2.2.8.1 Pemeriksaan laboratorium ................................................................ 21

2.2.8.2 Pemeriksaan penunjang .................................................................... 22

2.2.9 Penatalaksanaan Terapi CKD .................................................................. 22

2.2.9.1 Antihipertensi ................................................................................... 22

2.2.9.1.1 Angiotensin Converting Enzyme Inhibitor (ACEI) dan

Angiotensin Receptor Blockers (ARB) .................................. 23

2.2.9.1.2 Beta bloker .............................................................................. 24

2.2.9.1.3 Agonis Alfa 2 Sentral ............................................................. 25

2.2.9.1.4 Calcium-Channel Blockers (CCB) ........................................ 26

2.2.9.1.5 Diuretik ................................................................................... 27

2.2.9.1.5.1 Diuretik Tiazid ................................................................. 27

2.2.9.1.5.2 Loop Diuretik................................................................... 28

2.2.9.1.5.2.1 Karakteristik Kimia Furosemide .............................. 29

2.2.9.1.5.2.2 Dosis Furosemide ..................................................... 29

2.2.9.1.5.2.3 Farmakodinamik Furosemide ................................... 30

2.2.9.1.5.2.4 Farmakokinetik Furosemide ..................................... 30

2.2.9.1.5.2.5 Efek Samping dan Kontraindikasi Furosemide ........ 31

2.2.9.1.5.2.6 Interaksi Furosemide ................................................ 32

2.2.9.1.5.3 Diuretik Hemat Kalium ................................................... 32

2.2.9.2 Terapi Edema ................................................................................... 33

2.2.9.3 Terapi Anemia .................................................................................. 34

2.2.9.4 Terapi Mineral Bone Disease ........................................................... 34

2.2.9.5 Terapi Hiperkalemia ......................................................................... 35

Page 11: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

xii

2.2.9.6 Terapi Asidosis Metabolik ............................................................... 35

2.2.10Furosemide pada Chronic Kidney Disease (CKD) ................................ 36

BAB III KERANGKA KONSEPTUAL .......................................................... 40

3.1 Kerangka Konseptual ................................................................................... 40

3.2 Kerangka Operasional .................................................................................. 42

BAB IV METODE PENELITIAN .................................................................. 43

4.1 Rancangan Penelitian ................................................................................... 43

4.2 Populasi dan Sampel .................................................................................... 43

4.2.1 Populasi ................................................................................................... 43

4.2.2 Sampel ..................................................................................................... 43

4.2.3 Kriteria Data Inklusi ................................................................................ 43

4.2.4 Kriteria Data Eksklusi ............................................................................. 43

4.3 Bahan Penelitian .......................................................................................... 43

4.4 Instrumen Penelitian .................................................................................... 43

4.5 Tempat dan Waktu Penelitian ...................................................................... 44

4.6 Metode Pengumpulan Data .......................................................................... 44

4.7 Analisa Data ................................................................................................. 44

4.8 Definisi Operasional .................................................................................... 44

BAB V HASIL PENELITIAN ......................................................................... 47

5.1 Data Demografi Pasien ................................................................................ 48

5.1.1 Jenis Kelamin Pasien Chronic Kidney Disease (CKD) ......................... 48

5.1.2 Usia Pasien Chronic Kidney Disease (CKD) ......................................... 48

5.1.3 Status Pasien Chronic Kidney Disease (CKD) ...................................... 48

5.2 Klasifikasi Pasien Chronic Kidney Disease (CKD) .................................... 49

5.3 Penyakit Penyerta Pasien Chronic Kidney Disease (CKD) ........................ 49

5.4 Tindakan Hemodialisis Pasien Chronic Kidney Disease (CKD) ................ 50

5.5 Faktor Resiko Pasien Chronic Kidney Disease (CKD) .............................. 50

5.6 Manajemen Terapi pada Pasien Chronic Kidney Disease (CKD) .............. 50

5.6.1 Pola Penggunaan Furosemide pada Pasien Chronic Kidney Disease

(CKD) ........................................................................................................ 50

5.6.2 Pola Penggunaan furosemide tunggal pada Pasien Chronic Kidney Disease

(CKD) ....................................................................................................... 51

Page 12: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

xiii

5.6.3 Pola Penggunaan Terapi Kombinasi Furosemide Pada Pasien Chronic

Kidney Disease (CKD) ............................................................................. 51

5.6.4 Pola Penggunaan Terapi Furosemide dengan Pergantian (Switch) ........ 53

5.6.5 Lama Penggunaan Furosemide pada Pasien Chronic Kidney Disease

(CKD) ........................................................................................................ 54

5.6.6 Terapi lain yang diterima pasien Chronic Kidney Disease (CKD) ......... 54

5.7 Lama Perawatan Pasien Chronic Kidney Disease (CKD) .......................... 55

5.8 Kondisi Keluar Rumah Sakit Pasien Chronic Kidney Disease (CKD) ....... 56

BAB VI PEMBAHASAN .................................................................................. 57

BAB VII KESIMPULAN DAN SARAN ......................................................... 78

7.1 Kesimpulan .................................................................................................. 78

7.2 Saran ............................................................................................................ 78

DAFTAR PUSTAKA ........................................................................................ 79

LAMPIRAN ....................................................................................................... 80

Page 13: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

xiv

DAFTAR TABEL Tabel Halaman

II.1 (Klasifikasi CKD) ........................................................................................ 14

II.2 (Dosis antihipertensi golongan ACEI dan ARB pda CKD) ........................ 24

II.3 (Dosis antihipertensi golongan beta bloker) ................................................ 25

II.4 (Dosis antihipertensi golongan alfa agonis sentral) ..................................... 26

II.5 (Dosis antihipertensi golonganCCB) ........................................................... 26

II.6 (Dosis dan farmakokinetik diuretik thiazid pada CKD) .............................. 28

II.7 (Dosis loop diuretik pada CKD) ................................................................. 30

II.8 (Farmakokinetik loop diuretik) ................................................................... 31

II.9 (Dosis dan farmakokinetik diuretik hemat kalium pada CKD) ................... 33

II.10 (Terapi hiperkalemia) .................................................................................. 35

II.11 (Nama dagang, kandungan, dan bentuk sediaan furosemide) ..................... 38

V.1 (Jenis kelamin pasien Chronic Kidney Disease (CKD) ............................... 48

V.2 (Usia pasien Chronic Kidney Disease (CKD) ............................................. 48

V.3 (Status pasien Chronic Kidney Disease (CKD) ........................................... 48

V.4 (Klasifikasi pasien Chronic Kidney Disease (CKD) ................................... 49

V.5 (Penyakit penyerta pasien Chronic Kidney Disease (CKD) ........................ 49

V.6 (Tindakan hemodialisis pasien Chronic Kidney Disease (CKD) ................ 50

V.7 (Faktor resiko pasien Chronic Kidney Disease (CKD) ............................... 50

V.8 (Pola penggunaan furosemide pasien Chronic Kidney Disease (CKD) ...... 50

V.9 (Pola penggunaan furosemide tunggal pasien Chronic Kidney Disease

(CKD) .......................................................................................................... 51

V.10 (Pola penggunaan furosemide kombinasi pasien Chronic Kidney Disease

(CKD) .......................................................................................................... 51

V.11 (Pola penggunaan furosemide dengan pergantian (switch) Chronic Kidney

Disease (CKD)............................................................................................. 53

V.12 (Lama penggunaan furosemide pasien Chronic Kidney Disease (CKD) .... 54

V.13 (Terapi lain yang diterima pasien Chronic Kidney Disease (CKD) ............ 55

V.14 (Lama perawatan pasien Chronic Kidney Disease (CKD) .......................... 55

V.15 (Kondisi keluar rumah sakit pasien Chronic Kidney Disease (CKD) ......... 56

Page 14: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

xv

DAFTAR GAMBAR Gambar Halaman

2.1 (Anatomi ginjal)........................................................................................... 6

2.2 (Struktur nefron ginjal) ................................................................................ 7

2.3 (Aliran darah pada pembuluh darah ginjal) ................................................. 8

2.4 (Patofisiologi CKD degan aktivasi Sistem Renin Angiotensin) .................. 17

2.5 (Tekanan onkotik dan tekanana hidrostatik)................................................ 18

2.6 (Site of action diuretik pada nefron ginjal) ................................................. 27

2.7 (Struktur Furosemide) .................................................................................. 29

3.1 (Skema Kerangka Konseptual) .................................................................... 41

3.2 (Skema Kerangka Operasional) ................................................................... 42

5.1 (Skema inklusi dan eksklusi penggunaan furosemide pada pasien Chronic

Kidney Disease (CKD) di Rumah Sakit Umum Daerah sidoarjo ............... 47

Page 15: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

xvi

DAFTAR LAMPIRAN Lampiran Halaman

1 Daftar Riwayat Hidup .................................................................................. 89

2 Surat Pernyataan .......................................................................................... 90

3 Daftar Nilai Normal Data Klinik dan Data Laboratorium ........................... 91

4 Nota Dinas ................................................................................................... 92

5 Surat Ijin Penelitian ..................................................................................... 93

6 Kode Etik ..................................................................................................... 94

7 Perhitungan Pemberian Furosemide Melalui Pump .................................... 95

8 Lembar Pengumpulan Data Pasien Chronic Kidney Disease (CKD) di

Instalasi Rawat Inap RSUD Sidoarjo .......................................................... 96

9 Tabel Induk Pasien Chronic Kidney Disease (CKD) di Instalasi Rawat

Inap RSUD Sidoarjo ................................................................................ 180

Page 16: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

xvii

DAFTAR SINGKATAN

ACE : Angiotensin Converting Enzyme

ADH : Antidiuretik Hormon

ARB : Angiotensin II Receptor Blocker

BP : Blood Pressure

CCB : Calcium Channel Blocker

CKD : Chronic Kidney Disease

CCT : Clearance Creatinin Test

ESA : eritropoeitic-stimulating Agent

ESRD : End Stage Renal Disease

GFR : Glomelular Filtration Rate

KDIGO : Kidney Disease Improving Global Outcome

KDOQI : Kidney Disease Quality Outcome Initiative

NIDDK : National Institute of Diabetes and Digestive and Kidney Disease

LPD : Lembar Pengumpul Data

NKF : National Kidney Foundation

NO : Nitric Oxide

NSAID : Nonsteroidal Anti Inflamantory Disease

PERNEFRI : Persatuan Nefrologi Indonesia

PTH : Parathiroid Hormon

RAA : Renin-Angiotensin-Aldosteron

RISKESDAS : Riset Kesehatan Dasar

RMK : Rekam Medis Kesehatan

RRT : Renal Replacement Therapy

SHPT : Secondary-hyperparathyroidism

SIGN : Scottish Intercollegiate Guidelines Network

SLE : Systemic Lupus Erythematous

TGF : transforming growth factor

VDAE : Volume Darah Arteri Efektif

Page 17: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,
Page 18: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

79

DAFTAR PUSTAKA

Abboud, H., William, L., Henrich, 2010. Stage IV Chronic Kidney Disease, N

Engl J Med, No 362, p. 56-65.

Agarwal, R., Sinha, D., 2012. Thiazide diuretics in advanced chronic kidney

disease. Curr. Hypertens. Rep., Vol. 5 No. 6, p. 299-308.

Alfonso, A.A., Mongan, A.E., Memah, M.F., 2016. Gambaran kadar kreatinin

serum pada pasien penyakit ginjal kronik stadium 5 non dialisis. Jurnal

eBm, Vol. 4 No. 1, p. 178-183.

Alqahtani, F., Koulouridis, I., Susantitaphong, P., Dahal, K., Jaber, B. L., 2014.

A-meta-analysis of continous vs intermittent infusion of loop diuretics in

hospitalized patient. J Crit. Care, Vol. 29, p. 10-17.

Amalina,R., Respati, T., Budiman, 2015. Prevalensi dan Faktor Risiko Penyakit

Ginjal Kronik di RSUP Dr. Mohammad Hoesin Palembang Tahun 2015, p.

1086-1091.

Armiyati, R., Rahayu, D.A., 2014. Faktor Yang Berkorelasi Terhadap Mekanisme

Koping Pasien Ckd Yang Menjalani Hemodialisis Di Rsud Kota Semarang

(Correlating factors of coping mechanism on CKD patients undergoing

Hemodialysis in RSUD Kota Semarang), p. 1-7.

Askari, F.S.S., Sulaiman, S.A.S., Askari, N.S.S., 2016. Anticoagulation Therapy

in Patients with Chronic Kidney Disease. Adv Exp Med Biol, p. 101-114.

Ayaf, C., Beuscart, J.B., Briancon, S., Duhamel, A., Frimat, L., Kessler, M., 2016.

Competing risk of death and end-stage renal disease in incident chronic

kidney disease (stages 3 to 5): the EPIRAN community-based study, BMC

Nephrol, Vol. 17 No. 1, p. 1-13

Barret, K., Brooks, H., Boitano, S., Barman, S., 2010. Ganong`s review of

Medical Physiology 23rd Edition. United States: McGraw-Hill

Companies, p. 640.

Bellizi, V., Cupisti, A., Locatelli, F., Bollasco, P., Brunori, G., Cancarini, G.,

Cari, S., Nicola, L.D., Lorio B.R.D., Fiaccadori, E., Gariboto, G., Madreoli,

M., Minutolo, R., Oldrizzi, L., Piccoli, G.B., Quintaliani, G.,Santoro, D.,

Torraca, S.,Viola, B.F., 2016. Low-Protein Diets For Chronic Kidney

Disease Patients: The Italian Experience, BMC Nephrol, No.17, p. 1-17.

Bragatto, M.S., Santos, M.B., Pinto, A.M.P., Eduardo, Angonese, N.T., Fatima,

W., Vizze, G., Donaduzzi, C.M., Manfio, J.L., 2011. Comparison between

Pharmacokinetic and Pharmacodynamic of Single- Doses of Furosemide 40

mg Tablets. J. Bioequiv. Availab., Vol. 3 No. 8, p. 191-197.

Page 19: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

80

Brunton, L., Parker, K., Blumenthal, D, Buxton, L., 2011. Goodman & Gilman

Manual of Pharmacology and Therapeutics, United States of

America:McGraw-Hill, p. 484.

Chadban, S., Howell, M., Twigg, S., Thomas, M., Jerums, G., Cass, A., Campbell,

D., Nicholl, K.., Tong, A., Mongos, G., Stack A., Maclsaac, R.J., Girgis, S.,

Colagiuri, S., Craig, J., 2010. Pervention and management of chronic kidney

disease in type 2 diabetes, Nephrology, Vol. 15, p. 162-194.

Chandna, S.M., Gane, M.D.S., Marshall, C., Warwicker, P., Greenwood, R.N.,

Farrington, K. 2011. Survival of elderly patients with stage 5 CKD :

ccomparison of conservative management and renal replacement therapy,

Nephrol Dial Transplant, No. 26, p. 1608-1614.

Cho, S., Atwud, E., 2002. Peripheral Edema, Am J Med, No. 113, p. 580-586.

Chong, E., Kalia, V., Wilkie, S., 2014. Drug–drug interactions between

sucroferric oxyhydroxide and losartan, furosemide, omeprazole, digoxin and

warfarin in healthy subjects, J Nephrol, p. 1-8.

Dakappa, A., Narayanareddy, M., 2016. A cross-sectional study to asess the

rationality of fixed dose combination prescribed in geriatric patients in a

tertiary care hospital, Int J Basic Clin Pharmacol, Vol 5, p. 1441-1447.

Depkes RI, 2006. Buku Saku Hipertensi,

http://www.academia.edu/7994928/PHARMACEUTICAL_CARE_UNTU

K_PENYAKIT_HIPERTENSI diakses tanggal 2 Januari 2017.

Duffy, M., Jain, S., Harrell, N., Kothari, N., Reddi, A. S., 2015. Albumin and

Furosemide Combination for Management of Edema in Nephrotic

Syndrome: A Review of Clinical Studies. Cells, Vol. 4, p. 622-630.

Dussol, B., Frances, J. M., Morange, S., Delpero, C. S., Mundler, O., Berland, Y.,

2012. A Pilot Study Comparing Furosemide and Hydrochlorothiazide in

Patients With Hypertension and Stage 4 or 5 Chronic Kidney Disease. J.

Clin. Hypertens., Vol. 14 No. 1, p. 32-37.

Effendi, I., Markum, H.M.S., 2014. Pemeriksaan Penunjang Pada Penyakit Ginjal.

In: Setiati, S., Alwi, I., Sudoyo, A.W., Simadibrata, M., Setiyohadi, B.,

Syam, A.F., Buku Ajar Ilmu Penyakit Dalam Ed IV, Jakarta:

InternaPublishing, p. 2047.

Effendi, I., Pasaribu, R., 2014. Edema Patofisiologi dan Penanganan. In: Setiati,

S., Alwi, I., Sudoyo, A.W., Simadibrata, M., Setiyohadi, B., Syam, A.F.,

Buku Ajar Ilmu Penyakit Dalam Ed IV, Jakarta: InternaPublishing, p.

2059.

Page 20: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

Elizabeth, A.A., Glory, J., Darling, C.D., Punnagai, K., Vijaybabu, K., 2011.

Short-Term Furosemide Therapy In Chronic Renal Disease; Implications Of

Hypomagnesia And Potential For Improving Hyperkalaemia. J. Clin.

Diagn. Res., Vol. 5 No. 1, p. 91-95.

Ervina, L., Bahrun, D., . Lestari, H.I., 2015 Tatalaksana Penyakit Ginjal

Kronik pada Anak.

http://ejournal.unsri.ac.id/index.php/mks/article/download/2758/pdf,

Diakses tanggal 29 Sepetember 2016.

Garrido, J. B., Lobera, I. J., 2012. Interactions between antihypertensive drugs and

food. Nutr. Hosp., Vol. 27 No. 5, p. 1866-1875.

Giacoman, S.L., Madero, M., 2015. Biomarkers in Chronic Kidney Disease, from

Kidney Function to Kidney Damage,World J Nephrol, Vol 1 No.4, p. 57-

73

Goldsmith, D., Jayawardene, S., Ackland, P., 2013. ABC of Kidney Disease 2th

Edition, UK: John Willey & Sons Ltd, p. 1-6.

Granado, R.C.D., Mehta, R.L., 2016. Fluid overload in the ICU: evaluation and

management. BMC Nephrology, Vol. 17 No. 109, p. 1-9.

Grandman, A.H., Basile, J.N., Carter, B.L., Bakris, G.L., 2010. Combination

therapy in hypertension, J Am Soc Hypertens, Vol. 4 No.2, p. 90-98.

Granero, G.E., Longhi, M.R., Mora, M.J., Junginger, H.E., Midha, K.K., Shah,

V.P., Stavchansky, S., Dessman, J.B., Barends D.M., 2010. Biowaiver

Monographs for Immediate Release Solid Oral Dosage Forms: Furosemide.

J. Pharm. Sci., Vol. 99 No. 6, p. 1-13.

Gu, Q., Burt V.L., Dillon, C.F., Yoon, S., 2012. Trends in antihypertensive

medication use and blood pressure control among United States adults with

hypertension: the National Health And Nutrition Examination Survey, 2001

to 2010. Circulation, Vol 17 No. 126, p. 2105-2114.

Guyton, A.C., Hall, J.E., 2008. Buku Ajar Fisiologi Kedokteran Edisi 11.

Jakarta : EGC, p. 231-237 dan 326-327.

Halle, M.P., Hertig, A., Kengne, A.P., Ashutantang, G., Rondeau, E., Ridel, C.,

2012. Acute pulmonary oedema in chronic dialysis patient admitted into an

intensive care unit, Nephrol Dial Transplant, Vol. 27, p. 603-607.

Hendromartono, 2014. Nefropati Diabetik. In: Setiati, S., Alwi, I., Sudoyo, A. W.,

Simadibrata, M., Setiyohadi, B., Syam, A.F., Buku Ajar Ilmu Penyakit

Dalam Ed IV, Jakarta: InternaPublishing, p. 2159.

Page 21: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

82

Hermanson, T., Benett, C.L., Macdougall, C., 2016. Peginesatide for the treatment

of anemia due to chronic kidney disease – an unfulfilled promise. Expert

Opin Drug Saf., p. 2-7.

Ho, K.M., Power, B.M., 2010. Benefits and risks of furosemide in acute kidney

injury. Anaesthesia, Vol. 65, p. 283-293.

Horn, E.J., . Ellison, D.H., 2016. Diuretic Resistance. Am. J. Kidney Dis., p. 1-7.

Huda, Md.N., Alam, K.S., Rashid, H.U., 2012. Clinical Study Prevalence of

Chronic Kidney Disease and Its Association with Risk Factors in

Disadvantageous Population, Internationat Journal of Nephrology, Vol.

2012, p. 1-8.

Imanishi, Y., Nishizawa, Y., Inaba, M., 2013. Pathogenesis and Treatment of

Chronic Kidney Disease-Mineral and Bone Disorder.

https://www.intechopen.com/books/hemodialysis/pathogenesis-and-

treatment-of-chronic-kidney-disease-mineral-and-bone-disorder, diakses

tanggal 1 Deember 2016.

Iqbal, S., Alam, A., 2013. Renal Disease in Diabetes Mellitus: Recent Studies and

Potential Therapies. J Diabetes Metab, Vol S9 No. 006, p. 1-16.

ISO., 2013. Informasi Spesialis Obat Vol. 48. Jakarta: PT. ISFI Penerbitan.

Jayarman, R., Voort, J.V., 2010. Principles of management of chronic kidney

disease. Paediatr Child Health, Vol 20 No.6, p. 291-296.

Jalal, D.I., Decker, E., Perrenoud, L., Nowak, K.L., Bispham, N., Mehta, T.,

Smits, G., You, Z., Seals, D., Chonchol, M., Johnson, R.J., 2016. Vascular

Function and Uric Acid-Lowering in Stage 3 CKD. J. Am. Soc. Nephrol.,

Vol. 28, p. 1-10.

Jha, V., Garcia, G.G., Iseki, K., Li, Z., Naicker, S., Plattner, B., Saran, R., Wang,

A.Y.M., C. Yang, W., 2013. Chronic Kidney Disease: Global Dimension

and Prospective. Lancet, p. 1-13.

Johnston, S., 2016. Symptomp management in patients with stage 5 CKD opting

for conservative management, Healthcare, Vol. 4 No. 72, p.1-8.

KDIGO., 2013. Clinical practice guideline for the evaluation and management of

chronic kidney disease. Kidney Int Suppl, Vol. 3, p. 5.

Kitsios, G.D., Mascar, P., Ettunsi, R., Gray, A.W., 2014. Co-administration of

Furosemide with albumin for overcoming diuretid resistence in patients with

hypoalbuminemia: A meta-analysis. Vol. 29, p. 253-259.

Page 22: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

Koniewski, I., Wesson, D.E., 2013. Bicarbonate therapy for prevention of chronic

kidney disease progression. Kidney Int., Vol. 3 No. 85, p. 529-535.

Lemes, H. P., Araujo, S., Nascimento, D., Cunha, D., Garcia, C., Queiroz, V.,

Ferreira-Filho, S.R., 2011. Use of Small Doses of Furosemide in Chronic

Kidney Disease Patient with Residual Renal Function Undergoing

Hemodialysis. Clin. Exp. Nephrol., Vol. 15, p. 554-559.

Lenhardt, A., Kemper, M.J., 2011. Pathogenesis, diagnosis and management of

hyperkalemia. Pediatr Nephrol, Vol. 26, p. 377-384.

Levey, A.S., Coresh, J., 2012. Chronic Kidney Disease. Lancet, No. 379, p. 165-

180.

Lim, C. C., B. W. Peo, P. G. Ong, C. Y. Cheung, S. C. Lim, K. Y. Chow, C. C.

Meng, J. Lee, E. S. Tai, T. Y. Wong, C. Sabanayagam, 2014. Chronic

kidney disease, cardiovascular disease and mortality: A prospective cohort

study in a multi-ethnic Asian population. Eur J Prev Cardiol, p. 2-10.

Lim, L.M., Tsai, N.C.,Lin, M.Y., Hwang, D.Y., Lin, H.Y.H., Lee, J.J., Hwang,

S.J., Hung, C.C., Chen, H.C., 2016. Hyponatremia is Associated with Fluid

Imbalance and Adverse Renal Outcome in Chronic Kidney Disease Patients

Treated with Diuretics, Sci Rep, p. 1- 10.

Loho, I.K., Ramber, G.L., Woeow, M.F., 2016. Gambaran kadar ureum pada

pasien penyakit ginjal kronik stadium 5 non dialisis, Jurnal eBm, Vol. 4

No. 2, p. 1-6.

Mah, G.T., Tejani, A.M., Musini, V.M., 2009. Methyldopa for primary

hypertension, Cochrane Database of Systematic Review, Vol.4, p. 3-13.

Mallapallil, M., Friedman, E.A., Delano, B.G., McFarlane, S.I., Salifu, M.O.,

2014. Chronic kidney disease in the elderly: evaluation and management,

Clin Pract, Vol. 11 No.5, p. 525-535.

Mallat, S.G., 2012. What is preferred angiotensin II receptor blocker-based

combination therapy for blood pressure control in hypertensive patients with

diabetic and non-diabetic renal impairement?, Cardiovascular Diabetology,

Vol. 11 No. 32, p. 1-12.

Mandal, A.K., 2014. Effectiveness of Bumetanide Infusion in Treatment of

Generalized Edema and Congestive Heart Failure, Open Journal of

Internal Medicine, No. 4, p. 73-81.

Marieb, E.N., Hoehn, K., 2012. Human Anatomy and Phisiology 8th

edition.

California: Person Education Inc, p. 961.

Page 23: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

84

Martono, 2015. Penurunan Risiko Henti Jantung pada Asuhan Keperawatan

Pasien yang Dilakukan Hemodialisa Melalui Pengendalian Overload Cairan

Kalium Serum. Jurnal Terpadu Ilmu Kesehatan. 4 No. 1, p. 1-5.

Meola, M., Samoni, S., Petrucci, I., 2016. Imaging in Chronic Kidney Disease.

Contrib. Nephrol., No. 188, p. 69-80.

Mitsuyama, S.K., Ogawa, H., Matsui, K., Jinnouchi, T., Jinnouchi, H., Arakawa,

K., An angiotensin II receptor blocker-calcium channel blocker combination

prevents cardiovascular event in elderly high-risk hypertensive patients with

chronic kidney disease better than high-dose angiotensin II receptor

blockade alone, Kidney International, Vol. 83, p. 167-176.

Mok, 2012. Understanding lupus nephritis: diagnosis, management, and treatment

options. Int. J. Womens Health, p. 213-222.

Morton, R.L., Snelling, P., Webster, A.C., Rose, J., Masterson, R., Johnston,

D.W., Howard, K., 2012. Factors influencing patient choice of dialysis

versus conservative care to treat end-stage kidney disease, CMAJ,Vol.5 No.

184, p. 277-283.

Mozos, I., 2014. Laboratory Markers of Ventricular Arrythmia Risk in Renal

Failure, p.1-9

Muchtar, N.R., Tjitrosantoso, H., Bodhi, W., 2015. Studi penggunaan obat

antihipertensi pada pasien gagal ginjal kronik yang menjalani perawatan di

RSUP Prof. Dr. R. D. Kandou Manado, Jurnal Ilmiah Farmasi, Vol.4 No.

3, p. 2302-2493.

Nasir, K., Ahmad, A., 2014. Treatment of hyperkalemia in patients with chronic

kidney disease: a comparison of calcium polystyrene sulphonate and

sodium polystyrene sulphonate, J Ayub Med Coll Abbottabad, Vol 26 No.

4, p. 455-458.

NIDDK., 2015. Polycystic Kidney Disease. https://www.niddk.nih.gov/health-

information/kidney-disease/polycystic-kidney-disease, diakses tanggal 28

Desember 2016

NIDDK., 2014. Anemia in Chronic Kidney Disease.

https://www.niddk.nih.gov/health-information/kidney-disease/chronic-

kidney-disease-ckd/anemia, diakses tanggal 28 Desember 2016

NKF., 2004. Clinical Practice Guidelines on Hypertension and Antihypertensive

Agents in Chronic Kidney Disease.

http://www2.kidney.org/professionals/KDOQI/guidelines_bp/guide_7.htm,

diakses tanggal 1 Desember 2016.

Page 24: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

Novoa, J.M.L., Salgado, C.M., Pena, A.B.R., Hernandez, F. J.L., 2010. Common

Pathophisiological Mechanism of Chronic Kidney Disease: Thrapeutic

Perspective. Pharmacol. Ther., p. 61-81.

Nowling, T.K., Gilkeson, G.S., 2011. Mechanism of Tissue Injury in Lupus

Nephritis. Arthritis Res. Ther., Vol. 13 No. 250, p. 1-9.

Ogawa, H., Mitsuyama, S.K., Matsui,K.,Jinnouchi, T., Jinnouchi, H., Arakawa,

K., 2012. Angiotensin II receptor blocker-based therapy in Japanese elderly,

high-risk, hypertensive patients., Am J Med, Vol.125No. 10, p. 981-990.

Oh, S.W., Han, S.Y., 2015. Loop Diuretics in Clinical Practice. Electrolyte Blood

Press., p. 1-5.

Onuigbo, M..A.C., Agbasi, N., 2015. Diabetic Nephropathy and CKD-Analysis of

Individual Patient Serum Creatinine Trajectories: A Forgotten Diagnostic

Methodology for Diabetic CKD Prognostication and Prediction. J. Clin.

Med., Vol. 4, p. 1348-1368.

Orantes, C. M., R. Herrera, M. Almaguer, E. G. Brizuela, C. E. Hernandez, H.

Bayarre, J. C. Amaya, D. J. Calero, P. Orellana, R. M. Colindres, M. E.

Velazques, S. G. Nunez, V. M. Contreras, B. E. Castro, 2011. Chronic

Kidney Disease and Associated Risk Factors in the Bajo Lempa Region of

El Salvador: Nefrolempa Study, 2009. Medicc Rev., Vol. 13 No. 4, p. 14-

22.

Ortega, L.M., Arora, S., 2012. Metabolic acidosis and progression of chronic

kidney disease: incidence, pathogenesis, and therapeutic options.

Nephrologia, Vol. 6 No. 32, p. 724-730.

Parham, W.A., Mehdirad, A.A., Biermann, K.M., Fredman C.S., 2006.

Hyperkalemia revisited, Tex Heart Inst J, Vol 1 No. 33, p. 40-47.

PERNEFRI., 2014. Program Indonesia Renal Registry.

http://www.indonesianrenalregistry.org/data/INDONESIAN%20RENAL%2

0REGISTRY%202014.pdf, diakses pada 22 September 2016.

Phakdeekitcharoen, B., Boonyawat, K., 2012. The added-up albumin enhances the

diuretic effect of furosemide in patients with hypoalbuminemic chronic

kidney disease: a randomized controlled study. BMC Nephrol., Vol. 13 No.

92, p. 1-9.

Prodjosudjadi, W., 2014. Glumerulonefritis. In: Setiati, S., Alwi, I., Sudoyo, A.

W., Simadibrata, M., Setiyohadi, B., Syam, A.F.. Buku Ajar Ilmu

Penyakit Dalam Ed IV, Jakarta: InternaPublishing, p. 2072.

Page 25: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

86

Rhoades, R., Bell, D.R., 2009. Medical physiology Principle for Clinical

Medicine 3th

edition. London: Lippincot William &Walkins, Wolter

Kluwer, p. 392.

Riskesdas., 2013. Riset Kesehatan Dasar.

http://www.depkes.go.id/resources/download/general/Hasil%20Riskesdas%

202013.pdf, diakses tanggal 22 September 2016

Ritchling, N.H., Holzer, M., Herkner, H., Riedmuller, E., Havel, C., Kaff, A.,

Malzer, R., Schreiber, W., 2011. Randomized placebo controlled trial of

furosemide on subjective perception of dyspnoea in patient with pulmonary

oedema because of hypertensive crisis, Eur J Clin Invest, Vol.41 No. 6, p.

627-634.

Rule, A.D., Krambeck, A.E., Lieske, J.C., 2011. Chronic Kidney Dsease in

Kidney Stone Formers. Clin. J. Am. Soc. Nephrol., Vol. 6, p. 2069-2075.

Schena, F.P., 2011. Management of patients with chronic kidney disease, Intern

Emerg Med, Vol. 6 No. 1, p. 77-83.

Schrader, J., Salvetti, A., Calvo, C., Akpinar, E., Keeling, L., Weisskopf, M.,

Brunei, P., 2009. The combination of amlodipine/valsartan 5/150 mg

produces less peripheral oedema than amlodipin 10 mg in hypertnsive

patients not adequately controlled with amlodipin 5 mg, Int J Clin Pract,

Vol. 63 No.2, p. 217-225.

Sharma, S., Sharma, P., Tyler, L.N., 2011. Transfusion of Blood and Blood

Products: Indications and Complications, Am Fam Physician, Vol.6 No.

83, p. 719-724

Shemin, D., 2014. Anemia and Bone Disease of Chronic Kidney Disease:

Pathogenesis, Diagnosis, and Management. R. I. Med. J., p. 24-27.

SIGN, 2008. Diagnosis and management of chronic kidney disease :A national

clinical guideline. http://www.sign.ac.uk/pdf/sign103.pdf, diakses pada

tanggal 25 Desember 2016.

Sica, D. A., 2012. Diuretic use in renal disease. Nat. Rev. Nephrol., Vol. 8, p.

100-109.

Siswandono, 2008. Hubungan Struktur Aktifitas Senyawa Diuretika. In:

Siswandono, Soekardjo, B., Kimia Medisinal, Surabaya: Pusat Penerbitan

dan Percetakan Unair (AUP), p. 219.

Sja`bani, M., 2014. Batu Saluran Kemih. In: Setiati, S., Alwi, I., Sudoyo, A. W.,

Simadibrata, M., Setiyohadi, B., Syam, A.F,. Buku Ajar Ilmu Penyakit

Dalam Ed IV, Jakarta: InternaPublishing, p. 2121.

Page 26: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

Stamp, L.K., Barclay, M.L, O`Donnell, J.L., Zhang, M., Drake, J., Frampton, C.,

Chapman, P.T., 2012. Furosemide increases plasma oxypurinol without

lowering serum urate-a complex drug interaction: implications for clinical

practice. Rheumatology (Oxford), Vol. 9 No. 51, p. 1670-1676.

Stauffer, M.E., Fan, T., 2014. Prevalence of anemia in chronic kidney disease in

the united of state, PloS ONE, Vol. 9 No.1.

Sung, J., Jeong, J.K., Kwon, S.U., Won, K.H., Kim, B.J., Cho, B.R., Kim, M.K.,

Lee, S., Kim, H.J., Lim, S.H., Park, S.W., Park, J.E., 2016. Valsartan 160

mg/amlodipine 5 mg combination therapy versus amlodipine 10 mg in

hypertensive patients with inadequate respons to amlodipin 5 mg

monotherapy, Korean Circ J, Vol. 46 No.2, p. 222-228.

Susantitaphong, P., Sewaralthahab, K., Balk, E.M., Eiam-ong, S., Madias, N.E.,

Jaber, B.L., 2013. Efficacy and safety of combined vs single renin-

angiotensin-aldosterone system blockade in chronic kidney disease : A

Meta-Analysis, Am J Hypertens, Vol 26 No.3, p. 424-441.

Suwitra, K., 2014. Penyakit Ginjal Kronik. In: Setiati, S., Alwi, I., Sudoyo, A. W.,

Simadibrata, M., Setiyohadi, B., Syam, A.F., Buku Ajar Ilmu Penyakit

Dalam Ed IV, Jakarta: InternaPublishing, p. 2159.

Sweetman, S.C., 2009. Martindale The Complete Drug Reference 36th

Edition, London: Pharmaceutical Press, p. 1292.

Tai, R., Ohashi, Y., Mizuiri, S., Aikawa, A., Sakai, K., 2014. Association between

ratio of measured extracellular volume to expected body fluid volume and

renal outcomes in patients with chronic kidney disease: a retrospective

single-center cohort study. BMC Nephrology, Vol. 15 No. 189, p. 1-10.

Tedla, F.M., Brar, A., Browne, R., Brown, C., 2011. Hypertension in Chronic

KidneyDisease: Navigating the Evidence. Int. J. Hypertens., Vol. 2011, p.

1-10.

Thomas, J.R., Blanco, I., Putteerman, C., 2011. Urinary Biomarkers in Lupus

Nephritis. Clinic Rev. Allerg. Immunol, Vol 40, p 138-150.

Trinh, E., Bargman, J.M., 2016. Re Diuretics Underutillized in Dialysis Patients?.

Semin Dial, Vol. 29 No. 5, p.338-341.

Tjekyan, R.M.S., 2012. Prevalensi dan Faktor Risiko Penyakit Ginjal Kronik di

RSUP Dr. Mohammad Hoesin Palembang Tahun 2012. MKS, No. 4, p.

276-282

Trissel, L.A., 2009. Handbook on Injectable Drugs 15th Edition, United States

of America: American Society of Health-System Pharmacist.

Page 27: SKRIPSI - Universitas Muhammadiyah Malangeprints.umm.ac.id/42844/1/jiptummpp-gdl-desiimastu-48513-1-pendahul-n.pdf · hipertensi sebesar 75%, anemia 50%, hiperparatiroid, hiperfosfatemia,

88

Tylicki, L., Jakubowski, Lizakowsi, S., Swietlik, D., Rutkowski, B., 2015.

Management of renin angiotensin system blockade in patient with chronic

kidney disease under specialist care. Retrospective cross-sectional study,

jraas, Vol 16 No. 1, p.145-152.

Vazir, A., Cowie, M.R., 2013. The use of diuretics in acute eart failure: Evidence

based therapy?. World J. Cardiovasc. Dis., Vol. 3, p. 25-34.

Vongpatanasin, W., Kario, K., Atlas, S.A., Victor, R.G., 2011. Central

Simpatholitic Drugs, J Clin Hypertens, No. 13, p. 658-661.

Wang, W., Ma, L., Zhang, Y., Deng, Q., Liu, M., Liu, L., 2011. The combination

of amlodipine and angiotensin receptor blocker or diuretics in high-risk

hypertensive patients: rationale design and baseline characteristics, J Hum

Hypertens,Vol 25, p. 271-277

Wart, S.A.V., Shoaf, S.E., Mallikaarjun, S., Mager, D.E., 2014. Population-based

meta-analysis of furosemide pharmacokinetics. Biopharm. Drug Dispos.,

Vol. 35, p. 119-133.

Weber, M.A., Schiffrin, E.L., White, W.B., Mann, S., Lindholm, L.H., Kenerson,

J.G., Flack, J.M., Charter, B.L., Materson, B.J., Venkata, C., Cohen, D.L.,

Cadet, J.C., Charles, R.R.J., Taler, S., Kountz, D., Townsend, R.R.,

Chalmers, J., Ramirez, A.J., Bakris, G.L., Wang, J., Schutte, A.E.,

Bisognano, J.D., Touyz, R.M., Sica, D., Harrap, S.B., 2014. Clinical

Practice Guidelines for the Management of Hypertension in the Community

A Statement by the American Society of Hypertension and the International

Society of Hypertension. J Hypertens. Vol. 16, No. 1 1-13.

Weisberg, L.S., 2008. Management of severe hyperkalemia, Crit Care Med, Vol.

36, p. 3246-3251.

Wells, B.G., Dipiro, J.T., Schwinghammer, T.L., Dipiro, C.V., 2015.

Pharmacotheraphy Handbook, Ed 9th, United States of America:

McGrawHill Companies, Inc. p. 787.

Yang, F., Khin, L.W., Lau, T., Chua, H. R., Vathsala, A., Lee, E., Luo, N., 2015.

Hemodialysis versus Peritoneal Dialysis: A Comparison of Survival

Outcomes in South- East Asian Patients with End-Stage Renal Disease.

PLoS One, Vol 10 No. 10, p. 1-10.