Download Manajemen Nutrisi Pada Penyakit Ginjal

Manajemen Nutrisi
Pada Penyakit Ginjal
Sumber : Kuliah Gizi Nutritional Management on
Kidney Diseases by DR. dr. Haerani Rasyid, M.
Kes,SpPD ,K-GH, Sp.GK,Nutrition Department
/Nephrology Div School of Medicine Hasanuddin
University Makassar 2011
Tujuan Umum
• Mahasiswa mampu menjelaskan
manajemen nutris pada penyakit ginjal
Tujuan khusus
• Mahasiswa mampu menjelaskan
manajemen nutrisi pada penyakit Sindrom
Nefrotik, GGA, GGK, Batu Ginjal
Fungsi Ginjal
Bone Structure
Metabolic
End Products
Blood Formation
Calcium
Balance
Vitamin D
Activation
Erythropoietin
Synthesis
Removal of
Urea, Creatinine etc.
Functions
Water Balance
Potassium
Balance
Recovery of
Bicarbonate
Sodium
Removal
Cardiac Activity
Regulation of Blood pH
Blood Pressure
Peran nutrisi pada penyakit ginjal
• To prevent or reverse associated
malnourished states
• To minimize the adverse effect of
substances that are inadequately excreted
• Favorably affect the progression and
outcome of kidney disease
Dukungan nutrisi pada penyakit
ginjal
• Energy
- 25-40 kcal/kg BW
- to avoid weight loss
• Protein
- Renal disease  proteinuria
- Uremia
- restricting protein intake
• Lipids
- Aggressively lowering lipids profile (?)
• Fluids and electrolytes
- Sodium (1-3g/day) and Water ( 500
ml+UO+IWL)
- Potassium  Hyperkalemia (!)
- Phosporus, Calsium,magnesium
• Vitamins (?)
- poor oral intake
- decrease renal reabsorption
- losses from dialysis
• Trace elements
- iron deficiency ( poor oral intake/intestinal
absorption, laboratory, occult GIT 0 
ERYTROPOIETIN
Sindrom Nefrotik
• Patogenesis
• Loss of glom barrier to protein
• Hipoalbuminemia
• Hiperkolesterolemia
• Hiperkoaguability
• Abnormal bone metabolisme
• Causa:
• Primer
• Secunder
• CLINICAL SYMPTOM:
Oedem, hematuri,
proteinuria, hipoalbuminemia,
azotemia ( NH++ >>),
oligouri ( < 600cc).
• NUTRITION CARE
Energi
Range 35 – 60 /kg BB/hr
Protein
0,8 – 1 gr
Fat
Moderate
Na+
Moderate
K
Monitoring -hipokalemia
Goal
1. MAINTAIN OPTIMAL NUTRITION
2. MAINTAIN NUTRITIONAL STORES
3. MINIMIZE DISEASE METABOLISM
4. PREVENT PROGRESSIVITAS OF
DISEASE
5. SLOW DIALYSIS OCCURANCE
GGA
GGA
Penurunan
fungsi
mendadak
Penurunan
fungsi regulasi
Gangguan Metabolisme
Regulasi tekanan darah
Eskresi sisa metabolisme
Keseimbangan elektrolit
Regulasi hormonal
Penurunan fungsi
ekskresi
akumulasi air
Elektrolit
toksin uremi
PERUBAHAN METABOLIK PADA GGA
GGA
`
Penurunan
ekskresi
Infeksi
dan fungsi
penyembuhan
penurunan
fungsi
mendadak
Peningkatan produksi
Penurunan
fungsi regulasi
dan penurunan
klirens
sisa metabolik,
sitokin
protease dan hormone katabolik,
Gangguan transport oksigen dan
nutrient
Penurunan status nutrisi
Meningkatkan katabolisme
akumulasi air
Elektrolit
toksin uremi
perubahan metabolik
asidosis metabolik
perubahan respon glikemik
GGA
Keadaan sakit kritis
STRESS METABOLIK
Perlu energi lebih banyak
KOMPENSASI
Glikogenolisis
Glukoneogenesis
lipolisis
metabolisme Glukosa ↑
resistensi insulin, ↑
hormon "anti-insulin"
HIPERKATABOLISME
Glukcagon
Katekolamin
glukokartikoid
HIPERKATABOLISME
Gangguan Imunitas peningkatan katabolisme protein
Daya Tahan tubuh  keseimbangan nitrogen negatif
Infeksi
akumulasi toksin uremi.
survival rate
Metabolisme energi dan kebutuhan energi
• Metabolisme air, elektrolit dan asam basa,
 perubahan “milieu interieur” protein dan asam amino,
karbohidrat serta lipid.
• reaksi pro-inflamasi dan sistim antioksidasi.
• merupakan komplikasi dari sepsis, trauma atau kegagalan multi organ.
• Perubahan-perubahan metabolisme oleh penyakit yang mendasarinya
dan/atau disertai komplikasi
• adanya disfungsi organ lain
• ditentukan oleh tipe dan intensitas terapi pengganti ginjal
Chan, Curr Opin Clin Nutr Metab Care 2004:207
Metabolisme karbohidrat
• Terkait hiperglikemia
• Penyebab utama :
• resistensi insulin.
• peningkatan konsentrasi insulin plasma
dan aktivasi proses glukoneogenesis di
hepar terutama dari konversi pelepasan
asam amino selama katabolisme protein
Cano, Clin Nutrition 2006;25:295-310
Metabolisme lipid
kegagalan proses lipolisis
↓ aktifitas lipoprotein lipase perifer dan
trigliserida lipase hepar
• hipertrigliseridemia dan
• penurunan kolesterol total serta
• Penurunan kolesterol LDL
Cano, Clin Nutrition 2006;25:295-310
Metabolisme protein/asam amino
• aktivasi katabolisme protein,
• pelepasan asam amino yang berlebihan dari otot skelet dan
terjadi keseimbangan nitrogen negatif,
• peningkatan ekstraksi asam amino di hepar dari sirkulasi,
• peningkatan glukoneogenesis dan ureagenesis.
• Hati : sintesis protein
perangsangan sekresi protein fase akut.
plasma dan intra seluler :
perubahan metabolisme asam amino nonesensialesensial
klirens asam amino akan meningkat
Toigo,Clin Nutrition 2000;281
Faktor yang terlibat di dalam patogenesis
katabolisme protein pada GGA (1)
• Suplai nutrient tidak adekuat
• Toksin uremik
• Faktor endokrin :
• Resistensi insulin
• Peningkatan sekresi hormon katabolisme
• Resisten terhadap berkurangnya sekresi faktor
anabolik
Fiaccadori, J Nephrol 2008;21:645-656
Faktor yang terlibat di dalam patogenesis
katabolisme protein pada GGA (2)
• Sakit kritis/reaksi fase akut/respon inflamasi
sistemik (sitokin)
• Asidosis metabolik
• Protease (ubiquitin proteasome system)
• Kehilangan substrat nutrisi karena TPG
Fiaccadori, J Nephrol 2008;21:645-656
Kadar plasma asam amino rantai panjang (BCAA) menurun
 valline, leucine, dan iso leucine
• Asidosis :
menginduksi katabolisme BCAA
mengaktivasi ATP-ubiquetin-dependent
cytosolic proteolytic system,
 menginduksi proteolisis otot dan
 ↑ eksresi amonia di ginjal.
Leverve,Acute Kidney Injury,2007:112-118
• ↓ produksi : threonine, lysine, dan serine
• gangguan hidroksilasi phenyl alanin  kadar tyrosine
menurun
• Kadar Tryptopan menurun pada uremia
• ↑ glycine, citrolline, cystine, aspartate, methionine dan
metylhistidine
Leverve,Acute Kidney Injury,2007:112-118
Essential AA
Non-essential AA
Special AA
BCAA↓
valine ↓ ↓
leucine ↓
isoleucine ↓
threonine ↓
lysine ↓
serine ↓
decrease
production
oxidation in
muscles
metabolic
acidosis
glycine ↑
citruline ↑
cystine ↑
aspartate ↑
methionine ↑
methylhistidine
↑
KIDNEY
FAILURE
defective
phenylalanine
hydroxylation
tyrosine ↓
tryptophane ↓
arginine ↓
reduce
protein binding
Mitch WE. Handbook of Nutrition and the Kidney, 2005
Metabolisme mikronutrien
• Kadar vitamin yang larut dalam air berkurang  TPG
• kegagalan aktivasi vitamin D3
• ↓ kadar 25(OH)D3 dan 1,25-(OH)D3
 hiperparatiroidisme sekunder.
• ↓ kadar vitamin E dan vitamin A ,
• kadar vitamin K biasanya normal atau cenderung meningkat
MNT, Nephrol Nursing J 2007
Metabolisme trace elements
• tidak mengalami perubahan spesifik pada GgGA ,
• penurunan kadar konsentrasi selenium di plasma dan eritrosit .
• sakit kritis, pemberian selenium :
• memperbaiki outcome
• menurunkan insidensi kejadian GgGA yang memerlukan tindakan
TPG
MNT, Nephrol Nursing J 2007
PENGARUH TERAPI PENGGANTI GINJAL
(TPG) TERHADAP METABOLISME
Karena pemakaian yang berkesinambungan dan
adanya pergantian cairan yang tinggi (fluid
turnover),
terapi ini memberikan :
• pengaruh negatif terhadap
keseimbangan elektrolit dan nutrient.
• terdapat pembentukan reactive
oxygen species
Cano, Clin Nutrition 2006;25:295-3
STATUS NUTRISI PADA AKI
• Penderita sakit kritis dengan AKI  potensi
kehilangan nutrien
• Evaluasi status nutrisi sulit  perubahan di dalam
komposisi tubuh
• Protein Energy Wasting (PEW)
Fiaccadori, J Nephrol 2008;21:645-656
PENILAIAN STATUS NUTRISI
•
•
•
•
Biokimia (albumin dan prealbumin)
↓ berat badan
↓ massa otot
↓ asupan energi dan protein
Subjective Global
Assessment (SGA)
Fiaccadori, J Nephrol 2008;21:645-656
TUJUAN TERAPI NUTRISI PADA GGA
Mempertahankan status nutrisi optimal
Mencegah PEW
Menghindari kelainan metabolisme lebih
lanjut
Memperbaiki fungsi imun
Mengurangi akumulasi toksin uremia
Keseimbangan
nitrogen
Pemilihan jenis dan dosis nutrien
Pemberian Nutrisi GGA tergantung:
•
•
•
•
•
•
•
Ada / tidak adanya komplikasi pd GgGA
Kelainan Metabolisme karbohidrat
Kelainan Metabolisme Lipid
Kelainan Metabolisme Asam amino
Metabolisme mikronutrien
Metabolisme trace elements
TPG
Asupan nutrient yang optimal ditentukan oleh:
- tingkat keparahan penyakit yang mendasarinya
- komplikasi yang terjadi,
- tingkat katabolisme,
- status nutrisi
- tipe dan frekuensi TPG
Nutrisi yang tidak adekuat :
Kontribusi dalam hilangnya massa tubuh
pada GGA
Penentu utama dari morbiditas dan
mortalitas
PENATALAKSANAAN TERAPI NUTRISI PADA GGA
mengatasi gangguan fungsi ekskresi ginjal dan kelainan metabolisme
beserta komplikasinya
• cara pemberian
•Jenis nutrien
•Jumlah kebutuhan nutrisi
•Pemilihan regimen terapi
•Ada/tidak oliguria atau
anuria
JENIS DAN JUMLAH KEBUTUHAN NUTRISI
PADA GgGA
Kebutuhan energi / kalori
• GGA tanpa komplikasi, konsumsi oksigen sama dengan subjek yang sehat,
• adanya sepsis atau disfungsi multi organ terjadi peningkatan sekitar 25%.
• Ekspenditur energi ditentukan oleh penyakit yang mendasarinya tidak oleh
gagal ginjal
• Pemberian kalori adekuat sangat penting
 keseimbangan nitrogen menjadi positif.
MNT, Nephrol Nursing J 2007
•
•
•
•
Komplikasi : overfeeding dibandingkan underfeeding
Sebaiknya : 20 sampai 30 kkal/kg BB/hari
GgGA ringan : 35 kkal/kg BB/hari
hipermetabolik :
ekspenditur energi jarang melebihi 130%
asupan energi tidak melebihi 30 kkal/kg BB/hari
• gangguan respirasi ( respiratory distress) + ventilator :  25 kkal/kg
BB/hari
• Pada keadaan GgGA : jumlah cairan perlu di batasi
 produksi urine yang rendah.
• pemilihan sumber kalori harus hemat cairan misalnya :
• glukosa hipertonis (70% dextrose)
• infus lipid (20%)
• asam amino (10-15%)
Kebutuhan asam amino/protein
• GgGA ringan (risk) tanpa katabolik :
tidak kurang dari 0,8 gr/kg BB/hari
• GgGA + TPG intermiten (IHD) :
minimum 1,2 gr/kg BB/hari
• GgGA + Sakit kritis + TPG (CRRT) diperkirakan :
• protein catabolic rate (PCR) mencapai 1,5-1,7 gr/kg
BB/hari,
• asam amino/protein : 1,4-1,7 gr/kg BB/hari
• Dapat > tinggi : 2,5 gr/kg BB/hari (kontroversi )
Kebutuhan lipid
• Kalori dari lipid : 20-35% kalori total
• Pemberian parenteral 0,8 -1,2 g/kg bb/hari
 10 – 30% emulsi lipid
• Pemeriksaan kadar trigliserida
Fiaccadori, J Nephrol 2008;21:645-656
Kebutuhan mikronutrien
Di ICU : formula enteral 1500 – 2000 kkal
 Kebutuhan elektrolit cukup adekuat.
Monitor kadar elektrolit plasma :
 cegah refeeding syndrome
Fiaccadori, J Nephrol 2008;21:645-656
SODIUM :
• infus NaCl 0.45%
• Pada diet rendah sodium : NaCl 2 - 4 gram/hari.
• kecenderungan terjadi asidosis metabolik : konsentrasi bikarbonat
plasma dipertahankan > 20 mmol/l  diberikan 2 - 4 gram tablet Natrium
bikarbonat
MNT, Nephrol Nursing J 2007
KALIUM
• GFR < 15 ml/menit : 30 - 70 mEq/hari.
• Bila kadar kalium > 6.5 mmol/liter
Hindari asupan nutrisi yang mengandung banyak kalium.
 pemberian "potassium binding anion exchenge resins".
• Bahan makanan harus selektif
• Regimen terapi nutrisi parenteral
 monitor ketat pemberian cairan mengandung
kalium
MNT, Nephrol Nursing J 2007
VITAMIN
• defisiensi vitamin dan zat besi.
• Defisiensi asam folat, piridoksin, vitamin C ,B
complex  paling sering terjadi
• ↓kadar vit. D
• Vitamin K tidak membutuhkan suplementasi.
• ↑kadar vitamin A
MNT, Nephrol Nursing J 2007
• VITAMIN DAN MINERAL 100% DARI
RECOMMENDED DAILY ALLOWANCE
(RDA)
• IMMUNE MODULATING FORMULAE:
• ARGININ, GLUTAMINE, NUKLEOTIDA
• ANTIOKSIDAN, EPA, GLA
KEBUTUHAN NUTRISI PADA
PENDERITA GGA (ESPEN)
•
•
•
•
Energi
20-30 kkal/kg bb/hr
Karbohidrat
3-5 (maks 7) gr/kg bb/hr
Lemak
0,8-1,2 (maks 1,5) gr/kg bb/hr
Protein (asam amino esensial dan non-esensial)
Terapi konservatif 0,6-0,8 (maks 1,0) gr/kg bb/hr
TPG (CRRT/SLED)
1,0-1,5 gr/kgBB/hari
TPG (CRRT/SLED)
+hiperkatabolisme
maks 1,7 gr/kg BB/hari
Cano, Clin Nutrition 2006;25:295-310
KEBUTUHAN NUTRIEN PASIEN AKI SELAMA CRRT
Micronutrient
Losses/24mean Daily PN,
valuces
recommended
intakes
Range of
doses
provided by
industrial PN
supplement1
Chromium
Copper
Selenium
Zinc
Vitamin B1
Vitamin C
Vitamin E
25 μmol
0.41 mg
110 μg
0.2 mg
4.1 mg
10 mg
ND
10-15 μg
0.48-1.3 mg
24-70 μg
3.3-3.51 mg
3.0-3.51 mg
100-125 mg
10-10.2 IU
15 μg
1.0-1.2 mg
60 μg
6.5 mg
3 mg
100 mg
10 IU
Chiolero, Acute Kidney Injury 2008:267-274
Extent of Catabolism
Mild
Moderate
Severe
Excess urea appearance above
nitrogen intake (g)
>5
5 – 10
> 10
Clinical setting (examples)
Drug toxicity
Elective surgery
Sepsis ARDS, MODS
Mortality (S)
20
60
> 80
Dialysis/CRRT, frequency
Rare
As needed
Frequent
Route of nutrien administration
Oral
Enteral and / or
parenteral
Enteral/parenteral
Energy recommendation (kcal/kg
body weight/day
20-25
20-25
25-30
Energy subtrates
Glucose (g/kg bw/day)
Fat (g/kg bw/day)
Amino acidas/protein (g/kg/day)
Glucose
3.0-5.0
Glucose + fat
3.0-5.0
0.6-1.0
0.8-1.2
EAA + NEAA
Glucose + fat
3.0-5.0
0.8-1.2
1.0-1.5
EAA + NEAA
Enteral formulas
glucose 50-70%
lipid 10-20%
AA 6.5%-10%
micronutrients
Enteral formulas
glucose 50-70%
lipid 10-20%
AA 6.5%-10%
Micronutrients
Nutrient used
Oral/enteral
Parenteral
0.6-1.0
EAA(+NEAA)
Food
Druml, J of Ren Nutrition 2005;15:63-70
CARA PEMBERIAN TERAPI NUTRISI PADA
GGA
Secara Oral
Nutrisi Enteral (tube feeding)
Nutrisi Parenteral (NPE)
TERAPI GIZI
PARENTERAL
NUTRITION
ENTERAL
NUTRITION
FOOD
FORTIFICATION
ORAL
NUTRITIONAL
SUPPLEMENT
ENTERAL
NUTRITION
Fig. 1 - Decision tree for nutritional support in acute kidney injury
(AKI) patients with protein-energy wasting (PEW) or at risk of PEW.
GI = gastrointestinal.
Normal GI tract function
?
YES
NO
Enteral
feeding
Are nutritional
goals
achieved?
YES
Parenteral feeding
NO
Integratio
n with
parenteral
feeding
Peripheral
(shortterm with
or without
fluid
restriction
Central
(longterm, fluid
restriction
,
catabolis
Fiaccadori, J Nephrol 2008;21:645-656
m)
Terapi Nutrisi Secara Oral
pilihan pertama,
• penderita GgGA tanpa hiperkatabolik (kelompok 1).
• Awal : 40 gram protein (0.6 gr/kg BB/hari)
• Secara bertahap dinaikkan menjadi 0.8 gr / kg BB/hari jika kadar
ureum < 100 mg/dL.
hemodialisis atau dialysis peritoneal :
• protein sebaiknya dinaikkan menjadi 1,0-1,4 gr/kg BB/hari
Druml, J of Ren Nutrition 2005;15:63-70
Nutrisi Enteral (tube feeding)
• Sakit kritis
Keuntungan :
- mempertahankan fungsi gastro intestinal
khususnya fungsi barier dari mukosa intestinal.
- dapat menambah aliran plasma renal dan
memperbaiki fungsi ginjal.
• Memperbaiki prognosis
Druml, J of Ren Nutrition 2005;15:63-70
CARA PEMBERIAN EN
• KONTINYU:
•
•
10-25 mL/jam untuk12 jam pertama, dapat ditingkatkan
menjadi 50 mL/jam 12 jam kedua
Hari pertama1000 mL selama 24 jam, hari kedua 1500
mL selama 24 jam, hari ketiga sesuai kebutuhan
• INTERMITEN: 250-500 mL SETIAP KALI
PEMBERIAN, DIBERIKAN SELAMA 30-60
MENIT, 5-8 KALI SEHARI
Nutrisi Parenteral (NPE)
• sakit kritis :
sering disertai dengan keluhan gastrointestinal seperti mual dan
muntah,perdarahan SMBA
• kombinasi NPE dengan enteral atau oral
• Komposisi larutan nutrisi parenteral : glukosa, emulsi lipid, asam
amino
Druml, J of Ren Nutrition 2005;15:63-70
INDIKASI
•
•
•
•
NUTRISI ORAL/ENTERAL INADEKUAT SELAMA 7-10
HARI
GIZI BURUK, NUTRISI ORAL/ENTERAL INADEKUAT
SELAMA 3-5 HARI
HEMODINAMIK STABIL
SALURAN CERNA TIDAK BERFUNGSI ATAU HARUS
DIISTIRAHATKAN
TOTAL PN (TPN)
•
•
•
AKSES VENA SENTRAL
VOLUME & KONSENTRASI TINGGI
KEBUTUHAN ENERGI TINGGI
PERIPHERAL PN (PPN)
•
•
•
•
OSMOLARITAS ≤900 mOsml
PEMBERIAN JANGKA PENDEK: 7-10 HARI
KEBUTUHAN ENERGI TIDAK TINGGI
TIDAK ADA RESTRIKSI CAIRAN
Ringkasan
Terapi nutrisi rasional pd GGA bergantung kepada :
Ada / tidak adanya komplikasi pd GGA
Kelainan Metabolisme karbohidrat
Kelainan Metabolisme Lipid
Kelainan Metabolisme Asam amino
Metabolisme mikronutrien dan trace elements
TPG
Seleksi penderita
Cara pemberian dan komposisi nutrien
Tujuan terapi nutrisi pada GGA adalah peningkatan survival
CHRONIC KIDNEY DISEASE
(PENYAKIT GINJAL KRONIK)
59
Diabetes
• Hypertension
• Autoimmune diseases
• Systemic infections
• Exposure to drugs or procedures associated with acute
decline in kidney function
• Recovery from acute kidney failure
• Age > 60 years
• Family history of kidney disease
• Reduced kidney mass (includes kidney donors and
transplant recipients)
RISK FACTOR
60
Clinical symptom
-
Central nervous system
Ophtamic changes
Gastrointestinal
Dermatological
Cardiovascular system
Haematogical system
Respiratory system
Renal Osteodystrophy
61
Medical nutrition therapy
GOAL
1. ADEQUATE FOOD, NOT MAKE HEAVIER RENAL
FUNCTION
2. DECREASED OF UREUM & CREATININ LEVEL
3. MINIMIZED SALT RETENSION
REQUIREMENT
1. Low protein High Biologi value of Protein
2. Limitation of Salt ( Heavy HT, >> K, edema, Oligo /anurie)
3. Limitation of K (Glom function or prod urine << 400 cc)
4. Adequate food
5. >> fluid
62
VERY LOW PROTEIN  NEED KETO ACID
ANALOGUES
These agent are transaminated in the liver by non essential
amino acids to the corresponding essential amino acids
which are then use for protein synthesis
63
Keto acid supplemented protein
restriction diet should play a principle
role in the treatment of patients with
CKD because such diets
1. Improve symptomes
2. Maintains a good nutritional state
3. Limits proteinuria
4. Can delay the time until renal
replacement therapy is needed.
Specific International Guidelines &
Recommendation s for keto acid therapy
• Low protein diet (0.6-07 g/Kg b.w./dayCr Cl 50
ml/min/1.73 m2)
• Keto acid therapy indicated 20-25 ml/min/1.73 m2)
• Low protein diet +keto acid 0.4-0.6 gr/kg b.w./day
• Dosage of keto acid 0.1 gr/kg bw/day
• Daily energy intake of 35 kcal/kgb.w./day should be
recommended
• Protein calories must be replaced by complex CH
calories-not by lipid
Am J Nephrol 2005;25(suppl1):1-28
Aims of Dietary protein restriction :
• To slow the progression of kidney disease
• Minimize accumulation of uremic toxins
• Preserve protein nutritional status
• CKD stages 1-3 (GFR > 30 mL/min) :
- Protein 0.75 g/kg/d
• CKD stages 4-5 (GFR < 30 mL/min) :
- Protein 0.6 g/kg/d
MONITORING PROTEIN HOMEOSTASIS
1.
Based on renal damaged
indicator  higher / lower of muscle mass loss
2. Creatinine clearance
Gfr renal damaged– low creatinin clearance pada renal failure level of
creatine serum –high
3. SUN (SERUM UREA NITROGEN) OR BUN – indicator of renal function
Stabil  PROTEIN DIET
SUN increased  increased PROTEIN INTAKE.
Dehidrasion / catabolic state ( operasi, burn, infection, fracture  drug
catabolic: steroid
LEVEL 60- 80 mg/dl
 ACCEPTABLE
> 80
 uremia
< 40
 malnutrisi
4. Urea clearance  filtration capability
67
NUTRITION CARE
NUTRIENT
OLIGOURIE
DIURETIC
1. ENERGY
40-55 kcal/kg
40-55 kcal/kg
(High in trauma)
(high in trauma)
2. CHO
3. PROTEIN
4.
5.
6.
7.
Fluid
Na +
K+
Fat
50-70%
-
Need supplement
-
0,5g/kg 80% HBV
0,8 g/ kg or more
1-1,5 g/kg  dialysis If fasting
+ 500 cc
increasing as needed
500-1000 mg/d
replace losses
1000 mg/d
replace losses
= dialysis
= dialysis
68
OPTIONS- THERAPY OF ESRD
1.
CONSERVATIF MANAGEMENT
2.
DIALYSIS
A. HEMODIALISIS
B. PERITONEAL-DIALISIS
3.
TRANSPLANT
69
KONSERVATIF MANAGEMENT
1.
LIMITATION SYMPTOM
2.
PREVENT IRREVERSIBLE RENAL
DAMAGED
3.
MAINTAIN OF HEALTH BEFORE
DIALYSIS OR TRANSPLANTASION
70
TYPE OF DIALYSIS
A. HEMODIALYS
BY MACHINE ( venous )
3-4 hours /d, 3 – 4 x week
B. PERITONEAL DIALYSIS
Intermittent ( IPD)
Continous ambulatory ( CAPD)
Continous Cyclic
71
NUTRITION MANAGEMENT ON
RENAL TRANSPLANTASION
1. ADEQUATE FOOD
2. CHO 40 –50 % FROM TOTAL CALORIES
3. PROTEIN 1.2- 1.5 gr ADJUST TO NORMAL LEVEL (LAB
AND ELECKTROLYT BALANCE)
4. LIMITATION OF Na+ 2 - 4 gr / day
5. K+ AS NEEDED
72
KIDNEY STONES
 This disease is not
transmittable.
 Kidney stones can develop
when certain chemicals in
urine form crystals that
stick together.
 Stones may also develop
from a persistent kidney
infection.
 Drinking small amounts of
fluids.
 More frequent in hot
weather
Kidney stones cause pain when
they pass down the ureters to the
bladder and urethra
Based on: Mader, S., Inquiry Into Life, McGraw-Hill
• Increased risk : Low urine volume, oxalate,
uric acid, Sodium, acid PH, stasis, Calsium
• Decreased risk : High urine volume and
flow, citrate, glycoproteins, magnesium
75
Kidney Stones
• Basic cause is unknown
• Factors relating to urine or urinary tract
environment contribute to formation
• Present in 5% of U.S. women and 12% of
U.S. men
• Major stones are formed from one of three
substances:
• Calcium
• Struvite
• Uric acid
(Cont’d…)
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Slide 76
Kidney Stones
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Slide 77
(…Cont’d)
A. ENVIRONMENTAL FACTOR
1. CALSIUM ( 96%)
N  eksresi 100 –175 mg
hipersecresion  : high intake Ca, high Vit.D
long imobilisasion, hiperparathyroid
renal tubular asidosis, high calsiurie
idiopatik
Dietary factors associated with risk of calsium stones :
Increased risk ( animal protein, oxalate, sodium )
Decreased risk ( calsium, potassium, Magnesium, fluid
intake
2. CYSTEIN ( herediter )
homozygous cystinuria
78
Others :
- Urid acid
End product of purin metabolism
- Struvite
Magnesium ammonium phosphate,
carbonate apatite  Triple phosphate or
Infection stones
79
B. TRACTUS UROGENITAL
• CHANGED OF URINE PHYSICALLY
• CHANGED OF URINE CONCENTRATION
• CHANGED OF URINE BALANCED
80
C. MATRIX BATU ORGANIK
• RECURRENT INFECTION
• DEFICIENCY OF VITAMIN A
( DESQUAMATION OF CEL EPITHEL)
• DOT CALCIFICATION
RANDALL’S PLAQUE
81
Key Concepts
• Renal disease interferes with the normal
capacity of nephrons to filter waste
products of body metabolism.
• Short-term renal disease requires basic
nutritional support for healing rather than
dietary restriction.
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Slide 82
Dual Role of the Kidneys
• Kidneys make urine, through which they
excrete most of the waste products of
metabolism.
• Kidneys control the concentrations of most
constituents of body fluids, especially
blood.
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Slide 83
Treatments for Kidney Stones
• Small stones may pass with no pain
• Larger stones may pass but cause extreme of
pain, requiring a lot pain medication
• Stones that are too large to pass may require
surgical treatment including:
• using a ureteroscope to go up and snare the
stone
• using a nephroscope to crush the stone and
retrieve it
• using shock wave lithotripsy where a person
is submerged in water containing shock
waves to pulverize the stones
Risk Factors
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Slide 85
Calcium Stones
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• 70%-80% of kidney stones are composed
of calcium oxalate
• Almost half result from genetic
predisposition
• Other causes:
• Excess calcium in blood
(hypercalcemia) or urine
(hypercalciuria)
• Excess oxalate in urine (hyperoxaluria)
• Low levels of citrate in urine
(hypocitraturia)
• Infection
Slide 86
Examples of Food Sources of
Oxalates
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• Fruits: berries, Concord grapes,
currants, figs, fruit cocktail, plums,
rhubarb, tangerines
• Vegetables: baked/green/wax
beans, beet/collard greens, beets,
celery, Swiss chard, chives,
eggplant, endive, kale, okra, green
peppers, spinach, sweet potatoes,
tomatoes
• Nuts: almonds, cashews,
peanuts/peanut butter
• Beverages:
Slide 87 cocoa, draft beer, tea
Struvite Stones
• Composed of magnesium ammonium
phosphate
• Mainly caused by urinary tract infections
rather than specific nutrient
• No diet therapy is involved
• Usually removed surgically
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Slide 88
Other Stones
• Cystine stones
• Caused by genetic metabolic defect
• Occur rarely
• Xanthine stones
• Associated with treatment for gout and
family history of gout
• Occur rarely
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Slide 89
Kidney Stones: Symptoms and
Treatment
• Clinical symptoms: severe pain, other
urinary symptoms, general weakness, and
fever
• Several considerations for treatment
• Fluid intake to prevent accumulation of
materials
• Dietary control of stone constituents
• Achievement of desired pH of urine via
medication
• Use of binding agents to prevent absorption of
stone elements
• Drug therapy in combination with diet therapy
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Slide 90
VARIATION DIET
1. LOW CALCIUM HIGH ASH CAID
2. HIGH DIET ASH ALKALIS
3. LOW PURINE DIET
91
Acid ash and alkaline ash diet
• Dietary intake can influence the acidity or
alkalinity of the urine
• The acid forming : chloride, phosphorus,
sulfur ( high protein food, breads, cereal )
• The base forming : sodium, potassium,
calsium, magnesium ( Fruit, vegetables )
MILK ???
92
Nutrition Therapy:
Calcium Stones
• Low-calcium diet (approx. 400 mg/day)
recommended for those with
supersaturation of calcium in the urine and
who are not at risk for bone loss
• If stone is calcium phosphate, sources of
phosphorus (meats, legumes, nuts) are
controlled
• Fluid intake increased
• Sodium intake decreased
• Fiber foods high in phytates increased
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Slide 93
LOW CALCIUM DIET HIGH ASH ACID
• FLUID >
2500 cc/day
• Low calcium
• Limitation food intake contains:
PROTEIN : milk, cheese, schrimp, crab, rilis, salt fish, sarden,
animal brain, ren, liver, cor
CHO
: potatoes, sweet potatoes, cassava, biscuit, cake
contain milk
VEGETABLE : Spinach, mangkok leaf, melinjo leaf, papaya
leaf, lamtoro leaf, cassava leaf, talas (taro) leaf,
d.katuk leaf, kelor leaf, jtg pisang, melinjo, sawi,
leunca
FRUITS
: All Fermented Fruits
OTHERS : SOFT DRINK contains soda, alcohol, coclate, yeast
94
Low-Calcium Diet
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Slide 95
Nutrition Therapy:
Uric Acid Stones
• Low-purine diet sometimes recommended
• Avoid:
• Organ meats
• Alcohol
• Anchovies, sardines
• Yeast
• Legumes, mushrooms, spinach,
asparagus, cauliflower
• Poultry
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Slide 96
LOW PURINE DIET
LIMIT FOOD SOURCES OF URIC
ACID
LOST WEIGHT TO IDEAL BODY
WEIGHT
97
Nutrition Therapy:
Cystine Stones
• Low-methionine diet (essentially a lowprotein diet) sometimes recommended
• In children, a regular diet to support growth
is recommended
• Medical drug therapy is used to control
infection or produce more alkaline urine
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Slide 98
HIGH DIET ASH ALKALIS
Especially for Cysteine stone and Uric acid
1. Fluid > 2500 cc/day
2. Low AA (contain Sulfur)
3. Vegetables < 300 gr/day
4. Fruit < 300 gr/day
99
General Dietary Principles: Kidney Stones
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Slide 100
Diet & Fluid Advice
• High Fluid Intake
• Restrict Salt (Na)
• Oxalate Restrict
• Avoid high intake of Purine food
• Increased citrus fruits may help
• If hypercalciuria restrict Ca intake
Role of Potassium Citrate in preventing Cal Oxalate stone ds – KCit
lowers urinary calcium whereas Na Citrate does not lower Calcium due
to Sodium load
LIQUIDS
Moderate Amounts :
High Amounts :
Apple Juice
Cocoa
Beer
Fresh Tea
Coffee
Cola
FOODS :
Almonds, Asparagus, Cashew Nuts, Currants, Greens,
Plums, Raspberries, Spinach
General measures to prevent
recurrent stone formation
• Increase fluid intake to maintain urine output of 2-3
l/day:  increase in urine sodium as a result of increased
sodium intake. (Higher fluid intake alone will not prevent
recurrent stones in patients with hypercalciuria)
• Decrease intake of animal protein ( ≤ 52 g/day): Reduces
production of metabolic acids, resulting in a lower level of
acid induced calcium excretion; increases excretion of
citrate that forms a soluble complex with calcium; and
reduces supersaturation with respect to calcium oxalate
and limits the excretion of uric acid
• Restrict salt intake ( ≤ 50 mmol/day of sodium
chloride): Dietary and urinary sodium is directly
correlated with urinary calcium excretion, and lower
urinary excretion of sodium reduces urinary calcium
excretion
• Normal calcium intake ( ≥ 30 mmol/day): Low calcium
diets increase urinary oxalate excretion, which may
result in more stone formation and possibly a negative
calcium balance
• Decrease dietary oxalate: Reduce the intake of foods
rich in oxalate—spinach, rhubarb, chocolate, and nuts
• Cranberry juice: Decreases oxalate and phosphate
excretion and increases citrate excretion
Low
Purin
Diet
*
Goal :
1. Eliminate uric acid development
2. Lost weight ----obese or maintain ideal
body weight or normal weight
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Requirement
1.
2.
3.
4.
5.
Low purin contain 120-150 mg
Adequate calorie, protein, mineral and vitamin
High carbohydrate
Mild fat
High fluid
109
IMPORTANT !!
110
Penilaian Kebutuhan Kalori
• Sangat sulit
• BEE bisa meningkat
• Estimasi BEE:
a. Indirect calorimetri
b. Harris Benedict equation
c. REE
111
Penilaian Kebutuhan Protein
Ekskresi nitrogen 
Anjuran 1.5 – 2.2 g/kgBB/hari secara bertahap
Pemantauan: NUU dan kreatinin urin
Monitor: fungsi ginjal (ureum & kreatinin); fungsi
hepar.
• BCAA dapat dipertimbangan
• Serum albumin dipertahankan diatas 2.2 g/dL.
•
•
•
•
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Cara menghitung kebutuhan nitrogen
1. Berdasarkan sekresi urea pada urine [urinary urea
nitrogen = UUN] Untuk ini dibutuhkan urine tampung 24
jam. Langkah2 yang harus dilakukan:
•
•
Ukur UUN 24 jam
Hitung total UUN dengan menggunakan rumus:
totalUUN 
•
•
[UUN ][Vol.Urine]
100
Hitung asupan protein penderita/hari
Hitung nitrogen balans dengan menggunakan rumus:
N [ g / hari ] 
A sup an Pr otein
 [UUN  4]
6.25
Keterangan: asupan protein yang dikonversi ke Nitrogen = 6.25
UUN = 4 gr [rata-rata nitrogen yang dikeluarkan melalui urine]
113
Contoh:
Seorang penderita yang mempunyai asupan protein
62.5 g/hari sekresi urin 500 mg/dl UUN dalam 2000
ml urine
Maka:
UUN = 500 x 2000/100
= 10.000 mg atau 10 gr
ΔN[g/hari] = [62.5/6.25] – [10 + 4]
= 10 – 14
=-4
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2. Berdasarkan kebutuhan energi penderita:
• tentukan kebutuhan energi penderita dalam sehari
• Perkirakan ratio energi dan nitrogen, hal ini bervariasi
tergantung kondisi penderita. Dapat digunakan 1:150
untuk proses anabolisme dan atau 1:200 untuk
maintenance
• Hitung kebutuhan nitrogen dengan menggunakan rumus:
KebutuhanN[ g ] 
Kcal
Kcal : Nratio
Contoh:
Diasumsikan kebutuhan energi penderita sehari=2250
kcal, dan ratio kcal nitrogen 1:150, maka kebutuhan
nitrogen penderita tersebut adalah:
2250
N[ g ] 
 15 gNitrogen
150
• Dengan menggunakan hasil tersebut di atas dapat
ditentukan kebutuhan protein:
Pro[g] = Nitrogen [g] x 6.25
= 15 x 6.25
= 95.75 protein
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Penilaian Kebutuhan Elektrolit
• Monitor kadar elektrolit
dalam darah
Na, K, Cl ,
HCO3, Ca
• Monitor Blood gas
116