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Nutritional Management

on Kidney Disease

Dr Haerani Rasyid , MS,SpPD ,K-GH


Nutrition Department/Nephrology Div
School of Medicine Hasanuddin University
Makassar 2010

Nutrition aspect in Urogenitalia system


Acute nephritis
Nephrotic syndrome
Asymptomatic urinary abnormalities
Acute renal failure
Chronic kidney disease
Urinary tract infection
Urinary tract obstruction
Nephrolithiasis
Hypertension
Renal tubular defects

Kidney Function
Bone
BoneStructure
Structure

Metabolic
Metabolic
End
EndProducts
Products

Blood
BloodFormation
Formation
Calcium
Balance

Vitamin D
Activation
Erythropoietin
Synthesis

Removal of
Urea, Creatinine etc.

Functions

Water Balance

Potassium
Balance
Recovery of
Bicarbonate
Cardiac
CardiacActivity
Activity

R E NAL ANAE M I A

Sodium
Removal
Regulation
RegulationofofBlood
BloodpH
pH

Blood
BloodPressure
Pressure

The role of nutritional support in kidney


disease :
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

Nutrition support in kidney disease


Energy
- 25-40 kcal/kg BW
- to avoid weight loss
Protein
- Renal disease proteinuria
- Uremia
- restricting protein intake
5

Lipids
- Aggressively lowering lipids profile (?)
Fluids and electrolytes
- Sodium (1-3g/day) and Water ( 500
ml+UO+IWL)
- Potassium Hyperkalemia (!)
- Phosporus, Calsium,magnesium
6

Vitamins (?)
- poor oral intake
- decrease renal reabsorption
- losses from dialysis
Trace elements
- iron deficiency ( poor oral intake/intestinal
absorption, laboratory, occult GIT 0
ERYTROPOIETIN
7

NEPHROTIC SYNDROM
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

1.

MAINTAIN OPTIMAL NUTRITION

2.

MAINTAIN NUTRITIONAL STORES

3.

MINIMIZE DISEASE METABOLISM

4.

PREVENT PROGRESSIVITAS OF DISEASE

5.

SLOW DIALYSIS OCCURANCE

10

GgGA

Penurunan fungsi ekskresi

Penurunan fungsi mendadak


Penurunan fungsi regulasi

Gangguan Metabolisme
Regulasi tekanan darah
Eskresi sisa
metabolisme
Keseimbangan elektrolit
Regulasi hormonal

akumulasi air
Elektrolit
toksin uremi

PERUBAHAN METABOLIK PADA GgGA

GgGA

Penurunan
ekskresi
Infeksi danfungsi
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

Keadaan
sakit kritis
GgGA
STRESS METABOLIK

Perlu energi lebih banyak


KOMPENSASI

Glikogenolisis
Glukoneogenesis
lipolisis

metabolisme Glukosa
resistensi insulin
hormon "antiinsulin"
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;25:295-3

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 GgGA (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 GgGA (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,2007:112-1

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 GgGA

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 GgGA 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 GgGA
Penentu utama dari morbiditas dan
mortalitas

PENATALAKSANAAN TERAPI NUTRISI PADA GgGA

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


GgGA 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 GgGA


(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;25:295-3

KEBUTUHAN NUTRIEN PASIEN AKI SELAMA CRRT


Micronutrient

Losses/24mea
n valuces

Daily PN,
recommended
intakes

Range of
doses
provided by
industrial PN
supplement1

Chromium
Copper
Selenium
Zinc
Vitamin B1
Vitamin C
Vitamin E

25 mol
0.41 mg
110 g
0.2 mg
4.1 mg
10 mg
ND

15 g
1.0-1.2 mg
60 g
6.5 mg
3 mg
100 mg
10 IU

10-15 g
0.48-1.3 mg
24-70 g
3.3-3.51 mg
3.0-3.51 mg
100-125 mg
10-10.2 IU

Chiolero, Acute Kidney Injury 2008:267-

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


GgGA
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 GgGA bergantung kepada :
Ada / tidak adanya komplikasi pd GgGA
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 GgGA adalah peningkatan survival

CHRONIC KIDNEY DISEASE


(PENYAKIT GINJAL KRONIK)

59

Diabetes
RISK FACTOR
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)

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./dayCr 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
1. ENERGY

OLIGOURIE
40-55 kcal/kg
(High in trauma)

2. CHO

DIURETIC
40-55 kcal/kg
(high in trauma)

50-70%

Need supplement

3. PROTEIN
0,5g/kg 80% HBV
0,8 g/ kg or more
1-1,5 g/kg dialysis If fasting
4. Fluid
+ 500 cc
increasing as needed
5. Na +
500-1000 mg/d
replace losses
6. K+
1000 mg/d
replace losses
7. Fat
= 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
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(Contd)

Slide 76

Kidney Stones
(Contd)

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Slide 77

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
RANDALLS 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
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)
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Slide 86

Examples of Food Sources of


Oxalates
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: cocoa, draft beer, tea
Other: grits, tofu, wheat germ
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Slide 87

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

THERAPY
Susunan Kimia
1. Calsium
Phospat
Oxalat
2. As. Urat
3. Cystine

Modifikasi zat Gizi

low calsium
low phospat
low oxalat
low purine
low methionine

Diet Ash

acid ash

alkaline ash
alkaline ash

91

VARIATION DIET
1. LOW CALCIUM HIGH ASH CAID
2. HIGH DIET ASH ALKALIS
3. LOW PURINE DIET

92

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 ???
93

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 94

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

95

Low-Calcium Diet

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Slide 96

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 97

LOW PURINE DIET

LIMIT FOOD SOURCES OF URIC


ACID
LOST WEIGHT TO IDEAL BODY
WEIGHT

98

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 99

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

100

General Dietary Principles: Kidney Stones

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Slide 101

Diet & Fluid Advice


High Fluid Intake
Restrict Salt (Na)
Oxalate Restrict
Avoid high intake of Purine food
Increased citrus fruits may help
RoleIfofhypercalciuria
restrict Ca intake
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 :
Apple Juice
Beer

High Amounts :

Cocoa

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 oxalatespinach, 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

109

Requirement
1. Low purin contain 120-150 mg
2. Adequate calorie, protein, mineral and
vitamin
3. High carbohydrate
4. Mild fat
5. High fluid

110

IMPORTANT !!

111

Penilaian Kebutuhan Kalori


Sangat sulit
BEE bisa meningkat
Estimasi BEE:
a. Indirect calorimetri
b. Harris Benedict equation
c. REE

112

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.

113

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]
114

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
N[g/hari] = [62.5/6.25] [10 + 4]
= 10 14
=-4

115

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
116
= 95.75 protein

Penilaian Kebutuhan Elektrolit


Monitor kadar elektrolit dalam darah
Na, K, Cl , HCO3, Ca
Monitor Blood gas

117

Thankyou for your attention