Professional Documents
Culture Documents
on Kidney Disease
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
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
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.
2.
3.
4.
5.
10
GgGA
Gangguan Metabolisme
Regulasi tekanan darah
Eskresi sisa
metabolisme
Keseimbangan elektrolit
Regulasi hormonal
akumulasi air
Elektrolit
toksin uremi
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
akumulasi air
Elektrolit
toksin uremi
perubahan metabolik
asidosis metabolik
perubahan respon
glikemik
Keadaan
sakit kritis
GgGA
STRESS METABOLIK
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
survival rate
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
Metabolisme lipid
kegagalan proses lipolisis
aktifitas lipoprotein lipase perifer dan
trigliserida lipase hepar
hipertrigliseridemia dan
penurunan kolesterol total serta
Penurunan kolesterol LDL
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
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
Subjective Global
Assessment (SGA)
Fiaccadori, J Nephrol 2008;21:645-656
cara pemberian
Jenis nutrien
Jumlah kebutuhan nutrisi
Pemilihan regimen terapi
Ada/tidak oliguria atau
anuria
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
Kebutuhan mikronutrien
Di ICU : formula enteral 1500 2000 kkal
Kebutuhan elektrolit cukup adekuat.
Monitor kadar elektrolit plasma :
cegah refeeding syndrome
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
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
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
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
Extent of Catabolism
Mild
Moderate
Severe
>5
5 10
> 10
Drug toxicity
Elective surgery
Mortality (S)
20
60
> 80
Dialysis/CRRT, frequency
Rare
As needed
Frequent
Oral
Enteral and / or
parenteral
Enteral/parenteral
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
TERAPI GIZI
PARENTERAL
NUTRITION
ENTERAL
NUTRITION
FOOD
FORTIFICATION
ORAL
NUTRITIONAL
SUPPLEMENT
ENTERAL
NUTRITION
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)
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
INDIKASI
TOTAL PN (TPN)
PERIPHERAL PN (PPN)
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
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
-
61
62
63
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.
3.
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
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
Mosby items and derived
items 2006 by Mosby, Inc.
(Contd)
Slide 76
Kidney Stones
(Contd)
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
80
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.
Slide 82
Slide 83
Risk Factors
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)
Mosby items and derived
Infection
items
2006
by Mosby, Inc.
Slide 86
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
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
Slide 89
Slide 90
THERAPY
Susunan Kimia
1. Calsium
Phospat
Oxalat
2. As. Urat
3. Cystine
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
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
Mosby items and derived
items 2006 by Mosby, Inc.
Slide 94
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
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
Mosby items and derived
items 2006 by Mosby, Inc.
Slide 97
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
Slide 99
100
Slide 101
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
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
112
113
A sup an Pr otein
[UUN 4]
6.25
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
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
117