NUTRITIONAL ASPECTS

OF UROGENITAL
DISEASES

ARYANTI R. BAMAHRY
FK-UMI
2015

Kidney Function
Metabolic
Metabolic
End
EndProducts
Products

Bone
BoneStructure
Structure
Blood
BloodFormation
Formation
Calcium
Balance

Vitamin D
Activation
Erythropoietin
Synthesis

Removal of
Urea, Creatinine etc.

Water Balance
Potassium
Balance
Recovery of
Bicarbonate
Cardiac
CardiacActivity
Activity

Sodium
Removal
Regulation
RegulationofofBlood
BloodpH
pH

Blood
BloodPressure
Pressure

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

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/kgBW/d
- to avoid weight loss
Protein
- Renal disease proteinuria
- Uremia
restricting protein intake

Lipids
- Aggressively lowering lipids profile (?)
Fluids and electrolytes
- Water (500-600 ml +Urine Output)
- Sodium (1-3g/day)
- Potassium Hyperkalemia (!)
- Phosporus, calsium, magnesium

Vitamins
- poor oral intake
- decrease renal reabsorption
- losses from dialysis
Trace elements
- iron deficiency (poor oral intake/intestinal
absorption ERYTROPOIETIN

NEPHROTIC SYNDROME
An abnormal condition that is marked by deficiency of
albumin in the blood and its excretion in the urine due
to altered permeability of the glomerular basement
membranes.
CLINICAL SYMPTOMS :

Proteinuria > 3.5 g/day

Hyperlipidemia
Hypoalbuminemia (<3.5 g/dL)
Edema
Hiperkoagulability
Oligouria ( < 400cc)
Glomerular Diseases. Kidney Harrison.

NUTRITION THERAPY
GOAL :
Minimizing the effects of edema, proteinuria
& hyperlipidemia.
Replacing nutrients lost in the urine.
Reducing the risks of further renal
progression and atherosclerosis.

Nutrition therapy and pathophysiology. 2009

ACUTE RENAL FAILURE

Is characterized by a rapid decline in GFR over
hours to days.
Retention of nitrogenous waste products
Oliguria ( urine < 400 mL/day)
Electrolyte and acid-base abnormalities

ARF

Penurunan fungsi ekskresi

Penurunan fungsi mendadak

Penurunan fungsi regulasi

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

Akumulasi air
Elektrolit
Toksin uremi

PERUBAHAN METABOLIK PADA ARF

ARF

Penurunan
ekskresi
Infeksi danfungsi
penyembuhan

Peningkatan produksi
dan penurunan klirens

Sisa metabolisme
Sitokin
Protease & hormon katabolik
Gangguan transport oksigen
dan nutrien

Penurunan status nutrisi

Meningkatkan katabolisme

Akumulasi air
Elektrolit
Toksin uremi
Asidosis metabolik
Perubahan respon
glikemik

Keadaan sakit kritis

STRESS METABOLIK

Perlu energi lebih banyak

KOMPENSASI

Glikogenolisis
Glukoneogenesis
Lipolisis

metabolisme Glukosa
resistensi insulin
hormon "antiinsulin"

HIPERKATABOLISME

Glukagon
Katekolamin
Glukokortikoid

HIPERKATABOLISME
Gangguan Imunitas
Daya Tahan tubuh

Katabolisme protein
keseimbangan nitrogen (-)

Infeksi

Akumulasi toksin uremi

Survival Rate

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

Pemberian Nutrisi pada ARF

tergantung:

Ada / tidak adanya komplikasi pd ARF

Kelainan Metabolisme Karbohidrat
Kelainan Metabolisme Lipid
Kelainan Metabolisme Asam amino
Metabolisme Mikronutrien
Metabolisme Trace elements
TPG (terapi pengganti ginjal)

NUTRITION THERAPY IN ARF

(ESPEN, 2011)

Energy
25-30 (max 35) kkal/kg BW/d
Carbohydrate
3-5 (max 7) g/kg BW/d
Lipid
0,8-1,2 (max 1,5) g/kg BW/d
Protein
Conservatif therapy
0,6-0,8 (max 1,0) g/kg BW/d
Extracorporeal therapy 1,0-1,5 g/kgBW/d
+ hyperkatabolism
max 1,7 g/kg BW/d

NUTRITION THERAPY IN ARF

(ESPEN, 2011)

Vitamin
Requirement Water soluble vitamin increased
because of losses associated with renal replacement
therapy. (Vit. B6 10 mg/d, Vit. C 60-100 mg/d)
Fat soluble vitamin not lost during renal
replacement therapy supplementation not recommended

Electrolytes
Vary profoundly must be determined individually
Many patients ARF with hypokalemia/hypofosfatemia or during
CRRT with low electrolytes solutions.

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;25:295-310

STATUS NUTRISI PADA ARF

Penderita sakit kritis dengan ARF 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

25

CHRONIC KIDNEY DISEASE

Kelainan struktur atau fungsi ginjal > 3 bulan
dengan atau tanpa penurunan GFR
berdasarkan :
- kelainan patologis
- petanda kerusakan ginjal (proteinuria
atau kelainan pada radiologi).
GFR < 60 ml/menit/1,73m selama > 3 bulan
dengan atau tanpa kerusakan ginjal.

CHRONIC KIDNEY DISEASE

.Klasifikasi CKD berdasarkan penyebab, kategori GFR
dan kategori albuminuria.

Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the
Evaluation and Management of Chronic Kidney Disease. 2013

CHRONIC KIDNEY DISEASE

.Klasifikasi CKD berdasarkan penyebab, kategori GFR
dan kategori albuminuria.

RISK FACTORS :
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)

CHRONIC KIDNEY DISEASE

.Klasifikasi CKD berdasarkan penyebab, kategori GFR
dan kategori albuminuria.

Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the
Evaluation and Management of Chronic Kidney Disease. 2013

Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the
Evaluation and Management of Chronic Kidney Disease. 2013

Lang F. Color Atlas of Pathophysiology 2000

CLINICAL SYMPTOMS
Edema
Uremia
Hyperphosphatemia
Hyperkalemia
Metabolic acidosis
Azotemia

Oliguria
Hypertension
Anemia
Bone & mineral disorders
Gastrointestinal symptoms
Dermatological changes

INDIKATOR MALNUTRISI PADA PASIEN CKD

(Pernefri, 2011) :
1. Subjective Global Assessment (B) dan (C)
2. Albumin serum < 4,0 g/dL
3. Kreatinin serum < 10 mg/dL
4. Indeks massa tubuh < 20 kg/m 2
5. Kolesterol < 147 mg/dL
6. Prealbumin serum < 300 mg/L

OPTIONS - THERAPY OF ESRD

35

1.

CONSERVATIF MANAGEMENT

2.

DIALYSIS
A. HEMODIALISIS
B. PERITONEAL-DIALISIS

3.

TRANSPLANT

CONSERVATIF MANAGEMENT
1. LIMITATION SYMPTOMS
2. PREVENT IRREVERSIBLE RENAL
DAMAGED
3. MAINTAIN OF HEALTH BEFORE
DIALYSIS OR TRANSPLANTASION

36

NUTRITION THERAPY
GOAL :
To prevent malnutrition at an early stage of renal
disease/ maintain optimal nutritional status.
To reduce or control accumulation of waste products.
To prevent CVD disease by treating hyperlipidemia,
manage bone disease by treating vitamin D
deficiensies, and treating hyperparathyroidism.
To correct renal anemia to retard progression of renal
dysfunction.

Druml W, Cano N, Teplan V. Nutritional support in renal disease. In : Sobotka L (eds).

Basics in Clinical Nutrition. 4 th ed. Galen, ESPEN. 2011

NUTRITION THERAPY

(CKD STAGE 3-5)

Kebutuhan energi : 35 45 kkal/kg/hari

Kebutuhan lemak :
30% energi dari lemak, dengan lemak jenuh
< 10% total kalori, kolesterol < 300 mg/hari
Kebutuhan protein :
CKD stage 1-3 (GFR > 30 mL/min) : 0,75 g/kgBBI/hari
CKD stage 4-5 tanpa dialisis (GFR > 30 mL/min) :
0,6 g/kgBBI/hari.
CKD dgn dialisis : 1,2 g/kgBBI/hari.

TUJUAN DIET RENDAH PROTEIN

To slow the progression of kidney
disease
Minimize accumulation of uremic toxins
Preserve protein nutritional status

Diet rendah protein

Konvensional
Kebutuhan protein untuk pasien CKD :
Proteinuria < 1,5 g/hari : 0,6 0,8 g/kgBBI/hari.
Proteinuria >1,5 g/hari, sejumlah protein yang
sama harus ditambahkan melalui makanan.
Protein (High Biologycal Value) : 50-75%
Supplemented very low-protein (VLPD) diet
Diberikan pada CKD tahap lanjut (CKD stage 4-5),
dengan keto amino acids 0,3 0,4 g/kg/hari
(ESPEN, 2013 & NKF, 2013)

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.
The role of Keto Acid Analogues :

1. Improve symptoms
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 BW/day
Dosage of keto acid 0.1 gr/kg BW/day
Daily energy intake of 35 kcal/kg BW/day should be
recommended.
Protein calories must be replaced by complex CH
calories-not by lipid
Am J Nephrol 2005;25(suppl1):1-28

MONITORING PROTEIN HOMEOSTASIS

1.

Based on renal damaged

indicator higher / lower of muscle mass loss

2. Creatinine clearance
GFR renal damaged low creatinin clearance, creatinine
serum high
3. BUN (BLOOD UREA NITROGEN) indicator of renal function
Stabil PROTEIN DIET
BUN increased increased PROTEIN INTAKE.
Dehidration / catabolic state (surgery, burn, infection, fracture
drug catabolic: steroid
LEVEL 60- 80 mg/dl ACCEPTABLE
> 80
uremia
< 40
malnutrisi
4. Urea clearance filtration capability

NUTRITION THERAPY

(CKD-HD)

TUJUAN :
Mencegah, mendeteksi atau mengatasi
malnutrisi.
Mengurangi akumulasi cairan, sisa metabolisme,
kalium dan fosfor.
Mencegah komplikasi uremia (penyakit
kardiovaskuler dan penyakit tulang).

REKOMENDASI ASUPAN
VITAMIN LARUT AIR PADA CKD
Nutrien

Pre-Dialisis

Hemodialisis

Thiamine (B1)

1-1,5 mg/hari

1,1-1,2 mg/hari

Riboflavin (B2)

1-2 mg/hari

1,1-1,3 mg/hari

Niasin

Tidak ada

14-16 mg/hari

Asam Pantotenat (B5)

Tidak ada

5 mg/hari

Pyridoxine (B6)

5 mg/hari

10 mg/hari

Biotin

Tidak ada

30 g/hari

Asam Folat (B9)

200 g/hari

1 mg/hari

Cobalamin (B12)

Tidak ada

2,4 g/hari

Suplementasi untuk
meningkatkan
absorpsi Fe

75-90 mg/hari

Vitamin C

Dharmeizar dkk. Pernefri 2011.

REKOMENDASI ASUPAN
VITAMIN LARUT LEMAK PADA
CKD
Nutrien

Pre-Dialisis

Hemodialisis

Vitamin A

Tidak ada

700-900 g/hari

Vitamin D

Mulai dengan dosis

rendah dengan
monitor kadar Ca, P,
dan PTH

Individual

Vitamin E

Tidak ada

400-800 IU/hari

Vitamin K

Tidak ada

90-120 g/hari

Tidak dibatasi dengan

produksi urine normal

750-1000 mL/hari +
produksi urine

Cairan

Dharmeizar dkk. Pernefri 2011.

REKOMENDASI ASUPAN MINERAL

PADA CKD
Nutrien

Pre-Dialisis

Hemodialisis

< 5 g/hari

5-6 g/hari

Kalium

39 mg/kg/hari
tergantung nilai
laboratorium

8-17 mg/kg/hari

Kalsium

1200 mg/hari

2000 mg/hari dari

diet dan obat

800-1000 mg/hari (jika

fosfat serum > 4,6
mg/dL dan atau PTH >
114,9 pg/mL)

800-1000 mg/hari

Zinc (Zn)

Tidak ada

Jika perlu

Besi (Fe)

Individual

Individual

Selenium

Tidak ada

Tidak ada

NaCl

Fosfor

Dharmeizar dkk. Pernefri 2011.

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 electrolyte balance)
4. LIMITATION OF Na+ 2 - 4 gr / day
5. K+ as needed
49

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.

RISK FACTORS

Family history
Hypercalciuria
Hyperuricosuria
Hyperoxaluria
Low urine volume
Gout
Excess intake of vitamin D
Urinary tract infections
Urinary tract blockages

CLINICAL SYMPTOMS
Kidney stones cause pain when they pass
down the ureters to the bladder and urethra

Hematuria
Pain with urination
Urgency to urinate

Based on: Mader, S., Inquiry Into Life, McGraw-Hill

KIDNEY STONES

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 :
- Increased risk (animal protein, oxalate,
sodium )
- Decreased risk (Ca, K, Mg, fluid intake)
2. CYSTEIN ( herediter )
Homozygous cystinuria

3. Urid acid
End product of purin metabolism
4. Struvite
Magnesium, ammonium phosphate,
carbonate apatite Triple phosphate or
Infection stones

B. TRACTUS UROGENITAL
Changed of urine physically
Changed of urine concentration
Changed of urine balanced

C. MATRIX BATU ORGANIK

RECURRENT INFECTION
DEFICIENCY OF VITAMIN A
( DESQUAMATION OF CEL EPITHEL)

DOT CALCIFICATION
RANDALLS PLAQUE

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.

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

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)
Infection

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

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

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

KIDNEY STONES: 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

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

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 )

68

MILK ???

NUTRITION THERAPY:
CALCIUM STONES
Low-calcium (?) diet (approx. 800mg/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

LOW CALCIUM DIET HIGH ASH ACID

FLUID > 2500 cc/day

Low calcium (?)

Limitation food intake contains:
PROTEIN : milk, cheese, schrimp, crab, rilis,
salt fi sh, 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

LOW-CALCIUM DIET

NUTRITION THERAPY:
URIC ACID STONES
Low-purine diet sometimes recommended
Avoid:
Organ meats
Alcohol
Anchovies, sardines
Yeast
Legumes, mushrooms, spinach, asparagus,
cauliflower
Poultry

LOW PURINE DIET

Limit food sources of uric acid

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

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

HIGH DIET ASH ALKALIS

ESPECIALLY FOR :
CYSTEINE STONE & URIC ACID

1. Fluid > 2500 cc/day

2. Low AA (contain Sulfur)
3. Vegetables < 300 gr/day
4. Fruit < 300 gr/day

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

GENERAL MEASURES
TO PREVENT RECURRENT STONE FORMATION
Increase fluid intake to maintain urine output of 2-3 L/d:
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 NaCl):

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

THANK YOU