NUTRITIONAL ASPECTS

OF URONEFROLOGY
DISEASES

ARYANTI R. BAMAHRY
FK-UMI
2016
Kidney Function
Bone Structure
Metabolic Blood Formation
End Products
Calcium Vitamin D
Balance Activation

Erythropoietin
Removal of Synthesis
Urea, Creatinine etc.

Water Balance
Potassium
Balance

Recovery of Sodium
Bicarbonate Removal
Blood Pressure
Cardiac Activity
Regulation of Blood pH
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 Akumulasi air
Keseimbangan elektrolit Elektrolit
Regulasi hormonal Toksin uremi
 PERUBAHAN METABOLIK PADA ARF

ARF ` Penurunan
Infeksi dan fungsi ekskresi
penyembuhan

Penurunan status nutrisi

Peningkatan produksi
dan penurunan klirens Meningkatkan katabolisme

Sisa metabolisme Akumulasi air

Sitokin Elektrolit
Protease & hormon katabolik Toksin uremi
Gangguan transport oksigen Asidosis metabolik
dan nutrien Perubahan respon
glikemik
 Keadaan sakit kritis

STRESS METABOLIK

Perlu energi lebih banyak

KOMPENSASI

Glikogenolisis metabolisme Glukosa

Glukoneogenesis resistensi insulin
Lipolisis hormon "anti-insulin"
Glukagon
Katekolamin
HIPERKATABOLISME Glukokortikoid
 HIPERKATABOLISME

Gangguan Imunitas Katabolisme protein ↑

Daya Tahan tubuh  keseimbangan nitrogen (-)

Infeksi Akumulasi toksin uremi

Survival Rate
 Essential AA
Non-essential AA
Special AA
BCAA↓
threonine ↓
valine ↓ ↓
lysine ↓
leucine ↓
serine ↓
isoleucine ↓

decrease
oxidation in production
muscles

metabolic defective
phenylalanine
acidosis hydroxylation
KIDNEY
tyrosine ↓
glycine ↑ FAILURE
citruline ↑ tryptophane ↓
cystine ↑
reduce
aspartate ↑ arginine ↓ protein binding
methionine ↑
methyl-
histidine ↑ 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/1,73m² 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 Oliguria
Uremia Hypertension
Hyperphosphatemia Anemia
Hyperkalemia Bone & mineral disorders
Metabolic acidosis Gastrointestinal symptoms
Azotemia 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/m2
5. Kolesterol < 147 mg/dL
6. Prealbumin serum < 300 mg/L
 OPTIONS - THERAPY OF ESRD

1. CONSERVATIF MANAGEMENT

2. DIALYSIS
A. HEMODIALISIS
B. PERITONEAL-DIALISIS

3. TRANSPLANT

35
 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. 4th 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./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 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 μg/hari
Asam Folat (B9) 200 μg/hari 1 mg/hari
Cobalamin (B12) Tidak ada 2,4 μg/hari
Vitamin C Suplementasi untuk 75-90 mg/hari
meningkatkan
absorpsi Fe

Dharmeizar dkk. Pernefri 2011.

REKOMENDASI ASUPAN VITAMIN
LARUT LEMAK PADA CKD
Nutrien Pre-Dialisis Hemodialisis
Vitamin A Tidak ada 700-900 μg/hari
Vitamin D Mulai dengan dosis Individual
rendah dengan
monitor kadar Ca, P,
dan PTH
Vitamin E Tidak ada 400-800 IU/hari
Vitamin K Tidak ada 90-120 μg/hari
Cairan Tidak dibatasi dengan 750-1000 mL/hari +
produksi urine normal produksi urine

Dharmeizar dkk. Pernefri 2011.

REKOMENDASI ASUPAN MINERAL PADA
CKD
Nutrien Pre-Dialisis Hemodialisis
NaCl < 5 g/hari 5-6 g/hari
Kalium 39 mg/kg/hari 8-17 mg/kg/hari
tergantung nilai
laboratorium
Kalsium 1200 mg/hari ≤ 2000 mg/hari dari
diet dan obat
Fosfor 800-1000 mg/hari (jika 800-1000 mg/hari
fosfat serum > 4,6
mg/dL dan atau PTH >
114,9 pg/mL)
Zinc (Zn) Tidak ada Jika perlu
Besi (Fe) Individual Individual
Selenium Tidak ada Tidak ada
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

49 5. K+ as needed
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
RANDALL’S 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 )

MILK ???

68
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 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
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 low-
protein 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 oxalate—spinach,
rhubarb, chocolate, and nuts
Cranberry juice: Decreases oxalate and phosphate
excretion and increases citrate excretion