Nutritional Management on Renal Disease

Nurpudji A Taslim, Nutrition Department

School of Medicine Hasanuddin UniversityMakassar 2005

Renal Function1. WASTE FORMATION & HOMEOSTASIS

- UREA- REGULATION OF OSMOLALITY AND FLUID- REGULATION OF Na & K- REGULATION OF H+- REGULATION OF Ca & PO4- BALANCED

2. PROTEIN EXCRETION METABOLISM3. ENDOCRINE

- RENIN SINTHYSIS- ERYTHROPOETIN SINTHYSIS- ACTIVATIONI 25 OH CHOLECALCIFEROL- ADH ACTION- ALDOSTERON

DIAGNOSTIC TEST

1. BLOOD- CREATININE- BUN (BALANCED URINE NITROGEN)- CCT (CREATININE CLEARANCE TEST)

2. URINALISIS- UUN ( Urea Urine Nitrogen)-PROTEIN ALBUMIN

3. VISUAL- IVP (intra venous pyelography)- ARTERIOGRAM- BIOPSI- CT-SCAN-SONOGRAM

KLASIFIKASI

• Glomerular • Nephritic syndrom• Nephrotic syndrom

• Tubular & intertitium• ARF• Pyelonephritis• Others : others tubular or intertitium

• Progress nature of renal disease• ESRD• Nephrolithiasis

• Rheumatoid disorder

Patofisiologi inflamation

• Osteoarthritis• Rheumatoid arthritis• Sjogren• Sistemac Lupus Erythromatosus

NEPHRITIC SYNDROMGNA

GNA --- Inflamasi loop glom kapiler

akut, self limitimg, singkat, hematuria

infeksi sal. Nafas atas

GNC --- bila berlanjut menjadi kronis

Causa:

primer : Primer– IgA nepphropathy, hereditary nephritis

sekunder : SLE, Vasculitis, GNA associated endocarditis

Medical nutrition therapy

AKUT :

a. Antibiotic

b. Maintain nutrition status--- resolve spontaneously

c. Reduced protein and Kalium --- uremia

d. Reduced natrium---- hipertensi

CLINICAL SYMPTOM : DECREASED OF GRF

NEPHROTIC SYNDROMGNC

• Patogenesis• Loss of glom barrier to protein• Hipoalbuminemia• Hiperkolesterolemia• Hiperkoaguability• Abnormal bone metabolisme

• Causa:• DM, SLE, Amyloidosis• Peny utama pada ginjal

SINDROMA NEPHROTIC

• 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

GOAL1. MAINTAIN OPTIMAL NUTRITION

2. MAINTAIN NUTRITIONAL STORES

3. MINIMIZE DISEASE METABOLISM

4. PREVENT PROGRESSIVITAS OF DISEASE

5. SLOW DIALYSIS OCCURANCE

‘high protein diet --- increased urinary

losess (Mitch, 1996)

ACUT RENAL FAILURECausa : Sudden reduction in GFR

Renal shockdown ----- trauma or bleeding Decreased ability to excrete the daily

product of metabolic waste Clinical symptom:

a. Diuretic Phase : prod urine 450 ccb. Oligourie phase ( 7-12 hr)uremiaHigh level of K, Mg and Phospat Low level of Na, Calciumacidosis

Medical nutrition therapy• Manage for: • uremia, metabolic acidosis, imbalanced fluid and electrolyte

• Molina (95)• Early nutritional intervention --- positive affect patient survival

• Protein• PN --- in case of vomiting and diarrhea• CHO--- not effective--- decreased breaking of protein 50%• Mixed– CHO, lipid and AA --- prevent catabolism of protein• Protein --- 0,5 – 0,8 gr/KgBB/hr• Dialysis--- 1-2gr /KgBB

• Kalium• Especially---dialyses patients• Monitoring K• Glucose, insulin, bicarbonate ---- K inside cell

CHRONIC RENAL FAILURE• Causa : Chronic infection

Progressif glomerolus diseasesChronic Hipertension Nefrophaty DMHidronefrosis BilateralAnalgesic drug (Phenacetine)

• Symptom : uremiaAcid-base unbalanced Electrolyte unbalanced

• Clinical : anemia, anxiety, lose weight, pain (bone, joint), hypertension

Standard Nutrition Assessment on CRF

• Parameter Normal ModerateSevere

Dry weight % RBW 85-95 75-85 < 75

• TSFmen 4-6 <4Women 8-12 <8

• ACFmen 22-24 <22Women 18-20 <18

• LABAlbumin Serum 2,8 –3,3 <2,8

Transferrin 150-180 <150

Renal Failure DietGOAL

1. ADEQUATE FOOD, NOT MAKE HEAVIER RENAL FUNCTION2. DECREASED OF UREUM & CREATININ LEVEL3. MINIMIZED SALT RETENSION

REQUIREMENT1. HIGH Biologi value of Protein2. Limitation of Salt ( Heavy HT, >> K, edema, Oligo /anurie)3. Limitation of K (Glom function or prod urine << 400 cc)4. Adequate food5. >> fluid

Others Tubular & Intertitial disease • 1. Chronic Intertitial Nephritis

• Cause : – Analgesic abuse, Sickle cel anemia, DM, Vesico urethral

reflux

• Therapy :– Increased fluid intake

• 2. Fanconi’s Syndrom• In ability to re-absorbsi proper amount of glucose, AA,

phospate, bicarbonate in proximal tubulus

• ANAK• Polyurie• Ricketts• Growth retardation• vomiting

• GEJALA• Acidosis• Hipokalemia• Polyurie• Osteomalacia

GEJALA KLINIK

PYELONEPHRITIS

• Infection bacteria at the kidney• Avorn et al (94) & Hovell et al (98)

• Therapy cranberry or blueberry juice will decreased bacteria

SJOGREN’S SYNDROM

• Tabara & vara-Cristo,2000, Chronic inflammatory disorder,

characterized by poly-glandular tissue destructions leading to:

» Keratoconjunctivitis» Diminished prod of tears and saliva» Xerostomia» xeropthalmia

Dietary Management

• Relief of symptoms and eating discomfort• Lack of appetite, weight loss, fatigue,

difficulty chewing and swallowing • Ready-to-eat food• Sweetened lemon drops• Iron, B12 and folate as well balance diet–

(Lundstom and Lindstom,2001)

SCLERODERMA

• Escott-Stump,2002, Is a progressive characterized by deposition of fibrous connective tissue in the skin and visceral organs, including GIT

• One of manifestation of scleroderma—Raynaud’s Syndrome (ischemia or coldness in the small extremities—finger--- difficulty preparation and consumption of meal

• GIT symptoms , weight loss, renal dysfunction & multiple organ system dysfunction my result

Medical Management

• Disease is rogessive and current treatment produces are cure

• Side effects– may results as discussion above

• Medical Nutrition Therapy• Dysphagia• Malabs of lactose, vit, FA, minerals• Need high Energy, high protein – through NGF as a

supplement • PN – diarre persistent

SYSTEMIC LUPUS ERTHEMATOSUS (SLE)

• Etiologi tdk jelas• A genetic predisposition

• Genetic marker HLA• Human leukocyte Ag• Presence of anti-DNA ab• Environmental factors– viral infection

• Prevalence— women and childbearing age in Americans and Caucasians

• 1954– survival rate 50%, today 97%• 25% DEVELOPS SJOGREN’S SYNDROM

MEDICAL MANAGEMENT• SLE – autoimmune disease—affects all organ system

• Steroid—used as therapy– affect nutrient metabolism, needs and excretion

• Renal function is deranged– exessive excretion of protein, Na, fluid, calcium

• DRUGTHERAPY– Corticosteroid– alter of protein, Na, fluid, calcium need– Plaquenil ( antimalaria)– effective in clearing upskin lessions ( SE—

nausea,cramping abd, diarrhea)– Immunosuppresant—azathioprine---in the event of brain or renal

involment, but GIT effects may occur

MEDICAL NUTRITION THERAPY• No specific dietary guidelines• Diet based on individual need• Priorities—sequelae of disease and pharmacologic

effects on organ function and nutrition metabolism• Restricted---sodium and fluids intake• Limitations—fat intake• Leiba et al (2001)--- protein, calorie and diet low in

fat---reduction in immune-complex deposition in the kidney and protein urie and may prolong the lifespan

Diet Variation

1. LOW PROTEIN DIET I : 20 gr - CCT 5-20 cc/”, ureum 100 mg

2. LOW PROTEIN DIET II 40 gr - CCT 20 – 30 cc/”, Konservatif

3. LOW PROTEIN DIET III60 gr - CCT 30-50 cc/”, MILD CRF

PROTEIN LIMITATION BASED ON GFR

GFR PROTEIN ALLOWANCEcc/menit g/day g/kgBB/day

>25 no restriction no restriction20-25 60-90 1.315-20 50-70 1.010-15 40-55 0.7 5-10 40 u/ pria 0,5-0,6

35 u/ wanita

MONITORING PROTEIN HOMEOSTASIS

1. Based on renal damaged indicator higher / lower of muscle mass loss

2. Creatinine clearanceGfr renal damaged– low creatinin clearance pada renal failure level of creatine serum –high

3. SUN (SERUM UREA NITROGEN) OR BUN – indicator of renal functionStabil PROTEIN DIETSUN 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

NUTRITION CARE

NUTRIENT OLIGOURIE DIURETIC

1. ENERGY 40-55 kcal/kg 40-55 kcal/kg (High in trauma) (high in trauma)

2. CHO 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 needed5. Na + 500-1000 mg/d replace losses6. K+ 1000 mg/d replace losses7. Fat = dialysis = dialysis

Progresivitas of Diseases (CRF)

STAGE % LOST GFR (cc/min)

1. Decreased 55% 55-125 renal reserve

2. Renal Insuficiency 80% 30-55

3. Renal Failure 90% 12,5-30

4. Uremia / uremia >90% < 12,5 syndrome (ESRD)

OPTIONS- THERAPY OF ESRD

1. CONSERVATIF MANAGEMENT

2. DIALYSIS A. HEMODIALISISB. PERITONEAL-DIALISIS

3. TRANSPLANTASION

KONSERVATIF MANAGEMENT

1. LIMITATION SYMPTOM

2. PREVENT IRREVERSIBLE RENAL DAMAGED

3. MAINTAIN OF HEALTH BEFORE DIALYSIS OR TRANSPLANTASION

TYPE OF DIALYSIS

A. HEMODIALYSBY MACHINE ( venous )3-4 hours /d, 3 – 4 x week

B. PERITONEAL DIALYSIS Intermittent ( IPD)

Continous ambulatory ( CAPD)Continous Cyclic

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

RENAL STONE

Causa:1. Environment Factor2. Tractus Urogenitalia 3. Matrix Organik stone

A. ENVIRONMENTAL FACTOR

1. CALSIUM ( 96%)N eksresi 100 –175 mghipersecresion : high intake Ca, high Vit.D

long imobilisasion, hiperparathyroidrenal tubular asidosis, high calsiurie

idiopatik

2. CYSTEIN ( herediter )

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 CALCIFICATIONRANDALL’S PLAQUE

CLINICAL SYMPTOMSKOLIK, DEMAM, LEMAH

THERAPY1. High fluid2. Change pH from acid --- alkalis3. Elimination food contain nutrient---

contribute to stone development 4. Binding agent – ecretion through feses

e.g. sodium phytate --- for calsiumaluminium gel --- for phosfatGlycine --- for oksalat

THERAPY

Susunan Kimia Modifikasi zat Gizi Diet Ash1. Calsium low calsium acid ash

Phospat low phospatOxalat low oxalat

2. As. Urat low purine alkaline ash

3. Cystine low methionine alkaline ash

VARIATION DIET

1. LOW CALCIUM HIGH ASH CAID

2. HIGH DIET ASH ALKALIS

3. LOW PURINE DIET

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

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