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Foods and Diet for Chronic Kidney Disease (CKD)

In todays world, lifestyle related diseases like diabetes, hypertension and


obesity are the prime causes for initiating and enhancing the rate of
progression of chronic kidney disease. There are many categories of diseases
affecting the kidney but for the sake of brevity we focus on the ones where
diet has a role to play. We talk about where diet has a role to play. We talk
about renal stone disease, neprotic syndrome, and renal failure particularly
CKD (chronic kidney disease) where diet may have a role in preventing or
aggravating the condition.

Diet for Chronic Kidney Disease (CKD):

At the outset, the role of dietary modifications are most obvious in renal
failure, more so in chronic kidney disease (CKD). There are many
misconceptions in this regard, causing severe and often inappropriate
dietary restrictions of protein, salt and potassium in these patients.

Preventive Foods:
To prevent kidney disease in todays world it is important to eat a balanced,
nutritious diet. It is extremely important to restrict the amount of junk food
so that diabetes, hypertension and obesity can be avoided. Excess of animal
protein (particularly red meat), high carbohydrate and high salt content
foods, fructose-rich foods, artificial sweeteners, sweetened drinks
(particularly sodas) are to be avoided.

In the context of renal stones, certain foodstuffs are not recommended. As


calcium oxalate stones are the commonest, the usual recommendations for
preventing stone recurrence are to ensure adequate fluid intake, reducing
the consumption of salt and sugar, eating low fat dairy products and
reducing the intake of non-dairy animal protein. It is important to increase
the fruit and vegetable in take in these patients, restrict high oxalate foods
and not take vitamin C supplements in heavy doses for prolonged periods.

Diets rich in calcium are helpful in preventing renal stones and


recommended doses of calcium supplements do not increase the risk of
stone formation. Beverages like tea and coffee do not increase the stone
formation risk, while regular consumption of grapefruit juice does.

For patients with nephritic syndrome (in which case there is massive
amounts of protein in the urine), a balanced diet with salt and fat restriction
is prescribed. Fluid intake is restricted depending on the severity of the case
and whether renal failure has set in.
Note: Cranberry Juice or its extract is useful in preventing urinary tract
infections

Renal Diet Basics:


All meal plans, including the kidney-friendly diet, should follow the basic
rules of a balanced diet, ensuring that there are appropriate amounts of
calories, protein, carbohydrates, fats, minerals, vitamins and fluids. A proper
diet plan helps to control diabetes, high blood pressure, and
hypercholesterolemia and prevents obesity all of which are known factors for
the progression of renal failure.

Calories:
Calories come from the proteins, carbohydrates and fats in our diet. The
number of calories one needs depends on the age, gender, and body size
and activity level.

Protein:
The current recommendations are that patients with chronic kidney disease
(CKD) should take about 0.5-0.8/kg body weight of high biological value
proteins. There is no doubt that animal proteins have a high biological value,
but it is also true that they cause more acid secretion as compared to
vegetarian sources of proteins. Hence, a judicious mix of animal and
vegetarian proteins should be the best bet for such patients. Ask you
dietician or doctor for further details.

Protein Containing Foods in our Diet:

Non-Vegetarian Vegetarian
Egg white Pulses and legumes
Chicken Nuts and Oilseeds
Mutton Cheese and milk powder
Beef Yeast

Carbohydrates:
Healthy sources of carbohydrates include fruits and vegetables. Rice, wheat
and other cereals are all sources of carbohydrates in our daily diet. Sugar,
honey, hard candies, soft drinks and other sugary drinks contain a lot of free
sugar and are unhealthy sources of carbohydrates.

Fat:
We need some fat to stay healthy. Fat gives us energy and helps us use
some of the vitamins in our food. But too much fat can lead to weight gain
and heart disease. Try to limit fat in your meal plan, and choose healthier
fats when you can.

Sodium:
Too much sodium (salt) can lead to body swelling and raising the blood
pressure. This can damage the kidneys more and make the heart work
harder. Try eating fresh fruits and vegetable rather than crackers or other
salty snacks. Avoid pickles, papads and other namkeen items, bakery
products, tomato ketchups, soya sauce and other bottled sauces.

Note: Be careful not to consume salt substitutes or the low sodium salts like
Lona, it may contain high potassium and can be dangerous for renal failure
patients.
Potassium Diet for Chronic Kidney Disease (CKD):
The body needs some potassium to make muscles work, but too much
potassium can be dangerous. When the kidneys are not working well, the
potassium level may be too high or low. In patients of moderate or severe
CKD, potassium intake needs to be limited, otherwise there may be serious
consequences including death due to cardiac side effects, mainly
arrhythmias.

Low Potassium Diet (Eat These) High Potassium Diet (Avoid These)
Apple, pineapple, guava, cranberries, Bananas, melons, oranges, prunes, dry
grapes, strawberries, cucumber fruits and nuts
Beetroot, pink radish, bottle gourd,
snake gourd, ridge gourd, tinda, Coconuts and coconut water
parwal, onion, green mangoes
Rice, rice flakes, wheat semolina,
Tomatoes, green leafy vegetables
vermicelli
Potatoes, sweet potatoes, tapioca

Dried peas and beans

Fresh fish and chicken

Bran products and granola, ragi

Phosphorus:
Healthy kidneys keep the right balance of phosphorus in the body. When the
kidneys are not working well, phosphorus can build up in the blood. Too
much phosphorus in the blood can lead to weak bones that break easily.

Phosphate in Foods:

High Low
Wheat and wheat based products Rice and rice based products
Legumes, pulses and nuts Fruits and vegetables
Milk and milk products meat, poultry,
eggs and fish
Carbonated drinks

Fluids:
As kidney disease advances, the ability of the kidneys to excrete the water
decreases. Thus, if one is drinking too much water in severe renal failure the
water may accumulate in the body, causing swelling. It also may increase
blood pressure and precipitate heart failure causing severe breathing
difficulty. Depending on the stage of kidney disease you may foods that
contain a lot of water.

Vitamins:
Very frequently vitamin D, folic acid alone or with iron is added to the diet of
patients with CKD to make up for the deficit they have. But do not try taking
vitamins on your own; it may be harmful for you. Check with your doctor
first

2.8 Penatalaksanaan

Penatalaksanaan penyakit gagal ginjal kronik meliputi1:

1. Terapi spesifik terhadap penyakit dasarnya

Waktu yang paling tepat untuk terapi penyakit dasarnya adalah sebelum terjadinya penurunann
GFR, sehingga perburukan fungsi ginjal tidak terjadi. Pada ukuran ginjal yang masih normal
secara USG, biopsy, dan pemeriksaan histopatologi ginjal dapat menetukan indikasi yang tepat
terhadap terapi spesifik. Sebaliknya, bila GFR sudah menurun sampai 20-30% dari normal,
terapi terhadap penyakit dasar sudah tidak banyak bermanfaat.

1. Pencegahan dan terapi terhadap kondisi komorbid

Penting sekali untuk mengikuti dan mencatat kecepatan penurunan GFR pada pasien gagal ginjal
kronik. Hal ini untuk mengetahui kondisi komorbid yang dapat memperburuk keadaan pasien.
Faktor-faktor komorbid ini antara lain, gangguan keseimbangan cairan, hipertensi yang tidak
terkontrol, infeksi traktu urinarius, obstruksi traktus urinarius, obat-obat nefrotoksik, bahkan
radiokontras, atau peningkatan aktivitas penyakit dasarnya.

1. Memperlambat pemburukan (progression) fungsi ginjal

Faktor utama penyebab perburukan ginjal adalah terjadinya hiperfiltrasi glomerulus. Cara
penting untuk mengurangi hiperfiltrasi glomerulus adalah pembatasan asupan protein

1. Pencegahan dan terapi terhadap komplikasi

2. Terapi pengganti ginjal berupa dialisis atau transplantasi ginjal.

Tabel 5. Rencana Tatalaksanaan Penyakit GGK Sesuai dengan Derajatnya


LFG(ml/mnt/1,73m
Derajat Rencana tatalaksana
)
terapi penyakit dasar, kondisi
1 > 90 komorbid, fungsi ginjal,
memperkecil resiko kardiovaskuler
menghambat pemburukan
2 60-89
(progession) fungsi ginjal
3 30-59 evaluasi dan terapi komplikasi
persiapan untuk terapi pengganti
4 15-29
ginjal
5 <15 terapi pengganti ginjal

Terapi Nonfarmakologis1,6:

1. Pengaturan asupan protein:

Tabel 6. Pembatasan Asupan Protein dan Fosfat pada Penyakit Ginjal Kronik1

LFG Fosfat
Asupan protein g/kg/hari
ml/menit g/kg/hari
>60 tidak dianjurkan Tidak dibatasi
25-60 0,6-0,8/kg/hari 10 g
0,6-0,8/kg/hari atau tambahan 0,3 g
5-25 10 g
asam amino esensial atau asam keton
0,8/kg/hari(=1 gr protein /g proteinuria
<60 (sindrom
atau 0,3 g/kg tambahan asam amino 9g
nefrotik)
esensial atau asam keton.

1. Pengaturan asupan kalori: 35 kal/kgBB ideal/hari

2. Pengaturan asupan lemak: 30-40% dari kalori total dan mengandung jumlah yang sama
antara asam lemak bebas jenuh dan tidak jenuh

3. Pengaturan asupan karbohidrat: 50-60% dari kalori total

4. Garam (NaCl): 2-3 gram/hari

5. Kalium: 40-70 mEq/kgBB/hari

6. Fosfor: 5-10 mg/kgBB/hari. Pasien HD :17 mg/hari

7. Kalsium: 1400-1600 mg/hari


8. Besi: 10-18mg/hari

9. Magnesium: 200-300 mg/hari

10. Asam folat pasien HD: 5mg

11. Air: jumlah urin 24 jam + 500ml (insensible water loss)

Terapi Farmakologis1,2,3,6:

1. Kontrol tekanan darah

o Penghambat Ensim Konverting Angiotensin (Angiotensin Converting Enzyme/


ACE inhibitor) atau antagonis reseptor Angiotensin II evaluasi kreatinin dan
kalium serum, bila terdapat peningkatan kreatinin > 35% atau timbul
hiperkalemia harus dihentikan.

o Penghambat kalsium

o Diuretik

o Beberapa obat antihipertensi, terutama penghambat enzim konverting angotensin


(ACE inhibitor) dan angiotensin reseptor bloker melalui berbagai studi terbukti
dapat memperlambat proses perburukan fungsi ginjal, hal ini terjadi lewat
mekanisme kerjanya sebagai antihipertensi dan antiproteinuria. Jika terjadi
kontraindikasi atau terjadi efek samping terhadap obat-obat tersebut dapat
diberikan calcium channel bloker, seperti verapamil dan diltiazem.

2. Pada pasien DM, kontrol gula darah, hindari pemakaian metformin dan obat-obat
sulfonilurea dengan masa kerja panjang. Target HbA1C untuk DM tipe 1 0,2 diatas nilai
normal tertinggi, untuk DM tipe 2 adalah 6%

3. Koreksi anemia dengan target Hb 10-12 g/dl. Anemia pada penyakit ginjal kronis
terutama disebabkan oleh defisiensi eritropoetin. Hal-hal lain yang ikut berperan dalam
terjadinya anemia, yaitu defisiensi asam besi, kehilangan darah (perdarahan saluran
cerna, hematuria), masa hidup eritrosit yang pendek akibat hemolisis, defisiensi asam
folat, penekanan pada sumsum tulang, proses inflamasi akut maupun kronik. Evaluasi
terhadap anemia dimulai saat kada Hb 10 g% atau Hct 30%, meliputi evaluasi
terhadap status besi, mencari sumber perdarahan, morfologi eritrosit, kemungkinan
adanya hemolisis. Pemberian transfuse pada penyakit ginjal kronik harus dilakukan
secara hati-hati, berdasarkan indikasi yang tepat dan pemantauan yang cermat. Transfusi
darah yang dilakukan secara tidak cermat dapat mengakibatkan kelebihan cairan tubuh,
hiperkalemia, dan pemburukan fungsi ginjal.

4. Kontrol hiperfosfatemia: polimer kationik (Renagel), Kalsitriol


Pemberian diet rendah fosfat sejalan dengan diet pada pasien penyakit ginjal kronik secara
umum, yaitu tinggi kalori, rendah protein, dan rendah garam, karena fosfat sebagian besar
terkandung dalam daging dan produk hewan, seperti susu dan telor. Asupan fosfat dibatasi 600-
800 mg.hari. pembatasan asupan fosfat yang terlalu ketat tidak dianjurkan, untuk mencegah
terjadinya malnutrisi.

Pemberian pengikat fosfat dapat pula diberikan pada pasien penyakit ginjla kronik dengan
hiperfosfatemia. Pengikat fosfat yang banyak dipakai, adalah garam kalium, aluminium
hidroksida, garam magnesium. Garam-garam ini diberikan secara oral, untuk menghambat
absorbs fosfat yang berasal dari makanan. Garam kalsium yang banyak dipakai adalah kalsium
karbonat (CaCO3) dan kalsium asetat.

Pemberian bahan kalsium mimetic (calcium mimetic agent). Akhir-akhir ini dikembangkan
sejenis obat yang dapat menghambat reseptor Ca pada kalenjar paratiroid, dengan nama
sevelamer hidrokhlorida. Obat ini disebut juga calcium mimetic agent.

1. Koreksi asidosis metabolik dengan target HCO3 20-22 mEq/l

Asidosis menyebabkan keluhan mual, lemah, air hunger dan drowsiness. Pengobatan intravena
dengan NaHCO3 hanya diberikan pada asidosis berat, sedangkan jika tidak gawat dapat diberikan
secara peroral.

1. Pengendalian Gangguan Keseimbangan Elektrolit dan Asam-Basa

Gangguan keseimbangan elektrolit utama pada PGK adalah hiperkalemia dan asidosis.
Hiperkalemia dapat tetap asimptomatis walaupun telah mengancam jiwa. Perubahan gambaran
EKG kadang baru terlihat setelah hiperkalemia membahayakan jiwa. Pencegahan meliputi (1)
diet rendah kalium, menghindari buah (pisang, jeruk, tomat) serta sayura rendah; (2)
menghindari pemakaian diuretika K-sparring. Pengobatan hiperkalemia tergantung derajat
kegawatannya, yaitu:

1. Gluconas calcicus IV (10 20 ml 10% Ca gluconate)

2. Glukosa IV (25-50 ml glukosa 50%)

3. Insulin-dextrose IV dengan dosis 2-4 unit aktrapid tiap 10 gram glukosa

4. Natrium bikarbonat IV (25-100 ml 8,4% NaHCO3)

1. Kontrol dislipidemia dengan target LDL,100 mg/dl dianjurkan golongan statin

2. Terapi pengganti ginjal

Terapi pengganti ginjal dilakukan pada penyakit ginjal kronik stadium 5, yaitu pada GFR kurang
dari 15 ml/mnt. Terapi pengganti tersebut dapat berupa hemodialisis, peritoneal dialysis, atau
transplantasi ginjal. Pembuatan akses vaskular sebaiknya sudah dikerjakan sebelum klirens
kreatinin dibawah 15 ml.menit. Dianjurkan pmebuatan akses vaskular jika klirens kreatinin telah
dibawah 20 ml/menit.

2.9 Prognosis

Secara garis besar prognosis dari GGK yang tidak ditangani adalah buruk. Kebanyakan pasien
dengan GGK akan meninggal dengan komplikasi penyakit kardiovaskuler, infeksi, atau jika
dialisis tidak tersedia maka akan terjadi sindrom uremia yang progresif (hiperkalemia, asidosis,
malnutrisi, perubahan fungsi mental). Diantara pasien yang menjalani terapi pengganti ginjal,
penyakit kardiovaskuler merupakan penyebab mortalitas tersering kira-kira 40 % dari populasi.
Volume ekstraseluler yang overload dan hipertensi diketahui sebagai faktor prediktor terjadinya
hipertropi ventrikular kiri dan peningkatan risiko mortalitas akibat penyakit kardiovaskuler di
populasi. Setelah disesuaikan dengan umur, ras, jenis kelamin, dan etnik, dan keberadaan
diabetes, risiko penyakit kardiovaskuler tetap menjadi penyebab kematian tertinggi terutama
pada pasien muda

Circulation. 2007 Jul 3;116(1):85-97.

Nat Rev Nephrol. 2011 Mar;7(3):128-3

Nephrol Dial Transplant. 2002 May;17(5):723-31

Lancet. 2012 Jan 14;379(9811):165-80.

Cardiovascular disease (CVD)is the leading cause of death in patients with CKD.

o Reducing risk factors for development of CVD is beneficial.

E.g. treatment of hyperlipidemia, lifestyle and dietary changes

Tight blood pressure control:

o Reducing damage due to the end organ effects of hypertension on the kidney as
well as the heart.

o Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor


blockers(ARBs) block the effects of angiotensin II on (i) sodium and fluid
retention, (ii) vasoconstriction, (iii) stimulating ADH release, (iv) stimulating
aldosterone release, and (v) inducing a sympathetic response.

ACEIs and ARBs also slow down progression of proteinuria in patients


with diabetic CKD.

Diabetes management:
o Tight glucose management slows the progression of vascular and heart disease.

Avoidance of IV contrast, NSAIDs, and nephrotoxic drugs:

o These agents can potentially induce an acute kidney injury (AKI) on the
underlying kidney disease and therefore exacerbate the baseline CKD.

Diet:

o Mixed evidence exists whether dietary protein restriction is beneficial in slowing


disease progression.

o Proteins affect the renal hemodynamics, raising the GFR, in hypothesized 2 ways.

Hormonal effects proteins cause secretion of glucagon, IGF-1 and


kinins, all of which have been shown to raise the GFR.

Tubuloglomerular effects high amino acid (AA) filtration leads to


increased AA and hence the sodium uptake in the proximal convoluted
tubule. A decreased sodium delivery to the distal convoluted tubule leads
to the rennin-angiotensin system activation via the macula densa and these
work to raise the GFR (mechanisms above)

o Controlling hyperphosphatemia: Protein restriction also limits phosphorus


consumption. Hyperphosphatemia plays a major role in the progression of renal
osteodystrophy. Phosphate binders are used to reduce phosphate absorption
through the GI tract.