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Understanding Chronic renal failure

Chronic Renal Failure (CRF) or end-stage renal disease is a chronic renal failure is progressive
and irreversible. Where the ability of the body fails to maintain metabolism and fluid and
electrolyte balance, leading to uremia (retention of urea and other nitrogen wastes in the blood)
(KMB, Vol 2 p. 1448).
Etiology
Causes of chronic renal crow quite a lot but for clinical purposes can be divided into 2 groups:
1. Renal parenchymal disease
Primary renal disease: Glomerulonephritis, Mielonefritis, polycystic kidney, renal tuberculosis
Secondary renal disease: lupus nephritis, nephropathy, kidney Amilordosis, Poliarteritis nodasa,
progressive systemic sclerosis, gout, Dm
Etiology
2. Obstructive renal disease: an enlarged prostate, urinary tract stones, ureteric reflux,
Broadly speaking, the causes of kidney failure can be categorized
Infections are recurrent and the deteriorating nephron
Urinary tract obstruction
Destruction of blood vessels due to diabetes and hypertension of the old
Scar tissue and direct trauma to the kidney
Pathophysiology
Two theoretical approaches are usually proposed to explain the renal failure in chronic renal
failure:

1. Traditional viewpoint
To say that all units of the nephron have been stricken with the disease but in different stages,
and specific parts of the nephron is associated with certain functions can be completely destroyed
or changed its structure, such as organic lesion in the medulla will damage the anatomic
arrangement of the loop of Henle .
2. Bricker hypothesis approach or an intact nephron hypothesis
Argues that if the diseased nephron of its units will be destroyed, but the remaining intact
nephrons continue to work normally. Uremia will arise when the number of nephrons that have
been so reduced so that the fluid and electrolyte balance can not be maintained anymore.

Important adaptation performed by the kidneys in response to the threat of fluid and electrolyte
imbalance. Existing remnant nephrons hypertrophy in its effort to implement the entire kidney
workload, there is increased filtration speed, load and reabsorption of solutes in each nephron
tubules contained in normal kidney dibawab down.

Adaptation mechanism is quite successful in maintaining fluid and electrolyte balance of the
body to a low level of kidney function.
But eventually if 75% nephron mass has been destroyed, then the filtration speed and load for
each nephron solutes so high that the balance glomerolus-tubules can no longer be maintained.
Good flexibility in the process of excretion and the concentration of solutes and water to be
reduced.
Clinical course
General travel progressive renal failure can be divided into 3 atadium
Stage I
Decrease in reserve kidney (renal function between 40% - 75%). This is the lightest stage, in
which kidney function is still good. At this stage the patient is not yet merasasakan signs and
symptoms of renal physiology laboratory examination is still in still within normal limits. During
this stage, and serum creatinine levels of BUN (Blood Urea Nitrogen) within normal limits and
the patient asymptomatic. Impaired renal function may only be known by giving a heavy
workload, sepersti urinary concentration test of time or by conducting a thorough test GFR.
Stage II
Insufiensi renal (kidney function between 20% - 50%). At this stage the patient can perform
common tasks such as power and concentration but decreased kidney. At this stage of treatment
must be quickly overcome shortages daloam case of liquids, salt deficiency, heart disorders and
prevention of drug administration medications that are menggnggu kidney function. If these
steps as soon as possible with the right to prevent people with more severe ketahap entry. At this
stage more than 75% of a working network has been damaged. BUN levels began to rise above
normal limits. Increasing the concentration of BUN is slightly different, depending on the levels
of protein in this stage diit.pada serum creatinine levels begin to increase beyond normal levels.

Insufiensi renal (kidney function between 20% - 50%). At this stage the patient can perform
common tasks such as power and concentration but decreased kidney. At this stage of treatment
must be quickly overcome shortages daloam case of liquids, salt deficiency, heart disorders and
prevention of drug administration medications that are menggnggu kidney function. If these
steps as soon as possible with the right to prevent people with more severe ketahap entry. At this
stage more than 75% of a working network has been damaged. BUN levels began to rise above
normal limits. Increasing the concentration of BUN is slightly different, depending on the levels
of protein in this stage diit.pada serum creatinine levels begin to increase beyond normal levels.

Polyuria due to kidney failure is usually greater for a disease that mainly attacks the tubules,
although polyuria is moderate and rarely more than 3 liters / day. Usually found anemia in renal
failure with renal physiology between 5% - 25%. obviously decreased kidney function and
symptoms develop symptoms of blood deficiency, blood pressure will go up, patient activity
began to fail.
Stage III
Uremi kidney failure (renal function less than 10%)
All the symptoms are clear and the patient entered in a state of Diman unable to perform daily
tasks sebaimana hair properly. Gejal gejal that arise include nausea, munta, decreased appetite.,
Shortness of breath, dizziness, headache, decreased urine, lack of sleep, seizures seizures and
eventually a decline in consciousness to coma. Stadum end arise at about 90% of the nephron
mass has been destroyed. GFR value was 10% of normal and creatinine levels may be of 5-10 ml
/ min or less.

In this situation serum creatinine and BUN levels to rise sharply as the decline. At end-stage
renal failure, the patient began to feel the symptoms are quite severe because the kidneys no
longer able to maintain homeostasis caiaran and electrolytes in the body. Patients usually become
oliguric (urinary expenditure) is less than 500 per day because of the failure of glomerular
disease processes first though first attack of kidney tubules,

attack complex gijal tubules, the complex biochemical changes and symptoms symptoms of the
so-called uremic syndrome affects every system in the body. At end-stage renal failure, patients
would definitely menggal unless he received treatment in the form of a kidney transplant or
dialysis.
Clinical manifestations
Respiratory Disorders
Similarly, edema
Hypertension
Anorexia, nausea, vomitus
Gastric ulceration
Stomatitis
Proteinuria
Hematuria

Lethargy, apathy, concentration penuruna

Anemia
Bleeding
Poor skin turgor, gatak itchy skin
Renal dystrophy
Hyperkalemia
Metabolic Acidosis
Diagnostic Test
1. Urine:
Volume
Color
Sediment
Specific gravity
Creatinine
Protein

2. Blood:

Bun / Creatinine
A complete blood count
Red blood cells
Serum sodium
Potassium
Magnesium phosphate
Protein
Serum osmolarity

3. Pielografi intravenous
Showed abnormalities in renal pelvis and ureter
Pielografi retrograde
Done when there is suspicion of a reversible obstruction
Arteriogram kidney
Assessing kidney circulation and identify ekstravaskular, mass.

4. Sistouretrogram urination
Shows the size of the bladder, reflux into the ureter, retention.
5. Ultrasono kidney
Indicate bladder size, and the masses, cysts, obstruction in the upper urinary tract.
6. Renal biopsy
Probably done in endoscopy to determine the tissue cells for histological diagnosis

7. Endoscopic renal nefroskopi

Conducted to determine the renal pelvis; out stones, hematuria, and removal of the tumor
selective
8. ECG
It may show abnormal electrolyte and acid-base imbalance, arrhythmia, ventricular hypertrophy
and signs of pericarditis.
Management
1. Dialysis
Dialysis can be done to prevent complications of serious acute renal failure, such as
hyperkalemia, pericarditis and seizures. Pericarditis improve biochemical abnormalities; cause
caiarn, protein and sodium can be freely consumed; eliminate the bleeding tendency, and assist
wound healing.

2. Handling hyperkalemia
Fluid and electrolyte balance is a major problem in acute renal failure, hyperkalemia is the most
life-threatening condition in this disorder. Therefore, patients will be monitored through a series
of examinations of hyperkalemia serum electrolyte levels (potassium value> 5.5 mEq / L; SI: 5.5
mmol / L), ECG changes (T wave peak height is low or very high), and changes in clinical
status. Pningkatan potassium levels can be reduced by provision of a replacement ion resin
(sodium sulfonate polistriren [kayexalatel]), taken orally or by retention enema.

3. Maintaining fluid balance

Management of liquid keseimbanagan based on daily body weight, central venous pressure
measurement, urine and serum concentrations, fluid loss, blood pressure and clinical status of
patients. Enter and oral and parenteral output of urine, gastric drainage, feces, wound drainage
and perspirasi calculated and used as the basis for penggantia fluid therapy.
CONCLUSIONS ASSESSMENT
Hj client's name. H
Age 85 years.
Date admitted 30 April 2005 with a complaint can not urinate and right back pain .. These
complaints lasted 3 days at home. Initially 2 days ago clients use Dulcolaxthe client can not
defecate suppositories for 2 consecutive days and the client can BAB.
A day later the client difficulty urinating, straining even urine can not get out, then the family
took him to hospital. Arriving at Hospital mounted lancer urinary catheters and exit out the red
color somewhat and then comes out slightly brown colored like tea water.

When client assessments have been treated for 3 days focus data obtained:
General state of the client rather weak, leg weakness, not powered, wrinkled skin is not elastic.
odema pretibial. Less muscle tone. always lying in bed, ativitas a day, today assisted by his son,
urinary catheter inserted water brown like tea, pengalas cloth wet and smelly.

TD 160/90 mmHg. Nadi 82 x / min, body temperature of 36.2 o C, the sclera was pale, eye
secretions (+). Mouth / breath smelled of ammonia, talking softly sometimes less obvious,
Laboratory examination results
Date: 2 / 5 2005
U: 202.32
Creatinine: 3, 93
AST: 19
SGPT: 30
lWBC: 5.5 x 103 /
RBC: 3.90
HGB: 10.7
HCT: 32.5%
GDS: 161

Examination Support
Ultrasound Results:
Kidney: Looks both kidneys shrink with echodifferensiasi not clear (right kidney 5.9 x 3.1 cm
left kidney 5.8 x 2.5 cm).
Impression: PNC bilateral.

MEDICAL THERAPY
Drugs - Drugs:
IVFD NaCl 0.9% 20 tts / min
Allopurinol 300mg 1-0-0
10mg Zonidip 0-0-1
300mg Fibrat 0-0-1
Inj. Neurosanbe 1 amp / day / drips

Based on the assessment, nursing diagnosis is obtained:

1. Excess fluid volume associated with decreased urine output, fluid retention and sodium.
2. Impaired ADL compliance associated with physical weakness.
3. Oral mucous membrane changes associated with chemical irritants.
4. Risk of damage to the integrity of the skin associated with decreased activity, impaired
metabolic status.
Plan of action:
1. Excess fluid volume associated with decreased urine output, fluid retention and sodium.
1. Assess fluid status:
Weigh daily weight
Balance the input and output
Skin turgor and the presence of edema
Blood pressure, pulse and rhythm of the pulse.
2. Limit fluid intake

3. Identify potential sources of fluid

Medications and fluids used for the treatment of oral and intravenous.
Food
4. Explain rational restrictions on liquids
5. Assist clients in overcoming the discomfort due to fluid restriction.
6. Enhance and encourage oral hygiene.

2. Impaired ADL compliance associated with physical weakness.

Determine client's ability to berpartyisipasi in self-care activities. (Scale 0-4).
Provide assistance with the activities required
Encourage families to help meet the ADL client in bed.
Bantu family in the care of the client in bed.
Encourage families to change their butt pad when wet.
Help and motivation of families to maintain the cleanliness of the client's body,

3. Oral mucous membrane changes associated with chemical irritants.

1. Inspection of the oral cavity note the humidity, the character of saliva, the presence of
inflammation, ulceration.
2. Give fluids throughout the 24 hours within specified limits.
3. Give frequent mouth care.
4. Encourage oral hygiene after meals and at bedtime.
5. Encourage clients to avoid dessert lemon / ingredients that contain alcohol.
4. Risk of damage to the integrity of the skin associated with decreased activity, impaired
metabolic status.
1. Inspection of skin to change color, skin moisture, vascular.
2. Change position often, a client with a slow movement, give a soft cloth bearing the bony
ridge.
3. Maintain a dry linen free of kerip

GAGAL GINJAL

 Pengertian

Gagal ginjal kronis atau penyakit renal tahap akhir (ESRD) merupakan gangguan fungsi renal
yang progresif dan irreversibel dimana kemampuan tubuh gagal untuk mempertahankan
metabolisme dan keseimbangan cairan dan elektrolit. Gagal ginjal kronis terjadi dengan lambat
selama berbulan-bulan atau bertahun-tahun, dengan penurunan bertahap dengan fungsi ginjal dan
peningkatan bertahap dalam gejala-gejala, menyebabkan penyakit ginjal tahap akhir (PGTA).
Gagal ginjal kronis biasanya akibat akhir dari kehilangan fungsi ginjal lanjut secara bertahap.
Gangguan fungsi ginjal adalah penurunan laju filtrasi glomerulus yang dapat digolongkan ringan,
sedang dan berat. Azotemia adalah peningkatan nitrogen urea darah (BUN) dan ditegakkan bila
konsentrasi ureum plasma meningkat.

Etiologi

Gagal ginjal kronik merupakan suatu keadaan klinis kerusakan ginjal yang progresif dan
irreversible dari berbagai penyebab. Sebab-sebab gagal ginjal kronik yang sering ditemukan
dapat dibagi menjadi delapan kelas.
Klasifikasi sebab-sebab gagal ginjal kronik :

 Infeksi : Pielonefritis kronik

 Penyakit peradangan : Glomerulonefritis
 Penyakit vascular hipertensi : Nefrosklerosis benigna, nefrosklerosis maligna, stenosis arteria
renalis.
 Gangguan jaringan penyambung : Lupus eritematosus sistemik, Poliarteritis nodosa, sklerosis
sistemik progresif.
 Gangguan kongerital dan hereditas : Penyakit ginjal polikistik, asidosis tubulus ginjal.
 Penyakit metabolic : Diabetes militus, gout, hiperpara tiroidisme, amiloidosis.
 Nefropati toksik : Penyalahgunaan analgesik, nefropati timbale
 Nefropati obstruktif : Saluran kemih bagian atas kalkuli , neoplasma, fibrosisretroperitoneal.
Saluran kemih bagian bawah: hipertropi prostate, struktur urea, anomaly kongetal pada leher
kandung kemih dan uretra.

 Tanda dan gejala

Penurunan fungsi ginjal akan mengakibatkan berbagai manifestasi klinik mengenai dihampir
semua sistem tubuh manusia, seperti:

 Gangguan pada Gastrointestinal

Dapat berupa anoreksia, nausea, muntah yang dihubungkan dengan terbentuknya zat toksik
(amoniak, metal guanidin) akibat metabolisme protein yang terganggu oleh bakteri usus sering
pula faktor uremikum akibat bau amoniak dari mulut. Disamping itu sering timbul stomatitis,
cegukan juga sering yang belum jelas penyebabnya. Gastritis erosif hampir dijumpai pada 90 %
kasus Gagal Ginjal Kronik, bahkan kemungkinan terjadi ulkus peptikum dan kolitis uremik.
 Kulit
Kulit berwarna pucat, mudah lecet, rapuh, kering, timbul bintik-bintik hitam dan gatal akibat
uremik atau pengendapan kalsium pada kulit.
 Hematologi
Anemia merupakan gejala yang hampr selalu ada pada Gagal Ginjal Kronik. Apabila terdapat
penurunan fungsi ginjal tanpa disertai anemia perlu dipikirkan apakah suatu Gagal Ginjal Akut
atau Gagal Ginjal Kronik dengan penyebab polikistik ginjal yang disertai polistemi. Hemolisis
merupakan sering timbul anemi, selain anemi pada Gagal Ginjal Kronik sering disertai
pendarahan akibat gangguan fungsi trombosit atau dapat pula disertai trombositopeni. Fungsi
 leukosit maupun limposit dapat pula terganggu sehingga pertahanan seluler terganggu,
sehingga pada penderita Gagal Ginjal Kronik mudah terinfeksi, oleh karena imunitas yang
menurun.
 Sistem Saraf Otot
Penderita sering mengeluh tungkai bawah selalu bergerak-gerak (restlesslessleg syndrome),
kadang tersa terbakar pada kaki, gangguan syaraf dapat pula berupa kelemahan, gangguan
tidur, gangguan konsentrasi, tremor, kejang sampai penurunan kesadaran atau koma.
 Sistem Kardiovaskuler
Pada gagal ginjal kronik hampir selalu disertai hipertensi, mekanisme terjadinya hipertensi pada
Gagal Ginjal Kronik oleh karena penimbunan garam dan air, atau sistem renin angiostensin
aldosteron (RAA). Sesak nafas merupakan gejala yang sering dijumpai akibat kelebihan cairan
tubuh, dapat pula terjadi perikarditis yang disertai efusi perikardial. Gangguan irama jantung
sering dijmpai akibat gangguan elektrolit.
 Sistem Endokrin
Gangguan seksual seperti penurunan libido, ion fertilitas sering dijumpai pada Gagal Ginjal
Kronik, pada wanita dapat pula terjadi gangguan menstruasi sampai aminore. Toleransi glukosa
sering tergangu paa Gagal Ginjal Kronik, juga gangguan metabolik vitamin D.
 Gangguan lain
Akibat hipertiroid sering terjadi osteoporosis, osteitis, fibrasi, gangguan elektrolit dan asam basa
hampir selalu dijumpai, seperti asidosis metabolik, hiperkalemia, hiperforfatemi, hipokalsemia.

 Pemerikasaan Penunjang
Urine
Volume : Biasanya kurang dari 400 ml/24 jam (oliguria) atau urine tak keluar (anuria)
Warna : Secara abnormal urine keruh mungkin disebabkan oleh pus bakteri, lemak, partikel koloid,
forfat atau urat. Sedimen kotor, kecoklatan menunjukan adanya darah, HB, mioglobin.
Berat jenis : Kurang dari 1,015 (menetap pada 1,010 menunjukan kerusakan ginjal berat).
Osmolalitas : Kurang dari 350 mosm/kg menunjukan kerusakan tubular, dan rasio urine/serum sering
1:1
Klirens keratin : Mungkin agak menurun
Natrium : Lebih besar dari 40 m Eq/L karena ginjal tidak mampu mereabsorbsi natrium.
Protein : Derajat tinggi proteinuria (3-4+) secara kuat menunjukan kerusakan glomerulus bila SDM dan
fragmen juga ada.

Darah
BUN / Kreatin : Meningkat, biasanya meningkat dalam proporsi kadar kreatinin 16 mg/dL diduga tahap
akhir (mungkin rendah yaitu 5)
Hitung darah lengkap : Ht : Menurun pada adanya anemia Hb:biasanya kurang ari 78 g/dL
SDM : Waktu hidup menurun pada defisiensi aritropoetin seperti pada azotemia.
GDA : pH : Penurunan asidosis metabolik (kurang dari 7,2) terjadi karena kehilangan kemampuan ginjal
untuk mengeksresi hydrogen dan amonia atau hasil akhir katabolisme protein. Bikarbonat menurun,
PCO2 menurun .
Natrium Serum : Mungkin rendah (bila ginjal “kehabisan Natrium” atas normal (menunjukan status dilusi
hipernatremia).
Kalium : Peningkatan sehubungan dengan retensi sesuai dengan perpindahan seluler (asidosis) atau
pengeluaran jaringan. Pada tahap akhir, perubahan EKG mungkin tidak terjadi sampai kalium 6,5 MPq
atau lebih besar.
Magnesium/Fosfat : Meningkat
Kalsium : Menurun
Protein (khususnya Albumin) : Kadar serum menurun dapat menunjukkan kehilangan protein melalui
urine, perpindahan cairan, penurunan pemasukan, atau penurunan sintesis karena kurang asam amino
esensial.
Osmolalitas Serum : Lebih besar dari 285 mOsm/kg, sering sama dengan urine.
KUB fota : Menunujukkan ukuran ginjal / ureter / kandung kemih dan adanya obstruksi (batu)
Piolegram Retrograd : Menunujukkan abnormallitas pelvis ginjal dan ureter.
Arteriogram Ginjal : Mengkaji sirkulasi ginjal dan mengidentifikasi ekstravaskular massa.
Sistouretrogram Berkemih : Menunjukan ukuran kandung kemih, refluks ke dalam ureter, terensi.
Ultrasono Ginjal : Menentukan ukuran ginjal dan adanya massa, kista, obstruksi pada saluran
perkemihan bagian atas.
Biopsi Ginjal : Mungkin dilakukan secara endoskopik untuk menentukan sel jaringan untuk diagnosis
histoligis.
Endoskopi Ginjal, Nefroskopi : Dilakukan untuk menentukan pelvis ginjal, keluar batu, hematuria dan
pengangkatan tumor selektif.
EKG : Mungkin abnormal menunjukan ketidakseimbangan elektrolit dan asam/basa.
Foto Kaki, Tengkorak, Kolmna Spiral dan Tangan : Dapat menunjukan demineralisasi.
(Rencana Askep, Marilyn E Doenges dkk)

 Pencegahan

Pemeliharaan kesehatan umum dapat menurunkan jumlah individu yang menjadi insufisiensi. Sampai
menjadi kegagalan ginjal. Perawatan ditujukan kepada pengobatan masalah medis dengan sempurna
dan mengawasi status kesehatan orang pada waktu mengalami stress (infeksi, kehamilan).

 Pengobatan / Penatalaksanaan

Tujuan penatalaksaan adalah untuk mempertahankan fungsi ginjal dan homeostasis selama
mungkin. Adapun penatalaksaannya sebagai berikut :

 Diet tinggi kalori dan rendah protein

Diet rendah protein (20-40 g/hari) dan tinggi kalori menghilangkan gejala anoreksia dan nausea
dari uremia, menyebabkan penurunan ureum dan perbaikan gejala. Hindari masukan berlebihan
dari kalium dan garam.
 Optimalisasi dan pertahankan keseimbangan cairan dan garam.
Biasanya diusahakan hingga tekanan vena juga harus sedikit meningkat dan terdapat edema
 betis ringan. Pada beberapa pasien, furosemid dosis besar (250-1000 mg/hari) atau diuretic
100p (bumetanid, asam etakrinat) diperlukan untuk mencegah kelebihan cairan, sementara
pasien lain mungkin memerlukan suplemen natrium klorida atau natrium bikarbonat oral.
Pengawasan dilakukan melalui berat badan, urine, dan pencatatan keseimbangan cairan
(masukan melebihi keluaran sekitar 500 ml).
 Kontrol hipertensi
Bila tidak terkontrol dapat terakselerasi dengan hasil akhir gagal kiri pada pasien hipertensi
dengan penyakit ginjal, keseimbangan garam dan cairan diatur tersendiri tanpa tergantung
tekanan darah, sering diperlukan diuretik loop, selain obat anti hipertensi.
 Kontrol ketidaksemibangan elektrolit
Yang sering ditemukan adalah hiperkalemia dan asidosis berat. Untuk mencegah hiperkalemia,
dihindari masukan kalium yang besar (batasi hingga 60 mmol/hari), diuretik hemat kalium, obat-
obatan yang berhubungan dengan eksresi kalium (misalnya penghambat ACE dan obat anti
inflamasi non steroid), asidosis berat, atau kekurangan garam yang menyebabkan pelepasan
kalium dari sel dan ikut dalam kaliuresis. Deteksi melalui kadar kalium plasma dan EKG.
Gejala-gejala asidosis baru jelas bila bikarbonat plasma kurang dari 15 mmol/liter biasanya
terjadi pada pasien yang sangat kekurangan garam dan dapat diperbaiki secara spontan dengan
dehidrasi. Namun perbaikan yang cepat dapat berbahaya.
 Mencegah dan tatalaksana penyakit tulang ginjal
Hiperfosfatemia dikontrol dengan obat yang mengikat fosfat seperti alumunium hidroksida
(300-1800 mg) atau kalsium karbonat (500-3000mg) pada setiap makan. Namun hati-hati
dengan toksisitas obat tertentu. Diberikan supplemen vitamin D dan dilakukan paratiroidektomi
atas indikasi.
 Deteksi dini dan terapi infeksi
Pasien uremia harus diterapi sebagai pasien imuosupresif dan diterapi lebih ketat.
 Modifikasi terapi obat dengan fungsi ginjal
Banyak obat-obatan yang harus diturunkan dosisnya karena metabolitnya toksik dan
dikeluarkan oleh ginjal. Misalnya digoksin, aminoglikosid, analgesic opiat, amfoterisin dan
alupurinol. Juga obat-obatan yang meningkatkan katabolisme dan ureum darah, misalnya
tetrasiklin, kortikosteroid dan sitostatik.
 Deteksi dan terapi komplikasi
Awasi denagn ketat kemungkinan ensefelopati uremia, perikarditis, neurepati perifer,
hiperkalemia yang meningkat, kelebihan cairan yang meningkat, infeksi yang mengancam jiwa,
kegagalan untuk bertahan, sehingga diperlukan dialysis.
 Persiapan dialysis dan program transplantasi
Segera dipersiapkan setelah gagal ginjal kronik dideteksi. Indikasi dilakukan dialysis biasanya
adalah gagal ginjal dengan klinis yang jelas meski telah dilakukan terapi konservatif atau terjadi
komplikasi.