Acute renal failure

(ARF)/Acute kidney injury

(AKI)
Dr. Atma Gunawan SpPD.KGH
 Diagnostic criteria AKI
• Abrupt (within 48 hours)
• Absolute increase in the serum creatinine
concentration of ≥ 0.3 mg/dL (26.4 micromol/L)
from baseline,
• Or increase in the serum creatinine concentration
of ≥ 50 percent,
• Or oliguria of less than 0.5 mL/kg per hour for
more than six hours
• The diagnostic criteria should be applied only
after volume status had been optimized
• Urinary tract obstruction needed to be excluded if
oliguria was used as the sole diagnostic criterion.
 Acute or chronic ?
• The recent onset of symptoms or signs, such as fever
and discolored urine, suggests an acute process.
• Little or no output also suggests an acute component,
since prolonged oliguria (output less than 500 mL/day)
is associated with advanced renal failure.
• An increasing plasma creatinine concentration after the
initial evaluation is indicative of at least an acute or
rapidly progressive component to the disease, while a
stable value suggests a chronic disease.
• The plasma creatinine concentration tends to rise
progressively (at a rate greater than 0.3 to 0.5 mg/dL
per day) in acute tubular necrosis.
• A slower rate of rise is suggestive of prerenal disease.
• Ultrasonography, showing small, echogenic kidneys is
most consistent with a chronic disease . However, the
presence of normal-sized kidneys does not exclude
chronic disease.
AKI Criteria by the Acute Kidney Injury Network.
Causes
 The causes of AKI
• Acute tubular necrosis — 45 percent
• Prerenal — 21 percent
• Acute on chronic kidney disease — 13
percent (mostly due to acute tubular
necrosis and prerenal disease)
• Urinary tract obstruction — 10 percent
• Glomerulonephritis or vasculitis — 4 percent
• Acute interstitial nephritis — 2 percent
Atheroemboli — 1 percent

A report from Madrid, for example, evaluated all 748 cases of acute
renal failure at 13 tertiary hospital centers
 How AKI develops
Pre-renal Causes Intra-renal causes Post-renal causes
Damage to Renal Tubules

Hypoperfusion Intratubular Increased Renal Obstruction of

Obstruction vasoconstriction Urine Flow

Decreased Glomerular Increased

Filtration Rate Cellular
Intratubular Backup of urine
edema
Pressure
Increased Proximal Backleak of Decreased
Tubular Reabsorption of Tubular Fluid into Glomerular Capillary Compression of
SodIum and Water interstitium Permeability Renal Tubules

Decreased
Increased Secretion of Glomerular
Aldosterone and
Filtration Rate
Antidiuretic Hormone
Tubular Dysfunction (ATN)

Acute Kidney Injury

PATOFISIOLOGI ATN :
A. Normal
Arteriol aferen Arteriol eferen

Aliran plasma
glomerulus

Tekanan
hidrostatik
glomerulus
Filtrasi glomerulus
Tekanan
dalam tubulus
Contribution of ‘back-Leakage’ of glomerular
filtrate and intratubule obstruction to Renal
Failure in ATN
Diagnostic for the causes of
AKI
 Treatment
• Optimalization of volume status :
- rehydration
- fluid maintainance : 30-40 ml/kgBW/day
• Release post renal obstruction
• Correct electrolyte and acid-base imbalance:
- acidosis
- hyperkalemia, hypocalcemia
• Minimalize secondary organ damage due to AKI
(lung edema, arrhytmia,vomiting)
• Special adaptation due to decrease of renal
function
– Drug doses adjusment
– Low activity
 Nutritional Support
• Enteral nutrition is the recommended 
maintain gut integrity, ↓ gut atrophy and
↓ bacterial and endotoxin translocation
• General rule : 20-35 kcal/kg/day and up to
a maximum of 1.7g amino acids/kg/day if
hypercatabolic and receiving CRRT
• Electrolytes must be monitored closely to
avoid hypokalaemia and/or
hypophosphataemia following the initiation
of enteral nutrition.
 Pharmacological Treatment
• Loop diuretics
• Dopamine
• Fenoldopam
• Mannitol
• IGF and ANP
 Drug doses need to be adjusted
appropriately
 currently no evidence to support the
use of a specific pharmacological therapy
in the treatment of AKI
 Indications to Start RRT in AKI
serum urea >180 mg/dl (kali 6,01)

/Serum urea >180 mg/dl

 Modalitas terapi dialisis pada
ARF
• Intermiten hemodialisis
• Continuous renal replacement
therapy
• Acut peritoneal dialysis
Chronic kidney disease
 Definition of Chronic Kidney
Disease
Criteria
1. Kidney damage for ≥ 3 months, as defined by structural or
functional abnormalities of the kidney, with or without
decreased GFR, manifest by either :
• Pathological abnormalities; or
• Markers of kidney damage, including
Abnormalities in the composition of the blood or
urine, or abnormalities in imaging tests

2. GFR < 60 mL/min/1.73 m2 for ≥ 3 mounths, with or without

kidney damage
• The distinction between acute, subacute
and chronic kidney disease is arbitrary.
Clearly, a rise in the plasma creatinine
concentration or an abnormality on the
urinalysis that has developed within days
to weeks represents an acute process,
whereas evidence of renal disease
extending for months to years is a
chronic process that may be associated
with acute exacerbations.
 Differentiation of acute from
chronic kidney disease
• History Long-standing history suggests
CKD
• Renal osteodystrophy Ro” evidence of osteitis fibrosa
cystica or osteomalacia
suggests CKD
• Renal size (length)
-small (<9 cm) CKD
-normal AKI
-enlarged(>12 cm) Diabetec nephropathy
Amyloidosis
Obstructive uropathy
HIV
PKD
• Renal biopsy Histologic diagnosis
 K/DOQI 2003
Tahapan Penyakit Ginjal Kronik
GFR
Tahap Keterangan
(mL/men/1.73m2)
1 Kerusakan ginjal dengan GFR 90
normal atau 
2 Kerusakan ginjal dengan  60 – 89
GFR ringan
3  GFR sedang 30 – 59
4  GFR berat 15 – 29
5 Gagal ginjal < 15 (atau dialisis)
Penyakit ginjal kronik didefinisikan sebagai kerusakan ginjal atau GFR < 60
mL/men/1.73m2 selama > 3 months. Kerusakan ginjal didefinisikan sebagai kelainan
patologis atau adanya petanda adanya kerusakan, termasuk kelainan dalam test darah
atau urin atau pemeriksaan radiologis
 Penyebab CKD terbanyak yang membuat
pasien menjalani renal replacement therapy
(transplant,HD,CAPD)

Penyakit %

Diabetes mellitus 40
Hypertension 25
Glomerulonephritis 15
Polycystic kidney disease 4
Urologic 6
Unknown & miscellaneous 10
 Screening for CKD
• Rationale : early detection, early intervention, reduced
associated complications, high prevalence silent
kidney disease
• Whom ? Diabetes, hypertension, autoimmune diseases,
urinary tract infection or obstruction, heart failure,
cirrhosis, family of ESRD, family of nephropathy
(DM,HT,glomerulonephritis)
• How ?
- standart urine dipstick (spot urine): proteinuria
hematuria, lekosituria
- serum creatinine
- blood pressure
- ultrasound imaging(obstruction,stones,infection,PKD)
- serum electrolytes
- urinary concentration
 The risk for loss of kidney function
Type Definition Examples
Susceptibility Increased susceptibility to Older age, family history
factors kidney damage
Initiation factors Directy initiate kidney damage Diabetes, high blood
pressure, autoimmune
diseases, systemic
infections, urinary tract
infections, urinary stones,
lower urinary tract
obstruction, drug toxicity

Progression Cause worsening kidney Higher lavel of proteinuria,

factors damage and faster decline in higher blood pressure
kidney function after initiation level, poor glycemic
of kidney damage control in diabetes,
smoking
Endstage Increase morbidity and Lower dialysis dase (KW),
factors mortality in kidney failure temporary vascular access,
anemia, low serum
albumin, late referral
 Otak : - letargi, malaise
Manifestasi - bingung
- koma
- kejang Konjungtiva : - kemerahan
Klinik Uremia - kalsifikasi
- perubahan fundus karena hipertensi
Wajah : - pucat
- warna keabu-abuan
- uraemic frost
Mulut : - napas uremik
Tekanan vena jugularis :
- tinggi atau rendah

Jantung : - pembesaran jantung

Dada : - hiperventilasi karena asidosis
- perikarditis - edema paru, efusi

Abdomen : - ginjal & kandung kemih teraba

Tekanan darah : - meningkat - bruits ginjal
- turun saat berdiri
Lengan & tangan :
- lecet
- bekas garukan
- lekonikia
- tremor
- flap
- myoclonic jerks
Urin : - simptom penyakit ginjal
- poliuri, frekuensi, nokturi

Genital : - impotensi
- libido menurun Perifer : - edema tungkai
- amenore, mandul - neuropati perifer
- deformitas tulang pd anak
- peningkatan penyakit vaskuler
Manifestasi klinik CKD (biasanya manifes
pada KK<30 ml/minute ):

Anemia
Hipertensi
Overload syndrome
Uremia
 Perjalanan CKD
• Kerusakan ginjal bersifat irreversible
• Penurunan fungsi ginjal bersifat
progresif (4 ml/m pertahun)
• Kerusakan ginjal lebih lanjut bisa
diperlambat/dihambat dengan
melakukan intervensi terhadap
faktor-faktor yg mempercepat
kerusakan ginjal
 Koreksi faktor reversibel & correctable

 Faktor pre renal : hipovolemia ,dekompensasi kordis,hipotensi,

stenosis arteri renal
 Faktor post renal : membebaskan obstruksi post renal oleh karena
batu, prostat, keganasan rongga pelvis
 Mengobati penyakit dasar faktor renal : DM, hipertensi, Wegener’s
granulomatosis, lupus nefritis dll
 Eradikasi infeksi kuman t.u yg di traktus urogenitalis : ISK, sepsis
 Measures to prevent the
progression of CKD patients ?
• Life style modification : ideal BW,healty
eating,restrict dietary salt intake,cease
smoking,moderate alcohol
consumption,increase physical activity
• BP below 130/80. Hypertensive diabetics
and micro/macroalbuminuria treated with
ACE I or ARB
• Glycemic control : HbA1c <7%
• Reduction of proteinuria : ACEI,ARB
 Measures to prevent the
progression of CKD
• Dietary protein restriction : 0,6 – 0,8 g/kg BB
• Lipid lowering : cholesterol total
<200,LDL<100,HDL>45,TG<150
• Avoidance of nephrotoxic agents:
NSAID,aminoglycoside,radiocontrast media
Adjust doses depend on clearance creatinine
• Early referral to nephrologist :creatinine
clearance <30 ml/m,rapid progression of
renal failure,doubt to diagnosis or prognosis
• Others : Ca x P <55 mg/dl, PTH <3xN, fluid
balance,acidosis
Pengobatan Khusus Gejala & Keluhan
GGK
1. Anemia
- Fe
- asam folat
- eritropoetin
- transfusi
2. Gatal
- diet rendah protein
- difenhidramin
3. Mual
- diet rendah protein
4. Hiperuricemia : alupurinol
5. Hiperkalemi : glukose dan insulin,diit
rendah kalium,cation exchange resin
6. Asidosis : nabic infus dan tablet
7. Overload syndrome : balans cairan, diuretik
 Should be referred to
nephrologist

• When creatinine clearance <30

ml/min/1.73m2
• Patients at risk of rapid progression
• In whom doubt exists as to their
diagnosis and prognosis
 Kapan dilakukan renal
replacement therapy ?

 Klirens kreatinin < 15 ml/m (DM)

 Klirens Kreatinin < 10 ml/men (non DM)
 Sindroma Uremik
 Hiperkalemia
 Asidosis Metabolik
 Kelebihan Cairan (overload)
 Modalitas renal replacement
therapy
• Hemodialisis (HD)
• Chronic ambulatory peritoneal
dialysis (CAPD)
• Kidney transplant
HD
CAPD
KIDNEY
TRANSPLANT