Acute renal failure (ARF)

/Acute kidney injury (AKI)

PWM OLLY INDRAJANI

 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 %
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 < 500
mL/day) is associated with advanced renal failure.

An plasma creatinine [ ] 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 > 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

Cellular
Filtration Rate Intratubular Backup of urine
edema
Pressure
Increased Proximal Backleak of Decreased
Tubular Reabsorption of Compression of
Tubular Fluid Glomerular
SodIum and Water Renal Tubules
into Capillary
interstitium Permeability
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
B. Konstriksi
arteriolar C. Obstruksi D. Backleak
aferen

Tekanan Cast yang Kebocoran

glomerulus menyumbat filtrat
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
 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(kali6,01)

/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
 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
 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, Wegeners
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