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
Obstruction

Increased Renal
vasoconstriction

Decreased Glomerular
Filtration Rate

Increased
Intratubular
Pressure

Cellular
edema

Increased Proximal
Tubular Reabsorption of
SodIum and Water

Backleak of
Tubular Fluid into
interstitium

Increased Secretion of
Aldosterone and
Antidiuretic Hormone

Decreased
Glomerular Capillary
Permeability

Decreased
Glomerular
Filtration Rate
Tubular Dysfunction (ATN)

Acute Kidney Injury

Obstruction of
Urine Flow

Backup of urine

Compression of
Renal Tubules

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

Renal osteodystrophy

suggests
Renal size (length)
-small (<9 cm)
-normal
-enlarged(>12 cm)

Renal biopsy

Long-standing history suggests

CKD
Ro evidence of osteitis fibrosa
cystica or osteomalacia
CKD
CKD
AKI
Diabetec nephropathy
Amyloidosis
Obstructive uropathy
HIV
PKD
Histologic diagnosis

K/DOQI 2003

Tahapan Penyakit Ginjal Kronik

GFR
(mL/men/1.73m2)

Tahap

Keterangan

Kerusakan ginjal dengan GFR

normal atau

60 89

Kerusakan ginjal dengan

GFR ringan
GFR sedang

GFR berat

15 29

Gagal ginjal

< 15 (atau dialisis)

90

30 59

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
Susceptibility
factors

Definition
Increased susceptibility to
kidney damage

Examples
Older age, family history

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
factors

Cause
worsening
kidney
damage and faster decline in
kidney function after initiation
of kidney damage

Higher lavel of proteinuria,

higher blood pressure
level, poor glycemic
control in diabetes,
smoking

Endstage
factors

Increase
morbidity
and Lower dialysis dase (KW),
mortality in kidney failure
temporary vascular access,
anemia, low serum
albumin, late referral

Manifestasi
Klinik Uremia

Otak : - letargi, malaise

- bingung
- koma
- kejang
Konjungtiva : - kemerahan
- kalsifikasi
- perubahan fundus karena hipertensi

Wajah : - pucat
- warna keabu-abuan
- uraemic frost
Tekanan vena jugularis :
- tinggi atau rendah
Jantung : - pembesaran jantung
- perikarditis
Tekanan darah : - meningkat
- turun saat berdiri

Mulut : - napas uremik

Dada : - hiperventilasi karena asidosis

- edema paru, efusi
Abdomen : - ginjal & kandung kemih teraba
- bruits ginjal

Lengan & tangan :

- lecet
- bekas garukan
- lekonikia
- tremor
- flap
- myoclonic jerks
Urin : - simptom penyakit ginjal
- poliuri, frekuensi, nokturi

Genital : - impotensi
- libido menurun
- amenore, mandul

Perifer : - edema tungkai

- 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