ACUTE KIDNEY INJURY (AKI)

RSCM FKUI
FKUI

Pendahuluan
Sindrom yang ditandai oleh penurunan LFG
secara mendadak dan cepat (hitungan jam
minggu) yang mengakibatkan terjadinya
retensi produk sisa nitrogen seperti ureum
dan kreatinin
kreatinin.

Pendahuluan
Peningkatan kreatinin serum 0,5
0 5 mg/dL dari
nilai sebelumnya, penurunan CCT hitung
sampai 50% atau penurunan fungsi ginjal yang
mengakibatkan kebutuhan akan dialisis

Definitions

Acute Renal Failure

Acute
cute Kidney
d ey Injury
ju y

Etiologi Prerenal
I. Hipovolemia
A. Perdarahan, luka bakar, dehidrasi
B. Gastrontestinal: muntah, diare, drainase bedah
C. Renal: penggunaan diuretik,
diuresis osmotik (diabetes mellitus), hipoadrenal
D. Sekuestrasi cairan di ruang ekstravaskuler:
pankreatitis, peritonitis, trauma,
luka bakar, hipoalbuminemia berat
II. Curah jantung rendah
A. Penyakit
y
miokardium,, katup,
p, dan p
perikardium;;
aritmia; tamponade
B. Lainnya: hipertensi pulmoner, emboli paru masif,
ventilasi mekanik tekanan positif
p

Etiologi Prerenal
III. Perubahan rasio resistensi vaskular sistemik ginjal
A. Vasodilatasi sistemik:
sepsis, obat antihipertensi, anestesia, anafilaksis
B. Vasokonstriksi renal: hiperkalsemia,
norepinefrin, epinefrin, siklosporin, takrolimus, amfoterisin B
C. Sirosis dengan asites (sindrom hepatorenal)
IV. Hipoperfusi renal dengan gangguan respon autoregulasi ginjal:
Inhibitor siklooksigenase,
penghambat enzim pengkonversi angiotensin
V. Sindrom hiperviskositas
p
(jarang):
(j
g)
Myeloma multipel, makroglobulinemia, polisitemia

Etiologi renal
II. Obstruksi renovaskular
II. Penyakit glomeruli
III. Nekrosis
k i tubular
b l akut
k
IV. Nefritis interstitial
V. Obstruksi intratubular
VI Penolakan allograf
VI.

Etiologi post renal

I. Ureter
Batu, gumpalan darah, keganasan,
kompresi eksternal (fibrosis retroperitoneal)
II. Leher kandung kemih
N
Neurogenic
i bladder,
bl dd hipertrofi
hi t fi prostat,
t t batu,
b t
keganasan
III Uretra
III.
U t
Striktur, fimosis, katup kongenital

AKI: A Common, Serious Problem

AKI is present in 5%
% off allll h
hospitalized
l d
patients, and up to 50% of patients in ICUs
Mortality
li rate 50
0 80% in
i di
dialyzed
l d ICU
patients 4 Million die each year of AKI
AKI requiring
i i di
dialysis
l i iis one off the
h most
important independent predictors of death in
ICU patients
25% of ICU dialysis survivors progress to ESRD
within 3 years

RIFLE Criteria for Acute Renal Dysfunction

Category GFR Criteria

UO Criteria

Risk

Increased creatinin
x1.5 or GFR
decrease > 25%

UO < 0.5 ml/kg/h x 6 hr

Injury

Increased creatinine
x2 or GFR decrease
> 50%

UO < 0.5 ml/kg/h x 12 hr

Failure

Increase creatinine
x3 or GFR decrease
> 75%

UO < 0.3 ml/kg/h x 24 hr High

or Anuria x 12 hrs
Specivity

Loss

Persistent ARF = complete loss of kidney

f
function
ti > 4 weeks
k

ESKD

End Stage Kidney Disease (> 3 months)

High
Sensitivity

PROGNOSIS

GFR=Glomerular Filtration Rate

ARF; Acute Renal Failure
UO = Urine Output
ESKD; End Stage Kidney Disease
References :
Bellomo R, Kellum JA, Mehta R, Palevsky PM, Ronco C. Curr Opin Crit Care. 2002 Dec; 8(6):505-8.

Acute Kidney Injury Network (AKIN 2005)

C ti
Continuum
off th
the renall iinjury
j

STAGE I

STAGE II
STAGE III

RISK
(R)

INJURY
(I)

Severity

FAILURE
(F)

STAGE IV
LOSS
(L)

STAGE V
ESRD
(E)

Outcome

Etiology
gy of AKI

Diagnosis AKI
Anamnesis : harus terinci dan akurat
Pemeriksaan fisik : rutin
Laboratorium
b
i
: pemeriksaan
ik
standar
d
Kesulitan : membedakan akut dan kronik
Tanda kronik : fatigue,
fatigue weight loss
loss, anorexia
anorexia,
nocturia, and pruritus

Diagnosis of AKI is often delayed

Elevation in serum creatinine is the current gold
standard,
t d d b
butt thi
this iis problematic
bl
ti
Normal serum creatinine varies widely with age,
gender,
d di
diet, muscle
l mass, muscle
l metabolism,
b li
medications, hydration status
In AKI, serum creatinine can take
k severall d
days to
reach a new steady state

Initial diagnostic tools in AKI

History and Physical exam.
Urinalysis
SG, PH, protein, blood, crystals, infection
Urine microscopy
casts, cells (eosinophils)
Renal imaging
USG CT urografi
USG,
rografi non kontras
Markers of CKD
iPTH, size<9cm, anemia, high phosphate, low bicarb
Renal biopsy

AKI: Urgent Need for Early Diagnosis

Earlyy forms of AKI are often reversible

Early diagnosis may enable timely therapy
The paucity of early biomarkers has
impaired our ability to institute timely
therapy
h
iin h
humans

Biomarkers
Bi
k
for
f Early
E l Prediction
P di ti
of Acute Kidney Injury

SEPSIS

Current Clinical Scenario

SEPSIS

CPB

CPB
Normal
Creatinine

Early
Detection

Elevated
Creatinine
TRAUMA

TRAUMA

CONTRAST

WITH Early Biomarkers

Kidney
Injury

Acute
Kidney
Injury

MORTALITY

CONTRAST

Acute
Kidney
Injury

Kidney
Injury

MORTALITY
ARDS

TOXINS

ARDS

F il d
Failed
Intervention

TOXINS

Early
Detection

Opportunity
for Early
Intervention

Parikh CR, Kidney Int 2008;72:173946

Parikh CR, Kidney Int 2008;72:173946

Potential Roles of Biomarkers in AKI

Early
Detection
Defined Timing &
Single Insult
CPB
Contrast
Trauma
Chemotherapy

Undefined Timing &

Multiple Insults
Sepsis
ARDS
Critical
C i i l Ill
Illness

Prognosis
Differential
Diagnosis
Location
(proximal vs distal tubule)

Severity of AKI
Need for RRT
Duration of AKI

Etiology
(toxin ischemia
(toxin,
ischemia, sepsis)

Response to
Treatment

ATN vs Prerenal

Length of stay

Acute vs Chronic

Mortality

Parikh CR, Kidney Int 2008;72:173946

Potential Biomarkers in AKI

(Human Data)
Early
Detection
IL 18

Cystatin C

CPB (1)
ARDS (3)

ICU (9) (+)

ICU (10) (())

Prognosis
Differential
Diagnosis
IL 18

NGAL
CPB (4.5)
PCI (6)
D+HUS (8)

Tubular
Enzymes
ICU (11)

ATN vs other (13)

Mortality in ARDS (3)

Duration of AKI (1)

Cystatin C
Need for RRT (16)

KIM 1
ATN vs other (14)

KIM 1

IL 18

NGAL
Duration of AKI (1)

Na+ / H+
Exchanger
ATN vs other (15)

Parikh CR, Kidney Int 2008;72:173946

NGAL
(N t h l GelatinaseAssociated
(Neutrophyl
G l ti
A
i t d Lipocalin)
Li
li )
Protein
ote yang
ya g te
terikat
at pada ge
gelatinase
at ase da
dari se
sel
neutrofil
g kadar sangat
g rendah
Normal : diekskresi dengan
dari jaringan tubuh
Percobaan binatang : NGAL paling cepat dan
secara bermakna meningkat akibat gangguan
(injury) atau toksik pada ginjal
Diagnosis
Di
i dini
di i AKI 12
1 2 hari
h i terdeteksi
t d t k i sebelum
b l
kenaikan kreatinin
Dapat diperiksa dari darah dan urine
Ronco C,Int J Artific Organ 2008;31:19932000

The Emerging Plasma

AKI Panel

Devarajan,CLI April/May 2009

The Emerging
g g Urine
AKI Panel

Devarajan,CLI April/May 2009

Treatment of AKI
Treatment is largely supportive in nature!
Pharmacologic treatments under study:
Dopamine
Dopamine: no benefit
Atrial Natriuretic Peptide (ANP) or ANPanalogue
((Anaritide):
) p
promisingg
Human Insulin like growth factor 1: no benefit

Renal Replacement
p
therapy
py remains the
cornerstone of management of minority of
patients with severe AKI
p
Nephron Clin Pract 2009;112:c222c229

Is there a role for Dopamine in prevention or

t t
treatment
t off AKI in
i ICU setting?
tti ?
Clinical Outcomes:
No effect on mortality
No effect on the need for or incidence of Renal Replacement
Therapy (RRT)
Renal Physiologic Outcomes:
Diuretic effect and increased creatinine clearance on the first
day which was not significant on the following days.
Adverse effect:
on the immune, respiratory, and endocrine system.
Ann Intern Med. 2005;142:510524
ANZICS Clinical Trial Group. Lancet 2000;356:21392143

Role of ANP analogues

g
in AKI?
61 patients in 2 cardiothoracic ICU with postop AKI assigned
to receive
i recombinent
bi
ANP (50
(50ng/kg/min)
/k / i ) or placebo
l b
The need for RRT before day 21 after development of AKI was
significantly lower in ANP group (21% vs 47%)
The need for RRT or death after day 21 was significantly lower
in ANP group (28% vs 57%)

Crit Care Med. 2004 Jun;32(6):13105

Is there a role for diuretics in the treatment of AKI in

ICU setting?
tti ?
PICARD Study:
Cohort study of 552 pts in 4 UC hospitals:
Inhospital Mortality
Nonrecovery of renal function

Odds Ratio
1.77
1.68

IImproved
d urine
i output
t t and
d shorter
h t d
duration
ti off RRT ((none h
has
clinical relevance in ICU pts)
But diuretics continue to be used for volume control in AKI in
ICU setting!
JAMA. 2002 Nov 27;288(20):254753
Crit Care Resusc. 2007 Mar;9(1):608

Tatalaksana
Terapi berdasarkan etiologi :
1. Prerenal
2 Renall
2.
3. Postrenal

Terapi suportif
Asupan nutrisi :
Kebutuhan kalori 30 Kal/kgBB ideal/hari
ditambah
dit
b h 15
1520%
20% (t
(terdapat
d t kkomplikasi/stres)
lik i/ t )
Asupan protein : 11,5 gram/kgBB ideal/hari pada
GnGA berat
Asupan cairan: tentukan status hidrasi pasien

 Koreksi gangguan asam basa

Koreksi gangguan elektrolit

Terapi suportif indikasi dialisis

Oliguria
Anuria
Hiperkalemia (K >6,5 mEq/L)
Asidosis berat (pH <7,1)
Azotemia (ureum >200 mg/dL)
Edema paru
Ensefalopati uremikum
Perikarditis uremik
Neuropati/miopati uremik
Disnatremia berat ((Na >160 mEq/l
q/ atau <115 mEq/l)
q/ )
Hipertermia
Kelebihan dosis obat yang dapat didialisis (keracunan)

terimakasih