acute kidney injury (aki) imels

ACUTE KIDNEY INJURY (AKI)

RSCM FKUIRSCM –FKUI

PendahuluanPendahuluan

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

PendahuluanPendahuluan

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

Definitions

Acute Renal FailureAcute Renal Failure

Acute Kidney Injurycute d ey ju y

Etiologi PrerenalEtiologi Prerenal

I. HipovolemiaA. Perdarahan, luka bakar, dehidrasiB. Gastrontestinal: muntah, diare, drainase bedahC. Renal: penggunaan diuretik,

diuresis osmotik (diabetes mellitus), hipoadrenalD. Sekuestrasi cairan di ruang ekstravaskuler:

pankreatitis, peritonitis, trauma, luka bakar, hipoalbuminemia berat

II. Curah jantung rendahA. Penyakit miokardium, katup, dan perikardium; y , p, p ;

aritmia; tamponadeB. Lainnya: hipertensi pulmoner, emboli paru masif,

ventilasi mekanik tekanan positifp

Etiologi PrerenalEtiologi Prerenal

III. Perubahan rasio resistensi vaskular sistemik ginjalA. Vasodilatasi sistemik:

sepsis, obat antihipertensi, anestesia, anafilaksisB. Vasokonstriksi renal: hiperkalsemia,

norepinefrin, epinefrin, siklosporin, takrolimus, amfoterisin BC. Sirosis dengan asites (sindrom hepatorenal)

IV. Hipoperfusi renal dengan gangguan respon autoregulasi ginjal: Inhibitor siklooksigenase,

penghambat enzim pengkonversi angiotensinV. Sindrom hiperviskositas (jarang): p (j g)

Myeloma multipel, makroglobulinemia, polisitemia

Etiologi renalEtiologi renal

I Obstruksi renovaskularI. Obstruksi renovaskular

II. Penyakit glomeruli

k i b l kIII. Nekrosis tubular akut

IV. Nefritis interstitial

V. Obstruksi intratubular

VI Penolakan allografVI. Penolakan allograf

Etiologi post renalEtiologi post renal

I. UreterI. UreterBatu, gumpalan darah, keganasan, kompresi eksternal (fibrosis retroperitoneal)kompresi eksternal (fibrosis retroperitoneal)

II. Leher kandung kemihN i bl dd hi t fi t t b tNeurogenic bladder, hipertrofi prostat, batu,

keganasanIII U tIII. Uretra

Striktur, fimosis, katup kongenital

AKI: A Common, Serious Problem% f ll h l d• AKI is present in 5% of all hospitalized

patients, and up to 50% of patients in ICUs li 0 80% i di l d• Mortality rate 50 ‐ 80% in dialyzed ICU

patients– 4 Million die each year of AKIAKI i i di l i i f h• AKI requiring dialysis is one of the most important independent predictors of death in ICU patientsICU patients

• 25% of ICU dialysis survivors progress to ESRD within 3 yearswithin 3 years

RIFLE Criteria for Acute Renal Dysfunction

HighUO < 0.5 ml/kg/h x 6 hrIncreased creatininRisk

UO CriteriaGFR CriteriaCategory

UO < 0.5 ml/kg/h x 12 hrIncreased creatinineInjury

Sensitivityx1.5 or GFR decrease > 25%

x2 or GFR decrease > 50%

HighUO < 0.3 ml/kg/h x 24 hr Increase creatinineFailure

PROGNOSISPROGNOSISPersistent ARF = complete loss of kidney f ti 4 k

Loss

Specivityor Anuria x 12 hrsx3 or GFR decrease > 75%

End Stage Kidney Disease (> 3 months)ESKD

function > 4 weeks

GFR=Glomerular Filtration Rate ARF; Acute Renal FailureGFR=Glomerular Filtration Rate ARF; Acute Renal FailureUO = Urine Output ESKD; End Stage Kidney DiseaseReferences :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 f th l i jContinuum of the renal injury

STAGE ISTAGE I STAGE IISTAGE IISTAGE ISTAGE I STAGE II

INJURY

STAGE II

INJURY

STAGE VESRD

STAGE VESRD

STAGE III

FAILURE

STAGE III

FAILURE

STAGE IVLOSS

STAGE IVLOSS

RISK (R)

RISK (R)

INJURY (I)

INJURY (I)

(E)(E)FAILURE

(F)FAILURE

(F) (L)(L)

Severity OutcomeSeverity Outcome

Etiology of AKIgy

Diagnosis AKIDiagnosis AKI

• Anamnesis : harus terinci dan akuratAnamnesis : harus terinci dan akurat

• Pemeriksaan fisik : rutin

b i ik d• Laboratorium : pemeriksaan standar

• Kesulitan : membedakan akut dan kronik

• Tanda kronik : fatigue weight loss anorexiaTanda kronik : fatigue, weight loss, anorexia, nocturia, and pruritus

Diagnosis of AKI is often delayed

• Elevation in serum creatinine is the current gold t d d b t thi i bl tistandard, but this is problematic

• Normal serum creatinine varies widely with age, d di l l b ligender, diet, muscle mass, muscle metabolism,

medications, hydration status

k l d• In AKI, serum creatinine can take several days to reach a new steady state

Initial diagnostic tools in AKIInitial diagnostic tools in AKI

• History and Physical exam.• Urinalysis

SG, PH, protein, blood, crystals, infection• Urine microscopyUrine microscopy

casts, cells (eosinophils)• Renal imaging

USG CT rografi non kontrasUSG, CT urografi non kontras• Markers of CKD

iPTH, size<9cm, anemia, high phosphate, low bicarb• Renal biopsy

AKI: Urgent Need for Early DiagnosisAKI: Urgent Need for Early Diagnosis

• Early forms of AKI are often reversibley

• Early diagnosis may enable timely therapy

• The paucity of early biomarkers has• The paucity of early biomarkers has impaired our ability to institute timely h i htherapy in humans

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

SEPSIS Current Clinical Scenario SEPSIS

CPB

WITH Early Biomarkers

CPB

TRAUMA

NormalCreatinine

ElevatedCreatinine

CPB

TRAUMA

EarlyDetection

CONTRASTKidneyInjury

AcuteKidneyInjury MORTALITY

F il d

CONTRAST

ARDS

KidneyInjury

AcuteKidneyInjury

MORTALITY

ARDS

TOXINS

FailedIntervention

ARDS

TOXINS

Opportunityfor Early

InterventionEarly

Detection

a b

Parikh CR, Kidney Int 2008;72:1739‐46

Parikh CR, Kidney Int 2008;72:1739‐46

Potential Roles of Biomarkers in AKI

EarlyDetection Prognosis

DifferentialDiagnosisDefined Timing &

Single InsultSeverity of AKI

Need for RRT• CPB• Contrast• Trauma• Chemotherapy

• Location(proximal vs distal tubule)

• Etiology(toxin ischemia sepsis)

Need for RRT

Duration of AKI

Response to• Chemotherapy (toxin, ischemia, sepsis)

• ATN vs Pre‐renal

• Acute vs Chronic

Treatment

Length of stay

MortalityUndefined Timing & MortalityUndefined Timing &Multiple Insults• Sepsis• ARDS

C i i l Ill• Critical Illness

Parikh CR, Kidney Int 2008;72:1739‐46

Potential Biomarkers in AKI(Human Data)(Human Data)

EarlyDetection

PrognosisDetection

DifferentialDiagnosis

IL – 18Mortality in ARDS (3)Duration of AKI (1)

Cystatin CICU (9) (+)ICU (10) (‐)

IL – 18CPB (1)ARDS (3)

IL – 18ATN vs other (13) Cystatin C

Need for RRT (16)

KIM 1

ICU (10) ( )

NGALCPB (4.5)

TubularEnzymes

NGALDuration of AKI (1)

KIM – 1ATN vs other (14)

Na+ / H+

Exchanger

PCI (6)D+HUS (8)

ICU (11)

KIM ‐ 1

ExchangerATN vs other (15)

Parikh CR, Kidney Int 2008;72:1739‐46

NGAL (N t h l G l ti A i t d Li li )(Neutrophyl Gelatinase‐Associated Lipocalin)

• Protein yang terikat pada gelatinase dari selote ya g te at pada ge at ase da seneutrofil

• Normal : diekskresi dengan kadar sangat rendahg gdari jaringan tubuh

• Percobaan binatang : NGAL paling cepat dansecara bermakna meningkat akibat gangguan(injury) atau toksik pada ginjalDi i di i AKI 1 2 h i t d t k i b l• Diagnosis dini AKI 1‐2 hari terdeteksi sebelumkenaikan kreatinin

• Dapat diperiksa dari darah dan urine• Dapat diperiksa dari darah dan urineRonco C,Int J Artific Organ 2008;31:1993‐2000

The Emerging PlasmaThe Emerging PlasmaAKI Panel

Devarajan,CLI April/May 2009

The Emerging Urineg gAKI Panel

Devarajan,CLI April/May 2009

Treatment of AKITreatment of AKI

• Treatment is largely supportive in nature!Treatment is largely supportive in nature!

• Pharmacologic treatments under study:Dopamine no benefit– Dopamine: no benefit

– Atrial Natriuretic Peptide (ANP) or ANP‐analogue (Anaritide): promising( ) p g

– Human Insulin like growth factor 1: no benefit

• Renal Replacement therapy remains the p pycornerstone of management of minority of patients with severe AKIp

Nephron Clin Pract 2009;112:c222‐c229

Is there a role for Dopamine in prevention or t t t f AKI i ICU tti ?treatment of AKI in ICU setting?

Clinical Outcomes:• No effect on mortality• No effect on the need for or incidence of Renal Replacement

Therapy (RRT)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;142:510‐524ANZICS Clinical Trial Group. Lancet 2000;356:2139‐2143

Role of ANP analogues in AKI?g

• 61 patients in 2 cardiothoracic ICU with post‐op AKI assigned i bi ANP (50 /k / i ) l bto receive recombinent ANP (50ng/kg/min) or placebo

• The need for RRT before day 21 after development of AKI was• 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):1310‐5

Is there a role for diuretics in the treatment of AKI in ICU tti ?ICU setting?

• PICARD Study: Cohort study of 552 pts in 4 UC hospitals:Cohort study of 552 pts in 4 UC hospitals:

Odds Ratio In‐hospital Mortality 1.77Non‐recovery of renal function 1.68

I d i t t d h t d ti f RRT ( h• Improved urine output and shorter duration of RRT (none 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):2547‐53Crit Care Resusc. 2007 Mar;9(1):60‐8

TatalaksanaTatalaksana

• Terapi berdasarkan etiologi :Terapi berdasarkan etiologi :

1. Prerenal

2 l2. Renal

3. Postrenal

Terapi suportifTerapi suportif

• Asupan nutrisi :Asupan nutrisi :

Kebutuhan kalori 30 Kal/kgBB ideal/hari dit b h 15 20% (t d t k lik i/ t )ditambah 15‐20% (terdapat komplikasi/stres)

Asupan protein : 1‐1,5 gram/kgBB ideal/hari pada GnGA beratGnGA berat

Asupan cairan: tentukan status hidrasi pasien

• Koreksi gangguan asam basaKoreksi gangguan asam basa

• Koreksi gangguan elektrolit

Terapi suportif – indikasi dialisisTerapi 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 atau <115 mEq/l)( q/ q/ )– Hipertermia– Kelebihan dosis obat yang dapat didialisis (keracunan)

•

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