ACUTE KIDNEY INJURY (AKI)

Transkripsi

1 ACUTE KIDNEY INJURY (AKI) RSCM FKUI

2 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.

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

4 Definitions Acute Renal Failure Acute Kidney Injury

5 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 miokardium, katup, dan perikardium; aritmia; tamponade B. Lainnya: hipertensi pulmoner, emboli paru masif, ventilasi mekanik tekanan positif

6 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 (jarang): Myeloma multipel, makroglobulinemia, polisitemia

7 Etiologi renal I. Obstruksi renovaskular II. Penyakit glomeruli III. Nekrosis tubular akut IV. Nefritis interstitial V. Obstruksi intratubular VI. Penolakan allograf

8 Etiologi post renal I. Ureter Batu, gumpalan darah, keganasan, kompresi eksternal (fibrosis retroperitoneal) II. Leher kandung kemih Neurogenic bladder, hipertrofi prostat, t batu, keganasan III. Uretra Striktur, fimosis, katup kongenital

9 AKI: A Common, Serious Problem AKI is present in 5% of all hospitalized patients, and up to 50% of patients in ICUs Mortality rate 50 80% in dialyzed d ICU patients 4 Million die each year of AKI AKI requiring i dialysis i is one of the most important independent predictors of death in ICU patients 25% of ICU dialysis survivors progress to ESRD within 3 years

10 RIFLE Criteria for Acute Renal Dysfunction Category GFR Criteria UO Criteria Risk Injury Failure Loss ESKD Increased creatinin x1.5 or GFR decrease > 25% Increased creatinine x2 or GFR decrease > 50% Increase creatinine x3 or GFR decrease > 75% UO < 0.5 ml/kg/h x 6 hr UO < 0.5 ml/kg/h x 12 hr UO < 0.3 ml/kg/h x 24 hr or Anuria x 12 hrs Persistent ARF = complete loss of kidney function > 4 weeks End Stage Kidney Disease (> 3 months) High Sensitivity High Specivity 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 Dec; 8(6):505-8.

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12 Acute Kidney Injury Network (AKIN 2005) Continuum of the renal linjury STAGE I RISK (R) STAGE II INJURY (I) STAGE III FAILURE (F) STAGE IV LOSS (L) STAGE V ESRD (E) Severity Outcome

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16 Etiology of AKI

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

18 Diagnosis of AKI is often delayed Elevation in serum creatinine is the current gold standard, d but tthis is problematic Normal serum creatinine varies widely with age, gender, diet, muscle mass, muscle metabolism, medications, hydration status In AKI, serum creatinine can take several ldays to reach a new steady state

19 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 non kontras Markers of CKD ipth, size<9cm, anemia, high phosphate, low bicarb Renal biopsy

20 AKI: Urgent Need for Early Diagnosis Early 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 in humans

21 Biomarkers for Early Prediction of Acute Kidney Injury

22 SEPSIS Current Clinical Scenario SEPSIS WITH Early Biomarkers CPB CPB TRAUMA Normal Creatinine Elevated Creatinine TRAUMA Early Detection CONTRAST Kidney Injury Acute Kidney Injury MORTALITY CONTRAST Kidney Injury Acute Kidney Injury ARDS Failed Intervention ARDS MORTALITY TOXINS TOXINS Early Detection Opportunity for Early Intervention a b Parikh CR, Kidney Int 2008;72:

23 Parikh CR, Kidney Int 2008;72:

24 Potential Roles of Biomarkers in AKI Early Detection Defined Timing & Single Insult CPB Contrast Trauma Chemotherapy Undefined Timing & Multiple Insults Sepsis ARDS Cii Critical lillness Differential Diagnosis Location (proximal vs distal tubule) Etiology (toxin, ischemia, sepsis) ATN vs Pre renal Acute vs Chronic Prognosis Severity of AKI Need for RRT Duration of AKI Response to Treatment Length of stay Mortality Parikh CR, Kidney Int 2008;72:

25 IL 18 CPB (1) ARDS (3) NGAL CPB (4.5) PCI (6) D+HUS (8) Early Detection Cystatin C ICU (9) (+) ICU (10) ( ) Tubular Enzymes ICU (11) KIM 1 Potential Biomarkers in AKI (Human Data) Differential Diagnosis IL 18 ATN vs other (13) KIM 1 ATN vs other (14) Na + / H + Exchanger ATN vs other (15) Prognosis IL 18 Mortality in ARDS (3) Duration of AKI (1) Cystatin C Need for RRT (16) NGAL Duration of AKI (1) Parikh CR, Kidney Int 2008;72:

26 NGAL (Neutrophyl lgelatinase Associated i t dlipocalin) Protein yang terikat pada gelatinase ase dari sel neutrofil Normal : diekskresi dengan kadar sangat rendah dari jaringan tubuh Percobaan binatang : NGAL paling cepat dan secara bermakna meningkat akibat gangguan (injury) atau toksik pada ginjal Diagnosis i dinii AKI 1 2 hariterdeteksi t sebelum kenaikan kreatinin Dapat diperiksa dari darah dan urine Ronco C,Int J Artific Organ 2008;31:

27 The Emerging Plasma AKI Panel Devarajan,CLI April/May 2009

28 The Emerging Urine AKI Panel Devarajan,CLI April/May 2009

29 Treatment of AKI Treatment is largely supportive in nature! Pharmacologic treatments under study: Dopamine: no benefit Atrial Natriuretic Peptide (ANP) or ANP analogue (Anaritide): promising Human Insulin like growth factor 1: no benefit Renal Replacement therapy remains the cornerstone of management of minority of patients with severe AKI Nephron Clin Pract 2009;112:c222 c229

30 Is there a role for Dopamine in prevention or treatment t t of AKI in ICU setting? 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: ANZICS Clinical Trial Group. Lancet 2000;356:

31 Role of ANP analogues in AKI? 61 patients in 2 cardiothoracic ICU with post op AKI assigned to receive recombinent ANP(50 (50ng/kg/min) / or placebo 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 Jun;32(6):1310 5

32 Is there a role for diuretics in the treatment of AKI in ICU setting? PICARD Study: Cohort study of 552 pts in 4 UC hospitals: Odds Ratio In hospital Mortality 1.77 Non recovery of renal function 1.68 Improved urine output tand shorter duration of frrt( (none has clinical relevance in ICU pts) But diuretics continue to be used for volume control in AKI in ICU setting! JAMA Nov 27;288(20): Crit Care Resusc Mar;9(1):60 8

33 Tatalaksana Terapi berdasarkan etiologi : 1. Prerenal 2. Renal 3. Postrenal

34 Terapi suportif Asupan nutrisi : Kebutuhan kalori 30 Kal/kgBB ideal/hari ditambah 15 20% (terdapat t komplikasi/stres) i/ Asupan protein : 1 1,5 gram/kgbb ideal/hari pada GnGA berat Asupan cairan: tentukan status hidrasi pasien

35 Koreksi gangguan asam basa Koreksi gangguan elektrolit

36 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 atau <115 meq/l) Hipertermia Kelebihan dosis obat yang dapat didialisis (keracunan)

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