Acute Kidney Injury
Do we know what we mean?
Pembimbing : dr.Selli Muljanto, Sp.A
Gangguan ginjal akut yang sebelumnya disebut gagal ginjal
akut adalah penurunan fungsi ginjal mendadak, dalam
beberapa jam sampai beberapa minggu, diikuti oleh
kegagalan ginjal untuk mengekskresi sisa metabolisme
nitrogen dengan atau tanpa disertai terjadinya gangguan
keseimbangan cairan ataupun elektrolit Pertemuan organisasi ADQI (Acute Dialysis Quality Initiative) di Vicenza 2004 Acute Renal Failure (ARF) menjadi Acute Kidney Injury (AKI)
In 2004, a consensus definition for AKI was proposed by the Acute Dialysis Quality Initiative: the RIFLE criteria - R = risk for renal dysfunction - I = injury to the kidney
F = failure of kidney function
L = loss of kidney function E = end-stage renal disease
The Rifle Criteria
Risk
Injury
Increased creatinine 1.5 or GFR decrease > 25%
Increased creatinine 2 or GFR decrease > 50%
UO<0.5 ml/kg/hr 6 hours
UO <0.5 ml/kg/hr 12 hours
Failure
Increased creatinine 3 or GFR decrease UO < 0.3 ml/kg/hr 24 hours >75% or creatinine > 4 mg/dL or anuria 12 hours (acute rise >0.5 mg/dL)
Loss End-stage
Persistant AKI = complete loss of renal function > 4 weeks
End-stage kidney disease
Bellomo et al. Crit Care 2004;8:R204-R212.
eCCl determined by Schwartz formula Baseline eCCl from three months before PICU
100 ml/min/1.73m2 if no data available
pRIFLE differs from RIFLE in
Oliguria duration RIFLE-F limit eCCl
Pediatric RIFLE criteria definition and classifications of AKI Pediatric RIFLE criteria Estimated CCl (eCCl) Risk Injury Failure Loss End stage
eCCl decrease by 25% eCCl decrease by 50% eCCl decrease by 75% or eCCl <35 ml/min/1.73 m2 Persistent failure > 4 weeks Persistent failure > 3 months
Urine Output
< 0.5 ml/kg/hr for 8 h < 0.5 ml/kg/hr for 16 h < 0.3 ml/kg/hr for 24 h or anuric for 12 h
Clinical Approach to AKI: Pre-, Intra-, and Post-Renal
History Volume status Ultrasound Urinalysis Urinalysis Normal
US shows Hydronephrosis
Urinalysis Abnormal Pre-renal Post-Renal
Tubulointerstial Disorders
Glomerular and Vascular Disorders
Nephrologists Clinical Approach to AKI
Normal Urinalysis
History Volume Status Ultrasound Urinalysis
Hydronephrosis
Pre-Renal Abnormal urinalysis
Low ECF Volume GI losses Hemorrhage Diuretics Osmotic diuresis
Altered renal blood flow or hemodynamics Sepsis Heart failure Cirrhosis/Hepatorenal syndrome Hypercalcemia Medications NSAIDs/Cox-2 inhibitors ACE inhibitors Angiotensin II receptor blockers Vascular disease
Vascular Disorders
Post-Renal
Renal parenchymal disorders
Tubulointerstitial Disorders
Glomerular Disorders
Arterial Renal artery stenosis Renal artery thromboembolism Fibromuscular dysplasia Takayasu arteritis Medium vessel Polyarteritis nodosa Kawasaki disease Small vessel Glomerulonephritis Thrombotic microangiopathies Cholesterol emboli Renal vein Renal vein thrombosis Abdominal compartment syndrome
Prostate disease BPH Cancer Pelvic malignancy Stones Stricture Retroperitoneal fibrosis
Tubular obstruction Crystals Calcium oxalate (Ethylene glycol, orlistat) Indinivir Acyclovir Methotrexate Tumor lysis syndrome Myeloma cast nephropathy
Acute tubular necrosis Ischemic Nephrotoxic Contrast-induced Rhabdomyolysis
Acute interstitial nephritis Medication-induced Autoimmune Sjogren syndrome Sarcoidosis Infection-related
Patofisiologi GgGA Iskemik
Possible pathogenetic mechanisms in ATN.
Ischemia Nephrotoxins
Tubular damage (proximal tubules and ascending thick limb)
(1) Vasoconstriction Renin-angiotensin endothelin PGI2 NO
(2) Obstruction by casts
(3) Tubular backleak
(4) Interstitial inflammation
Intratubular pressure
Tubular fluid flow
(5) ? Direct glomerular effect
GFR
Oliguria
Gejala Klinis
Gejala pada intravasculer Takikardi Hipotensi Akral dingin Mukosa membrane kering Cappilary refill time > 2 detik Gejala Akibat Kelebihan Cairan Edem Hipertensi Irama Gallop Hepatomegali Krepitasi JVP meningkat
Gejala dari Penyakit Penyebab Purpura (Henoch_Schonlein purpura) Malar Rash (SLE) Pembesaran ginjal (Trombosis vena renalis, Hidronefrosis) Tender kidney (Pyelonefritis, penolakan transplantasi) Pembesaran ginjal (Uropati Obstruksi)
Clinical Features of AIN
Clinical Feature Leukocyturia Microhematuria Fever Eosinophilia Frequency 82% 67% 42% 34%
Rash Oliguria
23% 23%
Gonzlez E, et al. Kidney Int 2008; 73: 940946.
Pemeriksaan Penunjang
Urinalisis
Radiologis
Biopsi Ginjal
Perbedaan pemeriksaan urin antara gangguan ginjal akut prarenal dengan renal
Urine Volume Prarenal Sedikit Renal Sedikit
Protein
Sedimen Berat jenis Na urin (mmol/l) Urea urin (mmol/l) Osmolalitas (mmol/l) Rasio osmolalitas U/P
Negatif
Normal > 1020 < 10 > 250 > 500 > 1.3
Sering positif
Torak granular, eritrosit 1010 1015 > 25 < 160 200-350 < 1,1
FENa
<1
>1
Pemeriksaan Radiologis
Tujuan pemeriksaan USG ginjal adalah untuk menentukan apakah kedua ginjal ada, menentukan ukuran/besar ginjal, mengevaluasi parenkim ginjal, mengevaluasi adanya obstruksi pada saluran kemih, melihat aliran darah ginjal. Untuk mengevaluasi aliran darah ginjal dari arteri dan vena renalis, digunakan pemeriksaan radiologis USG Doppler.
Biopsi ginjal
Biopsi ginjal digunakan apabila hasil evaluasi pemeriksaan yang non-invasif tidak dapat menegakkan diagnosis etiologinya
Management
Fluids
Hyperkalemia
Metabolic Acidosis Hypertension Nutrition
Management: Intravascular Volume Fluids
Place foley catheter Fluid challenge - Isotonic saline 10-20 ml/kg
(+) response (> 1ml/kg/hr) indicates pre-renal cause (-) response indicates intrinsic cause
Prevent fluid overload - restrict
D5W or D10W with bicarbonate to replace insensible losses (approx 1/3 of maintenance) Replace urine losses with NS Lasix (1-5mg/kg) for signs of overload
Discontinue fluids/TPN with K
Management: Intravascular Volume Diuretics
Augmentation of Loop with addition of Thiazide
Augment loop diuretics by delivering more Cl to the distal tubule by blunting Na reaborption Fiser et al, Kid Int 1994 46:482
IV thiazide vs Control to augment loop in 10 adults with AKI
Thiazide addition resulted in sig improvement in UOP
5mg/kg/dose q6 Diuril followed by Lasix IV q6 or Lasix gtt
Management: Intravascular Volume Dopamine
Renal-dose dopamine (0.5 to 3-5 mcg/kg/min)
Increases RBF by promoting vasodilatation & may improve UOP
Not shown to alter course of renal failure Not proven to convert oliguric to non-oliguric AKI No effect in decreasing need for dialysis or improving survival in patients with AKI
Complications: tachycardia, arrhythmias, & myocardial ischemia
Management: Acidosis
Impaired acid excretion + increased acid production from underlying condition Administration
where max resp compensation is adequate and/or acidosis is contributing to hyperK
Plasma bicarb falls below 15 meq/L or arterial pH < 7.25
Management: Acidosis
Correction estimated by
HCO3 dose = (16-measured HCO3)(0.4)(wgt in kg)
Or empirically give HCO3 at dose of 1-2 meg/kg Avoid rapid correction HTN, fluid overload, intracranial hemorrhage If (+) hypoCa correct this 1st b/c HCO3 will decrease ionized Ca tetany or SZ
Management: Hipertensi
Prevent by avoiding fluid overload
Diuretics if responsive
Vasodilators usually drug of choice
Nitroprusside, Labetalol, or Nicardipine gtt Intermittent IV doses of Hydralazine or If taking po oral minoxadil or hydralazine
Management: Nutrition
AKI assoc w/ marked catabolism
Balance of volume and components
Enteral preferred (Nepro, RenaCal, etc.) over central Consider the following with TPN
Volume
High Dextrose, low rates; 20% lipids
Components
AA~ 1-1.5 gm/kg No K, Phos
Terapi Nutrisi Pada Pasien GgGA
Terapi nutrisi pada penderita GgGA harus
memperhatikan berbagai faktor: 1. Mempertimbangkan kelainan metabolisme yang terjadi 2. Mengurangi akumulasi toksin uremi 3. Mempertahankan status nutrisi secara optimal
Tabel Penatalaksanaan diit kalori dan protein Gangguan ginjal akut pada anak
Kalori kcal/kg berat badan ideal Protein kcal/kg berat badan ideal
Pengobatan konservatif 0 2 tahun
Anak / remaja
95 - 100 Minimal berdasarkan umur
1.0 - 1.8 1.0
Dialisis peritoneal 0 2 tahun Anak / remaja
95 - 100 Minimal berdasarkan umur
2.0 - 2.5 1.0 - 2.5
Hemodialisis 0 2 tahun Anak / remaja
95 - 150 Minimal berdasarkan tinggi badan
1.5 - 2.1 1.0 - 1.8
Prognosis
Highly dependent on underlying etiology, age of patient, and clinical presentation Children (retrospective)
> 3 system organ failure assoc with more than 50% mortality
