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