gangguan ginjal akut
Transcript of gangguan ginjal akut
Acute Kidney InjuryDo we know what we mean?
Pembimbing :
dr.Selli Muljanto, Sp.A
بسماهللالرحمنالرحي م
Definisi Gangguan Ginjal Akut
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
End-stage kidney disease
Persistant AKI = complete loss of renal function > 4 weeks
Increased creatinine × 3 or GFR decrease
>75% or creatinine > 4 mg/dL
(acute rise >0.5 mg/dL)
UO < 0.3 ml/kg/hr × 24 hours
or anuria × 12 hours
Increased creatinine × 2
or GFR decrease > 50%UO <0.5 ml/kg/hr × 12 hours
Increased creatinine × 1.5
or GFR decrease > 25%UO<0.5 ml/kg/hr × 6 hours
Bellomo et al. Crit Care 2004;8:R204-R212.
Olig
uria
Spe
cific
ity
Sen
sitiv
ity
Risk
Injury
Failure
Loss
End-stage
• 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
Estimated CCl (eCCl) Urine Output
Risk eCCl decrease by 25% <0.5 ml/kg/hr for 8 h
Injury eCCl decrease by 50% <0.5 ml/kg/hr for 16 h
Failure eCCl decrease by 75% or eCCl <35 ml/min/1.73 m2
<0.3 ml/kg/hr for 24 h or anuric for 12 h
Loss Persistent failure > 4 weeks
End stage Persistent failure > 3 months
Pediatric RIFLE criteria definition and classifications of AKI
Clinical Approach to AKI: Pre-, Intra-, and Post-Renal
HistoryVolume status
UltrasoundUrinalysis US shows
Hydronephrosis
Post-Renal
Urinalysis Normal
UrinalysisAbnormal
Tubulointerstial Disorders
Glomerular and Vascular Disorders
Pre-renal
Nephrologists Clinical Approach to AKIHistory
Volume StatusUltrasoundUrinalysis
Hydronephrosis
Post-Renal
Prostate disease BPH CancerPelvic malignancyStonesStrictureRetroperitoneal fibrosis
Normal Urinalysis
Pre-Renal
Low ECF Volume GI losses Hemorrhage Diuretics Osmotic diuresis
Altered renal blood flowor hemodynamics Sepsis Heart failure Cirrhosis/Hepatorenal syndrome Hypercalcemia Medications NSAIDs/Cox-2 inhibitors ACE inhibitors Angiotensin II receptor blockers Vascular disease
Vascular Disorders
TubulointerstitialDisorders
Glomerular Disorders
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
Arterial Renal artery stenosis Renal artery thromboembolism Fibromuscular dysplasia Takayasu arteritisMedium vessel Polyarteritis nodosa Kawasaki diseaseSmall vessel Glomerulonephritis Thrombotic microangiopathies Cholesterol emboliRenal vein Renal vein thrombosis Abdominal compartment syndrome
Renal parenchymal disorders
Abnormal urinalysis
Patofisiologi GgGA Iskemik
(1)Vasoconstriction
Renin-angiotensinendothelin
PGI2NO
(2)Obstruction
by casts
(3)Tubularbackleak
IschemiaNephrotoxins
Tubular damage(proximal tubules andascending thick limb)
(5)? Direct glomerular
effectGFR Oliguria
Tubularfluid flow
Intratubularpressure
Possible pathogenetic mechanisms in ATN.
(4)Interstitial
inflammation
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
González E, et al. Kidney Int 2008; 73: 940–946.
Clinical Feature Frequency
Leukocyturia 82%
Microhematuria 67%
Fever 42%
Eosinophilia 34%
RashOliguria
23%23%
Pemeriksaan Penunjang
• Urinalisis
• Radiologis
• Biopsi Ginjal
Perbedaan pemeriksaan urin antara gangguan ginjal akut prarenal dengan
renal
Urine Prarenal Renal
Volume Sedikit Sedikit
Protein Negatif Sering positif
Sedimen Normal Torak granular, eritrosit
Berat jenis > 1020 1010 – 1015
Na urin (mmol/l) < 10 > 25
Urea urin (mmol/l) > 250 < 160
Osmolalitas (mmol/l) > 500 200 -350
Rasio osmolalitas U/P > 1.3 < 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 ½ 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
Kalorikcal/kg berat badan ideal
Protein
kcal/kg berat badan ideal
Pengobatan konservatif 0 – 2 tahun
Anak / remaja95 - 100
Minimal berdasarkan umur
1.0 - 1.81.0
Dialisis peritoneal 0 – 2 tahun
Anak / remaja
95 - 100Minimal berdasarkan umur
2.0 - 2.51.0 - 2.5
Hemodialisis 0 – 2 tahun
Anak / remaja95 - 150
Minimal berdasarkan tinggi badan
1.5 - 2.11.0 - 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
Matur Nuwun