gangguan ginjal akut

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Acute Kidney Injury Do we know what we mean? Pembimbing : dr.Selli Muljanto, Sp.A ﺮﺮﺮﺮﷲﺮﺮﺮ ﺮﺮﺮﺮﺮﺮﺮﺮﺮ

Transcript of gangguan ginjal akut

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Acute Kidney InjuryDo we know what we mean?

Pembimbing :

dr.Selli Muljanto, Sp.A

بسماهللالرحمنالرحي م

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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)”

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• 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

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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

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• 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

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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

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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

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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

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Patofisiologi GgGA Iskemik

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(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

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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

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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)

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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%

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Pemeriksaan Penunjang

• Urinalisis

• Radiologis

• Biopsi Ginjal

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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

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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.

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Biopsi ginjal

Biopsi ginjal digunakan apabila hasil evaluasi pemeriksaan yang non-invasif tidak dapat menegakkan diagnosis etiologinya

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Management

• Fluids

• Hyperkalemia

• Metabolic Acidosis

• Hypertension

• Nutrition

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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

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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

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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

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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

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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

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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

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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

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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

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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

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Prognosis

• Highly dependent on underlying etiology, age of patient, and clinical presentation

• Children (retrospective) > 3 system organ failure assoc with more than

50% mortality

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Matur Nuwun