*

DIAGNOSIS GANGGUAN GINJAL AKUT (GgGA)

DAN INDIKASI TERAPI PENGGANTI GINJAL (TPG)

Rully Roesli
SubBagian Ginjal-Hipertensi, Bagian Ilmu Penyakit Dalam
Fakultas Kedokteran UNPAD/ RS dr. Hasan Sadikin Bandung
 DIAGNOSIS GANGGUAN GINJAL AKUT (GgGA)

Menurut KDIGO Clinical Practice Guideline for Acute

Kidney Injury. Kidney International. (2012). Definisi GgGA
adalah :

1 - Kenaikan kreatinin serum ≥ 0.3 mg/dl (≥26.5 μmol/l)

dalam 48 jam,atau

2 - Kenaikan kreatinin serum ≥ 1,5 kali dari nilai normal

(yang diketahui atau diukur < 7 hari sebelumnya)

3- Volume urin < 0,5 cc/kgBB/ dalam 6 jam

parison of Recent Consensus AKI Definitions
AKI Stage Urine Outputa KDIGO AKIN RIFLE
1 <0.5 mL/kg/h for Scr to 1.5-1.9 × Scr to 1.5-2 × Risk: Scr
6-12 h baseline over 7 d baseline to ≥1.5 ×
or ≥0.3 mg/dL or ≥0.3 mg/dL increase within 7
absolute increase absolute Scr d, sustained
over 48 h increase within for ≥24 h
48 h
2 <0.5 mL/kg/h Scr to 2.0-2.9 × Scr to >2-3 × Injury: Scr
for ≥12 h baseline baseline to ≥2 × increase
3 <0.3 mL/kg/h Scr to ≥3.0 × Scr to >3.0 × Failure: Scr
for ≥24 h or baseline, or Scr baseline, or Scr to ≥3.0 ×
anuria for ≥12 h increase increase increase or Scr
to ≥4.0 mg/dL or to ≥4.0 mg/dL increase
initiation of RRT (with increase of to ≥4.0 mg/dL
0.5 mg/dL) or (with increase of
initiation of RRT 0.5 mg/dL) or
initiation of RRT
Loss: Complete
Management of Acute Kidney Injury: Core Curriculum 2018 loss of kidney
Peter K. Moore, Raymond K. Hsu, Kathleen D. Liu
American Journal of Kidney Diseases function for >4
Volume 72, Issue 1, Pages 136-148 (July 2018 ) wk
ESKD: ESKD for
>3 mo
Table 2Causes of AKI
Type Examples of Specific Causes
Decreased kidney perfusion (“prerenal” states)
Hypovolemia Increased losses (hemorrhage, burns,
massive vomiting or diarrhea), poor
oral intake
Reduced cardiac output Heart failure, cardiac tamponade,
massive pulmonary embolism
Renal vasomodulation/shunting Medications (NSAID, ACEi/ARB,
cyclosporine, iodinated contrast),
hypercalcemia, hepatorenal
syndrome, abdominal compartment
syndrome
Systemic vasodilation Sepsis, SIRS, hepatorenal syndrome
Management of Acute Kidney Injury: Core Curriculum 2018
Peter K. Moore, Raymond K. Hsu, Kathleen D. Liu
American Journal of Kidney Diseases
Volume 72, Issue 1, Pages 136-148 (July 2018 )
Intrarenal causes
Vascular Renal artery stenosis, arterial/venous cross-clamping

Microvascular Thrombotic microangiopathies (TTP, HUS, aHUS, DIC, APS,

Glomerular
Tubulointerstitium
Management of Acute Kidney Injury: Core Curriculum
2018
Peter K. Moore, Raymond K. Hsu, Kathleen D. Liu
American Journal of Kidney Diseases
Volume 72, Issue 1, Pages 136-148 (July 2018
malignant hypertension, scleroderma renal crisis,
preeclampsia/HELLP syndrome, drug-induced),
cholesterol emboli
Rapidly progressive (crescentic) GN: anti–glomerular
basement membrane; immune complex diseases: IgA
nephropathy, postinfectious, lupus, mixed
cryoglobuminemia with MPGN; pauci-immune
glomerulonephritis: ANCA-associated vasculitides: GPA,
MPA, EGPA (Churg-Strauss); ANCA-negative; nephrotic-
range proteinuria with associated AKI: HIV-associated
nephropathy (secondary FSGS); other causes of nephrotic-
range proteinuria that commonly associate with AKI:
minimal change disease with ATN/AIN; membranous
nephropathy + crescentic GN or renal vein thrombosis;
myeloma + multiple different pathologies, but in
particular light chain cast nephropathy
AIN: medications, infection, lymphoproliferative disease;
pigment nephropathy: rhabdomyolysis (myoglobin),
massive hemolysis (hemoglobin); crystal nephropathy:
uric acid (tumor lysis), acyclovir, sulfonamides, protease
inhibitors (indinavir, azatanavir), methotrexate, ethylene
glycol, acute phosphate nephropathy, oxalate
nephropathy; myeloma-associated AKI (cast
nephropathy); ATN: ischemia (shock, sepsis),
inflammatory (sepsis, burns), medications (see Box 1;
osmotic nephrosis in setting of sucrose, mannitol and
) hydroxyethylstarch use)
Postrenal causes
Bladder outlet Benign prostatic hypertrophy, cancer,
strictures, blood clots
Ureteral Bilateral obstruction (or unilateral
with one kidney): stones, malignancy,
retroperitoneal fibrosis
Renal pelvis Papillary necrosis (NSAIDs), stones

Management of Acute Kidney Injury: Core Curriculum 2018

Peter K. Moore, Raymond K. Hsu, Kathleen D. Liu
American Journal of Kidney Diseases
Volume 72, Issue 1, Pages 136-148 (July 2018 )
 -
Medications Commonly Associated With Acute Tubular Necrosis

••Aminoglycosides (tobramycin, gentamycin)

••NSAIDs (ibuprofen, naproxen, ketorolac, celecoxib)
••ACEi (captopril, lisinopril, benazepril, ramipril)
••ARB (losartan, valsartan, candesartan, irbesartan)
••Amphotericin
••Cisplatin
••Foscarnet
••Iodinated contrast
••Pentamidine
••Tenofovir
••Zolendronic acid

Note: Although not a classic cause of acute tubular necrosis, volume

depletion caused by diuretics can exacerbate the effects of some of these
other medications. This table does not include common causes of pigment
or crystal nephropathy (which are described in Table 2) or medications
associated with osmotic injury. Abbreviations: ACEi, angiotensin-
converting enzyme inhibitor; ARB, angiotensin receptor blocker; NSAIDs,
nonsteroidal anti-inflammatory drugs.

Management of Acute Kidney Injury: Core Curriculum 2018

Peter K. Moore, Raymond K. Hsu, Kathleen D. Liu
American Journal of Kidney Diseases
Volume 72, Issue 1, Pages 136-148 (July 2018 )
Box 2
Key Medications Requiring Dose Adjustment (or Cessation) in AKI

••Analgesics (morphine, meperidine, gabapentin, pregabalin)

••Antiepileptics (lamotrigine)
••Antivirals (acyclovir, gancyclovir, valgancyclovir)
••Antifungals (fluconazole)
••Antimicrobials (almost all antimicrobials need dose adjustment in AKI,
with important exceptions of azithromycin, ceftriaxone, doxycycline,
linezolid, moxifloxacin, nafcillin, rifampin)
••Diabetic agents (sulfonylureas, metformin)
••Allopurinol
••Baclofen
••Colchicine
••Digoxin
••Lithium
••Low-molecular-weight heparin
••NOACs

Note: Medications that are associated with acute tubular necrosis (Box 1)
should be withheld, if possible. Abbreviations: AKI, acute kidney injury;
NOAC, novel anticoagulants.

Management of Acute Kidney Injury: Core Curriculum 2018

Peter K. Moore, Raymond K. Hsu, Kathleen D. Liu
American Journal of Kidney Diseases
Volume 72, Issue 1, Pages 136-148 (July 2018 )
INDIKASI
TUJUAN TPG PADA GgGA

a. Mencegah perburukan fungsi ginjal

lebih lanjut.
b. Membantu mempercepat proses
penyembuhan penyakit dan
pemulihan fungsi ginjal dan fungsi
organ lain yang terganggu.
c. Memungkinkan dilakukan tindakan
pengobatan yang banyak
memerlukan cairan misalkan :
resusitasi cairan , pemberian nutrisi ,
obat-obatan,dll. INDIKASI TPG PADA GgGA

Bila direncanakan inisiasi (memulai) TPG pada

pasien GgGA dalam kondisi kritis terutama
yang dirawat di ICU, yang selalu menjadi
pertanyaan adalah :

 kapan harus memulai

 apa pilihan pengobatan,
 bagaimana dosisnya
 kapan harus menghentikannya
Indikasi dan kriteria untuk inisiasi TPG pada GgGA di ICU
Dikutip dari : Bellomo R, Ronco C. Kidney Int 1998;53(66):S 106-109

1 Oliguria ( output urin <200 cc/12 jam)

2 Anuria/oliguria berat ( output urin < 50 cc/12 jam)
3 Hiperkalemia ( K+ > 6.5 mmol/L)
4 Asidosis berat (pH< 7.1)
5 Azotemia (Urea > 30 mmol/liter)
6 Gejala klinik berat ( terutama edema paru) BUKAN BERDASAR
Kadar KREATININ DARAH
7 Ensefalopati uremik
8 Perikarditis uremik
9 Neuropati/miopati uremik
10 Disnatremia berat ( Na >160 atau < 115 mmol/L )
11 Hipertermia / hipotermia
12 Overdosis obat –obatan yang terdialisis
Bila didapatkan :
- satu gejala diatas sudah dapat merupakan indikasi untuk inisiai dialisis
dua gejala diatas merupakan indikasi untuk segera inisiasi dialisis
- lebih dari dua merupakan indikasi untuk segera inisiasi dialisis walaupun
kadarnya belum mencapai yang tertera dalam table
INDIKASI TERAPI PENGGANTI GINJAL PADA GgGA

1 Oliguria ( output urin <200 cc/12 jam)

2 Anuria/oliguria berat ( output urin < 50 cc/12 jam)

3 Hiperkalemia ( K+ > 6.5 mmol/L)

4 Asidosis berat (pH< 7.1)

5 Azotemia (Urea > 30 mmol/liter)

6 Gejala klinik berat ( terutama edema paru)

7 Ensefalopati uremik

8 Perikarditis uremik

9 Neuropati/miopati uremik

10 Disnatremia berat ( Na >160 atau < 115 mmol/L)

11 Hipertermia / hipotermia

12 Overdosis obat –obatan yang terdialisis

PILIHAN UNTUK GgGA
*What Works?
Filtrasi
Dialisis
 Acute Renal Replacement Therapy
INTERMITTENT CONTINOUS
(< 12 jam /hari) (24 jam)

Intermittent Hemodialysis (IHD) Peritoneal dialysis

Single pass Acute Peritoneal Dialysis
Sorbent based
Continous Renal Replacement Therapy (CRRT) :
Hybrid dialysis : CAVH Continous Arterio-Venous Hemofiltration
Extended Daily Dialysis (EDD) CVVH Continous Veno-Venous Hemofiltration
Slow Continous Dialysis (SCD) CAVHD Continous Arterio-Venous Hemodialysis
Sustained Low Efficiency Dialysis (SLED) CVVHD Continous Veno-Venous Hemofdialysis
Sustained Low Efficiency Daily Dialysis (SLEDD) CAVHDF Continous Arterio-Venous Hemodia- filtration
Sustained Low Efficiency Daily Dial-filtration CVVHDF Continous Veno-Venous- Hemodia-filtration
(SLEDD-f)
SCUF Slow Continous Ultra-Filtration
HYBRID DIALYSIS

Adapted from Mehta RL. Supportive therapies; intermittent hemodialysis, continuous renal replacement therapies and
peritoneal dialysis. In : Schrier RW, editor. Atlas of diseases of the kidney, Current Medicine, Philadelphia: Blackwell
Science; 1998: with permission.
 * Types of RRT for acute renal failure (aRRT)

Mode of Complexity Efficiency Anti- Volume

Therapy coagulation control

PD Low Moderate No Moderate

CAVHD High Moderate and Yes Good

variable

CVVH Moderate High Yes Good

CVVHD High High Yes Good

IHD Low Moderate Optional Moderate

EDD-f Low High Optional Excellent

SLED
HYBRID DIALYSIS/PIRRT
Mark R Marshall
Chair , New Zealand National Renal Advisory Board

Bandung, Indonesia
18th May 2011
Continous vs Intermittent

CRRT iHD

Intensivist Nephrologist
HYBRID dialysis

SLOW SOLUTE
REMOVAL OVER A
CRRT IHD
LONG DURATION TO
THE NEPHROLOGIST
PIRRT

PROLONGED
INTERMITTENT
CRRT RENAL iHD
REPLACEMENT
THERAPIES
KONSEP Prolonged Intermittent Renal Replacement Therapy (PIRRT),
Seminars in Dialysis, terbitan bulan Maret-April 2011 dan Nephrology Dialysis and Transplantation (NDT) volume 26 tahun 2011
 *
(PROLONGED
INTERMITTENT Examples:
PIRRT RENAL REPLACEMENT
THERAPY)
Lower QB 70
EF Efficiency QD 70
(EXTENDED T 18 hours
FILTRATION) Ref: Lonnemann et al, 2000

ED
(EXTENDED
DIALYSIS) Higher QB 283
Efficiency
QD 200
EDF QF 100
(EXTENDED T 7.1 hours
DIAFILTRATION) Ref: Marshall et al, 2004

Marshall et al, Semin Dial, 24, pp142-148, 2011

Me-Resepkan (prescription) Terapi SLED

MEMECAHKAN PERMASALAHAN

Gagal Jantung kurangi

Resiten diuretik pre-load
Syok kardiogenik

DIURETIK Filtrasi

INDIKASI &
Gagal Nafas hilangkan
TARGET TERAPI dalam ventilator edem paru

Bic Nat

AKI FAILURE
Anuri ekskresi kalium Dialisis
Hiperkalemi perbaiki acidosis
Asidosis metabolik
 *
* [] Stabilize the cardiovascular
preparation
* [] Stabilize the respiratory
* [] Control acidosis and hyperkalemia

prescription

* [] UF goals determined by clinical need

* [] UF rate determined by cardiovascular stability
* [] Once the patient tolerance to UF is established, other
parameters can be set
[] dapat mengatur Qb
(100 – 300 cc / menit)
[] dapat mengatur Qd
(300 - 500 cc/menit ) memilih
[] dapat mengatur temperatur MESIN
( 35’ C)
[] dapat mengatur natrium
( natrium profile)
[] dapat mengatur bikarbonat
(bicarbonate profiling)
*