ACUTE

KIDNEY
INJURY
POST RENAL

A I S YA H N A U L I S I H O TA N G

F A K U LT A S K E D O K T E R A N

C 111 12 128

I L M U P E N YA K I T D A L A M

IDENTITAS PASIEN
Nama

: Tn. AA

No. RM: 774371

Umur

: 46 tahun

Pekerjaan : PNS
Alamat: BTN Griya Alauddin Permai

ANAMNESIS
Keluhan Utama : Nyeri pinggang kiri atas
Anamnesis Terpimpin : Nyeri pinggang disebelah kiri atas dirasakan sejak dua minggu
yang lalu hilang timbul, nyeri seperti tertusuk-tusuk dan terasa tembus ke belakang. Nyeri
dirasakan terutama pada pagi hari dan pada saat nyeri, pasien tidak mampu beraktivitas.
Nyeri berkurang dengan obat anti nyeri. Tidak ada keluhan yang sama sebelumnya.
Anamnesis Sistematik : Demam menggigil tidak ada, sakit kepala tidak ada, sakit menelan
tidak ada, batuk tidak ada, sesak tidak ada, nyeri dada tidak ada, nyeri ulu hati tidak ada,
mual muntah tidak ada, pasien mengaku BAK sedikit, frekuensi jarang, warna kuning tua
dan agak kasar sehingga pasien merasa tidak nyaman saat berkemih, minum 5 gelas
sehari. BAB konsistensi lunak, frekuensi normal. Pasien juga mengeluh nyeri sendi terus
menerus terutama sendi jari tangan dan kaki disertai benjolan sejak 3 bulan, berobat 2
hari yang lalu di RSUD Syekh Yusuf dan mendapat Allopurinol 100 mg. Riwayat Hipertensi
ada sejak tahun 2012 tidak terkontrol, berobat dengan amlodipine 10 mg. Riwayat DM
tidak ada. Riwayat merokok ada sejak muda, sudah berhenti 10 tahun yang lalu.

PEMERIKSAAN FISIS
General status:
BB : 55 kg

TB : 157 cm

IMT : 22.3 kg/m2

Sakit ringan / Gizi Cukup/ Composmentis

Vital sign:
Tekanan Darah
Nadi

: 170/100 mmHg

: 90 kali/menit regular, kuat angkat

Respiratory Rate : 20 kali/menit, tipe thoracoabdominal

Suhu

: 36.5 oC

VAS

: 3/10

PEMERIKSAAN FISIS
Head Examination
Konjungtiva : Anemis ()
Skera : Ikterik ()
Bibir
: Sianosis ()
Leher : Lymphadenopathy (), JVP
R + 0 cmH2O (30)

Thorax Examination

Insp. : Simetris D=S, normochest

Palp. : Gerak napas D=S
Perc.: Sonor
Ausc.: Vesicular
Ronchi -/ Wheezing -/Bunyi Jantung 1/II murni
reguler

PEMERIKSAAN FISIS
Pemeriksaan Abdomen
Insp.

: Datar, mengikuti gerak napas

Ausc. : Peristaltik (+), kesan normal

Palp. : Tenderness (-), Liver and spleen tidak teraba
Perc. : Tympany, shifting dullness (-)

Pemeriksaan Punggung
Insp.

: Normal

Ausc. : Normal
Palp. : Normal
Perc. : Nyeri ketok tidak ada

Ekstremitas
Edema: -/-, Krepitasi -/-, limited ROM pada pedis d/s, hangat pada
perabaan -/-

LABORATORIUM
2-10-2016 RSUD Syekh Yusuf
Hb : 12,4 gr/dl
Ureum : 69 mg/dl
Creatinine : 1,5 mg/dl
Asam urat : 9,3 mg/dl

4-10-2016
HEMATOLOGY
WBC
RBC
HGB
HCT
MCV
MCH
MCHC
PLT
Ureum
Creatinin
SGOT
SGPT
Uric Acid
Natrium
Kalium
Klorida

RESULT
20,2
4,22
11,6
37
87
27
31
240
123
4,11
18
22
8,7
139
3,5
104

NORMAL VALUE
4.00-10.00
4.00-6.00
12.0-16.0
37.0-48.0
80.0-97.0
26.5-33.5
31.5-35.0
150-400
10-50
M(<1,3); F(<1.1)
<48
<41
F(2.4-5.7); M(3.4-7)
136-145
3.5-5.1
97-111

DIAGNOSIS KERJA
Acute Kidney Injury Stage 3 DD
s/ Nephropathy Obstruksi
Gout Arthritis
Hipertensi on treatment

TERAPI
Diet rendah garam, purin, kalium, protein
Amlodipine 10 mg/24 jam/oral
Allopurinol 100 mg/24 jam/oral

RENCANA PEMERIKSAAN
USG Abdomen
Urinalisa
X-Ray Ekstremitas

DISKUSI
ACUTE KIDNEY
I N J U RY

DEFINISI
Acute kidney injury (AKI) : Penurunan fungsi
ginjal yang terjadi secara mendadak (<48 jam)
Biasanya ditandai dengan :
1. Peningkatan kreatinin >0,5 mg% jika
kreatinin awal <2,5 mg% atau peningkatan
kreatinin >20% jika kreatinin awal >2,5 mg
%
2. Penurunan urin output (<0,5 ml/kgbb/jam
selama 6 jam)

KLASIFIKASI AKI
Stage
1

2
3

Serum creatinine

Urine output

Stage
Cr Criteria
UOP
Criteria
1.5-1.9 baseline
<0.5
ml/kg/hr
for 6-12 hrs
OR
1>0.3 mg/dL
Crby1.5-2x baseline or < 0.5 ml/kg/hr
Crby 0.3 mg/dl
for 6hr
<0.5 ml/kg/hr > 12 hrs
2-2.9 baseline
2
Crby 2-3x
< 0.5 ml/kg/hr
for 12hr
3 times baseline
<0.3
ml/kg/hr > 24 hrs
3OR
Crby more than 3x or
Crby
if baseline
increase
in Cr 0.5
to 4.0
mg/dL
>4mg/dl
OR
Initiation of RRT

< 0.3 ml/kg/hr

OR
for 24hr
Anuria
> 12 hrs
Or anuria for
12h

Sumber : KDIGO AKI Guideline. 2012.

KLASIFIKASI AKIN
Stage
1

2
3

Serum creatinine

Urine output

Stage
Cr Criteria
UOP
Criteria
1.5-2 baseline
<0.5
ml/kg/hr
for hrs
OR
1>0.3 mg/dL
Crby1.5-2x baseline or < 0.5 ml/kg/hr
Crby 0.3 mg/dl
for 6hr
<0.5 ml/kg/hr > 12 hrs
>2-3.0 baseline
2
Crby 2-3x
< 0.5 ml/kg/hr
for 12hr
>3x times baseline
<0.3
ml/kg/hr > 24 hrs
3OR
Crby more than 3x or
Crby
if baseline
increase
in Cr 0.5
to 4.0
mg/dL
>4mg/dl
OR
Need for RRT

< 0.3 ml/kg/hr

OR
for 24hr
Anuria
for 12 hrs OR need
OrRRT
anuria for
for
12h

EPIDEMIOLOGI
5-10% pada pasien rawat
inap
70% pada pasien sakit berat
5-6% pasien ICU memerlukan
RRT (Renal Replacement
Therapy)

KLASIFIKASI BERDASARKAN ETIOLOGI

KLASIFIKASI BERDASARKAN ETIOLOGI

Harrisons Ed.19th. Acute Kidney Injury. Sushrut S.W, Joseph V.B. 2015

AKI PRERENAL
Penurunan Volume Cairan
Intravaskular
Extracellular fluid loss: burns, diarrhea, vomiting,
diuretics, salt-wasting renal disease, primary
adrenal insufficiency, gastrointestinal hemorrhage
Extracellular fluid sequestration: pancreatitis,
burns, crush, injury, nephrotic syndrome,
malnutrition, advanced liver disease

AKI PRERENAL
Penurunan Cardiac Output
Myocardial dysfunction: MI, arrhythmias, ischemic
heart disease, cardiomyopathies, valvular disease,
hypertensive disease, severe cor pulmonale

Vasodilatasi Perifer
Drugs: antihypertensive agents
Sepsis,
Miscellaneous: adrenal cortical insufficiency,
hypermagnesemia, hypercapnia, hypoxia

AKI PRERENAL
Vasokonstriksi Renal Berat
Sepsis
Drugs: nonsteroidal anti-inflammatory agents,
-adrenergic agonists.
Hepatorenal syndrome

Oklusi Mekanik Arteri Renalis

Thrombotic occlusion
Miscellaneous: emboli, trauma (e.g.,
angioplasty)

DIAGNOSIS AKI PRERENAL

Etiology
Clinical Features
Prerenal History of poor fluid intake or fluid
azotemia loss (hemorrhage, diarrhea,
vomiting,
sequestration into extravascular
space); NSAID/ACE-I/ARB; heart
failure;
evidence of volume depletion
(tachycardia,
absolute or postural hypotension,
low jugular venous pressure,
dry mucous membranes), decreased
effective circulatory volume
(cirrhosis,
heart failure)
SepsisSepsis, sepsis syndrome, or septic
associat shock. Overt hypotension not always
ed AKI
seen in mild to moderate AKI

Ischemia
associat
ed AKI

Systemic hypotension, often

superimposed
upon sepsis and/or reasons
for limited renal reserve such as
older

Laboratory Features
BUN/creatinine ratio above 20,
FeNa
<1%, hyaline casts in urine
sediment,
urine specific gravity >1.018,
urine
osmolality >500 mOsm/kg

Comments
Low FeNa, high specific gravity
and
osmolality may not be seen in
the
setting of CKD, diuretic use; BUN
elevation out of proportion to
creatinine
may alternatively indicate upper
GI bleed or increased catabolism.
Response to restoration of
hemodynamics
is most diagnostic.

Positive culture from normally

sterile
body fluid; urine sediment
often
contains granular casts, renal
tubular
epithelial cell casts
Urine sediment often contains
granular
casts, renal tubular epithelial
cell
casts. FeNa typically >1%.

FeNa may be low (<1%),

particularly
early in the course, but is usually
>1%
with osmolality <500 mOsm/kg

AKI RENAL

Harrisons Ed.19th. Acute Kidney Injury. Sushrut S.W, Joseph V.B. 2015

PATOFISIOLOGI AKI RENAL

Harrisons Ed.19th. Acute Kidney Injury. Sushrut S.W, Joseph V.B. 2015

ACUTE TUBULAR NECROSIS (ATN)

Etiologi of ATN

Sepsis (48%)

Ischemia (32%)
prolonged prerenal
azotemia
Hypotension
hypovolemic shock
cardiopulmonary arrest
cardiopulmonary bypass

Direct toxic Injury (20%)

Exogenous
Radiocontrast
Aminoglycosides
Vancomycin
Amphotericin B
Cisplatin
Acyclovir
Calcineurin inhibitors
HIV meds (tenofovir)
Endogenous (pigment
nephropathy)
Rhabdomyolysis
Hemolysis

PATO P H Y S I O L O G I A C U T E T U B U L A R N E C R O S I S

ACUTE TUBULAR NECROSIS

Index
BUN/PCr Ratio

Prerenal
Azotemia

Oliguric AKI (ATN)

>20:1

10-15:1

Urine sodium (UNa),

meq/L

<20

>40

Urine osmolality,
mosmol/L H2O

>500

<400

-Fractional
excretion of sodium
(FENa)

<1%

>2%

-FEUrea

<35%

Response to volume

Cr improves with IVF

Urinary Sediment

Bland, Hyaline

>35%
Cr wont improve much
Muddy brown granular
casts, cellular debris,
tubular epithelial cells

DIAGNOSIS OF RENAL AKI

Nephrotoxin-Associated AKI: Endogenous
Etiology
Clinical Features
Laboratory
Features
Rhabdom Traumatic crush
Elevated
yolysis
injuries, seizures,
myoglobin,

immobilization
creatine kinase;

urine heme
positive with
few red
blood cells
Hemolysi Recent blood
Anemia,
s
transfusion with
elevated LDH,
transfusion
low haptoglobin
reaction

Tumor
Recent
Hyperphosphate
lysis
chemotherapy
mia,

hypocalcemia,
hyperuricemia
Multiple
Age >60 years,
Monoclonal
myeloma constitutional
spike in urine or

Comments
FeNa may be low
(<1%)

FeNa may be low

(<1%); evaluation
for
transfusion reaction

Bone marrow or
renal biopsy can be

DIAGNOSIS OF RENAL AKI

Nephrotoxin-Associated AKI: Exogenous
Etiology
Clinical Features
Contrast
Exposure to iodinated contrast
nephropath
y

Tubular
injury

Interstitial
nephritis

Aminoglycoside antibiotics,
cisplatin,
tenofovir, zoledronate,
ethylene glycol,
aristolochic acid, and
melamine (to
name a few)
Recent medication exposure;
can have
fever, rash, arthralgias

Laboratory Features
Comments
Characteristic course is FeNa may be low (<1%)
rise in SCr
within 12 d, peak
within 35 d,
recovery within 7 d
Urine sediment often
Can be oliguric or
contains granular
nonoliguric
casts, renal tubular
epithelial cell
casts. FeNa typically
>1%.

Eosinophilia, sterile
Urine eosinophils have
pyuria; often
limited diagnostic
nonoliguric
accuracy; systemic signs of

drug reaction often absent;

kidney
biopsy may be helpful

DIAGNOSIS AKI RENAL

Other Causes of Intrinsic AKI
Etiology
Clinical Features

Laboratory
Features
Glomerulon Variable features
ANA, ANCA, AGBM
ephritis/va include
antibody, hepatitis
sculitis
skin rash, arthralgias,
serologies,

sinusitis (AGBM
cryoglobulins,
disease), lung
blood culture,
hemorrhage (AGBM,
decreased
ANCA, lupus), recent
complement
skin infection or
levels,
pharyngitis
ASO titer
(poststreptococcal)
(abnormalities of

these tests
depending on
etiology)
Interstitial Nondrug-related causes Eosinophilia,
nephritis
include tubulointerstitial sterile pyuria;

nephritis-uveitis (TINU) often

syndrome, Legionella
nonoliguric

Comments
Kidney biopsy may be
necessary

Urine eosinophils have

limited diagnostic
accuracy; kidney biopsy
may be

DIAGNOSIS OF RENAL AKI

Other Causes of Intrinsic AKI
Etiology
Clinical Features
TTP/HUS

Atheroembolic
disease

Laboratory
Features
Neurologic abnormalities and/or Schistocytes
AKI;
on peripheral
recent diarrheal illness; use of
blood
calcineurin
smear,
inhibitors; pregnancy or
elevated LDH,
postpartum;
anemia,
Spontaneous
thrombocytop
enia

Recent manipulation of the

aorta or
other large vessels; may occur
spontaneously
or after anticoagulation; retinal
plaques, palpable purpura,
livedo
reticularis, GI bleed

Hypocomplem
entemia,
eosinophiluria
(variable),
variable
amounts of
proteinuria

Comments
Typical HUS refers to AKI with a diarrheal
prodrome, often due to Shiga
toxin released from Escherichia coli or
other bacteria; atypical HUS is due
to inherited or acquired complement
dysregulation. TTP-HUS refers to
sporadic cases in adults. Diagnosis
may involve screening for ADAMTS13
activity, Shiga toxinproducing E. coli,
genetic evaluation of complement
regulatory proteins, and kidney
biopsy.
Skin or kidney biopsy can be diagnostic

AKI POSTRENAL
Level of obstruction
Upper tract (ureters)
Lower tract (bladder outlet or
urethra)

Degree of obstruction
Partial vs. Completee
Anatomic lesion (unilateral vs.
bilateral)
Functional

Duration (Acute vs
Chronic)
Cause (Congenital vs
Acquired)

LOWER TRACT
OBSTRUCTION
BPH or prostate
cancer
Bladder cancer
Urethral strictures
Bladder stones
Blood clots
Functional
obstruction as a
result of neurogenic
bladder

UPPER TRACT OBSTRUCTION

Intrinsic:
Nephrolithiasi
s
Blood clot
Papillary
necrosis
Cancer

Extrinsic:
Retroperitoneal or
pelvic malignancy
Endometriosis/Prol
apsed uterus
Abdominal aortic
aneurysm or Iliac
artery aneurysm
Retroperitoneal
fibrosis

PATOFISIOLOGI AKI POST RENAL

Reduced GFR: underperfusion of
glomeruli and changes in the
glomerular ultrafiltration coefficient
An initial period of hyperemia from
afferent arteriolar dilation is followed
by intrarenal vasoconstriction from
the generation of angiotensin II,
thromboxane A2, vasopressin and a
reduction in NO production.

DIAGNOSIS OF POST RENAL AKI

Post Renal AKI
Etiology
Clinical Features

Laboratory
Features
History of kidney stones, No specific
prostate
findings other than
disease, obstructed
AKI;
bladder catheter,
may have pyuria
retroperitoneal or pelvic or hematuria
neoplasm

Comments
Imaging with computed
tomography
or ultrasound

COMPLICATIONS OF AKI
Intravascular overload
Electrolyte disturbance
Hyperkalemia (serum K+ >5.5 mEq/L)
Hyponatremia (serum Na+ < 135 mEq/L)
Hyperphosphatemia (serum phosphate concentration of
>5.5 mg /dl)
Hypocalcemia (serum Ca++ < 8.5 mg/dl)
Hypercalcemia (serum Ca++ > 10.5 mg /dl)

Metabolic acidosis (arterial blood PH < 7.35)

Hyperuricemia
Bleeding tendency
Seizure

PENCEGAHAN AKI
Renal AKI can be avoided: close attention to
cardiovascular function and intravascular volume in
high-risk patients (elderly & preexisting renal
insufficiency)
Aggressive restoration of intravascular
volume renal AKI after major surgery,
trauma or burns.
Nephrotoxic: tailoring the dosage of
potential nephrotoxins to body size and GFR

MANAGEMENT OF AKI
Preliminary measures
Exclusion of reversible causes: Obstruction should be relived,
infection should be treated
Correction of prerenal factors: intravascular volume and cardiac
performance should be optimized
Maintenance of urine output: Loop diuretics may be
usefully to convert the oliguric form of ATN to the
nonoliguric form.
High doses of loop diuretics such as Furosemide (up
to 200 to 400 mg intravenously) may promote diuresis
in patients who fail to respond to conventional doses

MANAGEMENT AKI PRERENAL

Replacement fluids due to hypovolemia must be
tailored according to the composition of the lost
fluid.
Severe hypovolemia due to hemorrhage should be
corrected with packed red blood cells
isotonic saline is usually appropriate replacement
for mild to moderate hemorrhage or plasma loss
(e.g., burns, pancreatitis).

MANAGEMENT AKI PRERENAL

Hypotonic solutions (e.g., 0.45% saline): recommended as
initial replacement in patients with prerenal AKI due to
increased urinary or gastrointestinal fluid losses,
although isotonic saline may be more appropriate in
severe cases.
Subsequent therapy should be based on
measurements of the volume and ionic
content of excreted or drained fluids.
Serum potassium and acid-base status should
be monitored carefully.

MANAGEMENT AKI RENAL

No specific therapies for established renal AKI due
to ischemia or nephrotoxicity.
Focus on elimination of the causative
hemodynamic abnormality or toxin, avoidance of
additional insults, and prevention and treatment of
complications.
Specific treatment of other causes: depends on the
underlying pathology.

MANAGEMENT AKI POST RENAL

Requires close collaboration between
nephrologist, urologist and radiologist.
Obstruction of the urethra or bladder neck:
transurethral or suprapubic placement of a bladder
catheter
Ureteric obstruction: treated initially by
percutaneous catheterization of the dilated renal
pelvis or ureter.

T E R A P I KON S E R VATI F
1. MANAGEMENT DIET
Protein 1.25 g/kgBB untuk menjaga
balance nitrogen.
Membatasi diet protein 0.6 0.8 g/kg
perhari misalnya protein yang high
biologic value (kaya asam amino esensial)
untuk azotemia berat.

2 . F L U I D A N D E L E C T R O LYT E M A N A G E M E N T
After hypovolemia corrected, total oral and
intravenous fluid administration = daily sensible
losses (via urine, stool, and NG tune o surgical
drainage)+estimated IWL (400500 ml/day).
Strict input output monitoring is
Hypervolemia: can usually be managed
by restriction of salt and water intake and
diuretics.

 Hyperkalemia:
Restrict dietary K+ intake
Give calcium gluconate 10 ml of 10% solution over
5 minutes
Glucose solution 50 ml of 50 % glucose plus
Insulin 10 units IV
Potassiumbinding ion exchange resin
Dialysis: therapy fails or the patient is very toxic

 Hyperphosphatemia:
restriction
of
dietary
phosphate and by oral aluminum hydroxide or
calcium carbonate, which reduce gastrointestinal
absorption of phosphate.
Hypocalcemia does not usually require treatment.

3. MANAGEMENT ASAM BASA

Asidosis Metabolik: diterapi jika serum bicarbonate
dibawah 15 mmol/L or pH arteri jatuh dibawah 7.2.
Asidosis yang lebih berat dikoreksi dengan Natrium
bikarbonat oral atau intravena.
Perkiraan
penggantian
penurunan
bikarbonat tergantung jumlah serum.
Komplikasi
pemberian
bikarbonat:
hypervolemia,
metabolic
alkalosis,
hypocalcemia and hypokalemia.

DIALYSIS / RENAL REPLACEMENT THERAPY (RRT)

Indications :
Oliguria/Anuria
Hyperammonemia
Hyperkalemia
Severe acidemia
Severe azotemia
Pulmonary Edema
Uremic
complications
Severe electrolyte
abnormalities
Drug overdose
with a filterable
toxin
Anasarca

PROGNOSIS
Tergantung berat-ringannya penyakit
yang mendasari dan manifestasi klinisnya
Morbiditas dan Mortalitas: dipengaruh dari ada
tidaknya oliguria, GI bleeding, septicemia,
metabolic acidosis and neurologic abnormalities
(pasien oliguric > nonoliguric ).
Mortality rate: oliguric=50 %,
nonoliguric= 26 %

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