AKI CKD

Fakultas Kedokteran
Universitas Sebelas Maret
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 Definisi
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AKI (acute kidney injury) adalah penurunan

mendadak fungsi ginjal (GFR) yang bersifat
sementara, ditandai dengan peningkatan
kreatinin serum dan hasil metabolisme nitrogen
lainnya, serta adanya ketidakmampuan ginjal
untuk mengatur homeostasis cairan dan
elektrolit.
 Definition of AKI

• a sudden, sustained, and usually

reversible decrease in the glomerular
filtration rate (GFR) occurring over a
period of hours to days.

> 30 definitions used in published

studies
 KDIGO Definition of AKI ( 2012 )
Defined by any of the following:

• Increase in SCr by ≥0.3 mg/dL within 48 hours

• Increase in Scr by ≥1.5 times baseline, which is

known or presumed to have occurred within the
prior seven days

• Urine volume <0.5 mL/kg/h for six hours

 KDIGO Classification of AKI ( 2012 )

Stage Serum creatinine Urine output

1 1.5-1.9× baseline <0.5 ml/kg/hr for 6-12 hrs

OR
>0.3 mg/dL 
<0.5 ml/kg/hr > 12 hrs
2 2-2.9× baseline

3 3 times baseline <0.3 ml/kg/hr > 24 hrs

OR OR
increase in Cr to ≥4.0 mg/dL Anuria > 12 hrs
OR
Initiation of RRT

KDIGO Clinical Practice Guideline for AKI. Kidney Int 2012

 Definitions of
Terminology
• Azotemia - the accumulation of
nitrogenous wastes (high BUN)

• Uremia – clinical manifestation

(symptomatic renal failure)

• Oliguria – UOP < 400-500 mL/24 hours

• Anuria – UOP < 100 mL/24 hours
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Patofisiologi
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 Classification of the Etiologies of
AKI
Acute
Renal
Injury

Prerenal Intrinsic Postrenal

AKI AKI AKI

Acute Acute Acute

Acute Intratubular
Tubular Interstitial Vascular
GN Obstruction
Necrosis Nephritis Syndromes
 Prerenal AKI
• Intravascular volume depletion:
-bleeding, GI loss, Renal loss, Skin loss (burn), Third space loss,
poor oral intake (NPO, AMS, anorexia)

• Decreased effective circulating volume:

-congestive heart failure, cirrhosis, nephrotic syndrome, sepsis

• Decreased flow through renal artery:

-RAS or occlusion (compartment syndrome), hepatorenal
syndrome, hypercalcemia
-pharmacologic impairment (RAAS blocker, NSAIDs, CNI)
 Prerenal Azotemia Tx
• In early stages can be rapidly corrected by
aggressive normalization of effective arterial
volume.

• Correction of volume deficits

• Optimization of cardiac function
• Discontinuation of antagonizing medications
o NSAIDs/COX-2 inhibitors
o Diuretics
o RAAS blockers
 Renal / Intrinsic AKI
• Tubule: ATN (sepsis, ischemic, toxins)
• Interstitium: AIN (Drug, infection, neoplasm)
• Glomerulus: AGN (primary, post-infectious,
rheumatologic, vasculitis, HUS/TTP)
• Vasculature:
o Atheroembolic dz, renal artery thromboembolism, renal artery
dissection, renal vein thrombosis

• Intratubular Obstruction
o myoglobin, hemoglobin, myeloma light chains,
uric acid, tumor lysis, drugs (bactrim, indinavir,
acyclovir, foscarnet, oxalate in ethylene glycol toxicity)
 Acute Tubular Necrosis (ATN)
• Direct toxic Injury (20%)
• Sepsis (48%)
o Exogenous
• Ischemia (32%) • Radiocontrast
• Aminoglycosides
o prolonged prerenal • Vancomycin
azotemia • Amphotericin B
o Hypotension • Cisplatin
o hypovolemic shock • Acyclovir
• Calcineurin inhibitors
o cardiopulmonary arrest • HIV meds (tenofovir)
o cardiopulmonary bypass
o Endogenous (pigment
nephropathy)
• Rhabdomyolysis
• Hemolysis
 Laboratory Findings in Acute Kidney Injury

Index Prerenal Oliguric AKI

Azotemia (ATN)

BUN/PCr Ratio >20:1 10-15:1

Urine sodium (UNa), <20 >40

meq/L
Urine osmolality, >500 <400
mosmol/L H2O
-Fractional excretion <1% >2%
of sodium
-FEUrea <35% >35%
Response to volume Cr improves with IVF Cr won’t improve much

Urinary Sediment Bland, Hyaline Muddy brown granular

casts, cellular debris,
tubular epithelial cells
 Pitfalls: Fractional
Excretion of Na
• Pre-existing CKD: FeNa 2-3 even without tubular
injury
• Poor sensitivity with diuretics use
• Picture might be muddied by fluid therapy

• Etiologies of FeNa < 1%

o hepatorenal syndrome
o contrast nephropathy
o rhabdomyolysis
o acute glomerulonephritis
o early obstructive uropathy
 Postrenal AKI:
Classification
o Level of obstruction
• Upper tract (ureters)
• Lower tract (bladder outlet or urethra)
o Degree of obstruction
• Partial vs. Complete
o TypeAnatomic lesion (unilateral vs. bilateral)
• Functional
o Duration (Acute vs Chronic)
o Cause (Congenital vs Acquired)
Etiologies: Upper tract obstruction

o Intrinsic:  Extrinsic:
• Nephrolithiasis Retroperitoneal or
• Blood clot pelvic malignancy
• Papillary necrosis Endometriosis/Prolapse
• Cancer d uterus
Abdominal aortic
aneurysm or Iliac
artery aneurysm
Retroperitoneal fibrosis
 Etiologies: Lower tract obstruction

o BPH or prostate cancer

o Bladder cancer
o Urethral strictures
o Bladder stones
o Blood clots
o Functional obstruction as a result of
neurogenic bladder
 Postrenal AKI tx
• Prompt recognition and relief of obstruction can
prevent the development of permanent structural
damage.
o Lower tract obstruction (bladder catheter)
o Upper tract obstruction
• ureteral stents
• percutaneous nephrostomies
• Monitor for post-obstructive diuresis
• Recovery of renal function dependent upon duration
of obstruction.
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How do we assess a pt with
AKI?
• Is this acute or chronic renal failure?
o Establish baseline Cr and assess Cr trend
o History and examination
o Small kidneys on ultrasound (except for in -
Diabetes, PCKD, Urinary Tract Obstruction)
 AKI: Focused History
• Prenal hx: N/V/D? Oral intake? Diuretics? Hx of
heart dz, liver dz, previous renal dz?
• Post-renal sxs: hesitancy, frequency, urgency, weak stream,
dribbling, feeling of incomplete bladder emptying, flank
pain. h/o kidney stones or BPH? Spinal cord injury?
Anticholingergic meds?
• Any recent illnesses? Fever? Rashes?
• Any recent surgery?
• Cardiovascular instability?
• Toxin exposure: new medications (Abx, NSAIDs)? IV contrast?
• Change in urination, any edema/SOB/Wt. gain?
o Look for temporal link of exposure or risk factor to
elevation of Cr or decline in UOP
How to assess volume?
History (intake, fluid loss, meds)
Postural blood pressure and pulse
Daily weights
In’s/Out’s, fluid balance/fluid challenge

 Signs of volume depletion:

-Dry mouth, Increased thirst, Lightheadedness, Muscle
cramps, extremities are cool to the touch, palpitations,
reduced and dark urine, syncope
-PE: Listlessness/AMS/LOC, tachycardic, weak rapid pulse,
hypotensive (orthostatic vitals), tachypnic, increased
Temp, poor capillary refill, decreased skin turgor, flattened
neck veins, little or no urination for several hrs
 U/A, Urine protein/Cr, Urine Eosinophilla
 FeNa, FeUrea
 CPK, uric acid
 Urine microscopy:
Muddy brown casts in ATN
WBC casts in AIN
RBC casts in AGN

 Post-void residual (>100-150 ml c/w voiding dysfunction)

 bladder catheterization
 renal ultrasound
 Management of AKI: general principle

• No therapy to date have shown efficacy in

treating AKI.
• Identify the etiology and treat the underlying
cause
• Optimization of hemodynamics to increase
renal perfusion
• Lack of benefit – low dose dopamine, loop
diuretics only if markedly fluid overload
o Identify and aggressively treat infection (early
removal of foley catheters, and minimize
indwelling lines)
 Management of AKI:
treat complications
• Correct fluid imbalances: strict I/O’s, daily wts. determine
fluid balance goals daily, fluid selection or diuresis,
readjust for UOP recovery, post diuresis or dialysis
• Electrolyte imbalances (low K/phos diet, binder)
• Metabolic acidosis (Bicarb deficit, mode and rate of
replacement)
• Nutrition: adjust TPN/protein intake
• Medication dosing: adjustment for eGFR to avoid under
or over dosing, timing for dialytic therapy, reassess dosing
for renal recovery or dialysis modality)
• Procedural considerations (prefer non-contrast CT,
appropriate to delay contrast exposure, prophylaxis)
Penatalaksanaan
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Nephrotoxic Drug Exposure
• Minimizing nephrotoxin
o Avoid Aminoglycosides, Amphotericin,
Bactrim, Vancomycin, NSAIDs, IV
contrast, Fleet’s enemas

• Renal dose medications – especially

antibiotics and monitor level

• Cautious use (metformin, long acting oral

hypoglycemic agents, insulin, gemfibrozil
and statins, neurotin,
colchicine/allopurinol,
morphine/codeine, lmwh)
Ancient Chinese Medical
Text
 The inferior doctor treats actual illness.
 The mediocre doctor attends to impending
illness.
 The superior doctor prevents illness.

2600 BC - Huang Dee Nai-Chang

Be aware of pts who are at risk for AKI
Volume depletion or Hypotension
Sepsis
Pre-existing renal, hepatic, or cardiac dz
Diabetes mellitus
Elderly
Exposure to nephrotoxins
Aminoglycosides, amphotericin,
immunosuppressive agents, chemo.,
NSAIDs,, RAAS blockers, intravenous
contrast media
Post cardiac or vascular Surgery pts or ICU
pts with multiorgan failure
 Take Home Messages:
AKI
• AKI is increasingly common.
• It involves high cost of management, carries a high
morbidity and mortality risks.
• The most common cause of in-hospital AKI is ATN that
results from multiple acute insults (sepsis, ischemia, or
nephrotoxin).
• No drug treatment has been shown to limit the
progression of, or speed up recovery from AKI.
• Review medications and adjust dose
• Recognize risk factors
• The Best Treatment is PREVENTION and avoid further
renal damage!!!
• Examine pt: BP? Dry? Septic (vasodilated)?
• Flush foley (sediment can obstruct outflow)
• Check I/Os (has he been drinking?)
• Give IV BOLUS (250-500cc IVF), see if pt pees in next
30-60 min
o If he pees, then he was dry
o If he doesn’t pee, then he’s either REALLY dry or in
renal failure
• Check UA, UCx, urine lytes
• Consider Renal U/S if reasonable
 Definisi

Gagal ginjal adalah suatu keadaan klinis yang ditandai

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dengan penurunan fungsi ginjal yang ireversibel.

Kriteria penyakit ginjal kronik

1. Kerusakan ginjal yang terjadi lebih dari 3 bulan,
berupa kelainan struktural atau fungsional dengan
atau tanpa penurunan laju filtrasi glomerulus dengan
manifestasi :

Terdapat kelainan patologis

Terdapat tanda kelainan ginjal termasuk kelainan
dalam komposisi darah atau urin atau kelainan
dalam tes pencitraan
2. Laju filtrasi glomerulus kurang dari
60ml/menit/1m73m2 selama 3 bulan, dengan atau
tanpa kerusakan ginjal (PAPDI, 2010)
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 Manifestasi klinis
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 Manifestasi klinis

Anamnesis
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Keluhan utama
Riwayat hipertensi, DM, ISK, batu di saluran kemih,
hiperurisemia, infeksi saluran kemih, dan faktor-faktor
risiko lain
Sindroma uremia : lemah, nafsu makan berkurang, berat
badan berkurang, mual, muntah, dll
Riwayat penyakit ginjal pada keluarga
Riwayat paparan kronis nefrotoksin
Px Fisik
Hipertensi
Tanda-tanda anemia
Edema
Pemeriksaan ren : pembesaran, nyeri
Komplikasi uremia
 Penunjang
1. Darah
Fungsi ginjal : ureum, kreatinin, elektrolit, ABG, Gula darah,
albumin
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Komplikasi CKD :
Anemia : Darah lengkap, SI, TIBC, Feritin
PTH : paratiroid
Hyperparatirioid : PTH
Coagulopati : PT APTT

2. EKG
3. Urinalisis
4. Radiologis
Foto polos abdomen
Anatomis dan fungsi renal :
BNO & USG : adanya obstruksi, batu radiolucent tidak
terlihat di bno
IVP : jika cr<2
Komplikasi cardiac failure : echo
 Diagnosis
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Penghitungan GFR yang paling baru

menggunakan rumus GFR CKD-Cys epi

Bisa di akses di
https://www.kidney.org/professionals/kdoqi/gfr
_calculator

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Protein
•Pre-dialisis : 0.6-075
g/KgBB/hari
•Hemodialisis : 1.2
g/KgBB ideal/hari
•Dialisis peritoneal : 1.2-
1.3 g/KgBB ideal/hari
•Pasca transplantasi :
0.8-1 g/KgBB iedal/hari
Tatalaksana
Cairan Garam NaCl
•Pre-dialisis : cairan •Predialisis : &lt; 5
tidak dibatasi dengan g/hari
produksi urin normal •Hemodialisis : 5-6
•Hemodialisis : 500 g/hari
mL/hari + produksi •Dialisis peritoneal : 5-
urin 10 g/hari
•Dialisis peritoneal : •Transplantasi ginjal :
1500-2000 mL/hari &lt;6-7 g/hari pada fase
dengan pemantauan akut.
harian
 Tatalaksana

Anemia
Dislipidemia
Tinjauan pustaka

1. Meneksklusi kemungkinan
anemia defisiensi besi
Target : LDL <100 mg/dL, 2. Terapi eritropoetin apabila Hb
apabila trigliderida > 200 ≤ 10 mg/dL dan Hct ≤ 30%
mg/dL, maka targetnya dengan target terapi Hb 10-12
kolesterol non HDL < 130 g/dL dan Hct > 30%
mg/dL. 3. Dosis penggunaan EPO 2000-
4000 IU SC selama 4 minggu 2-
3 kali seminggu. Apabila tidak
Terapi : Statin dan perbaikan maka dosis dinaikan
konsumsi rendah lemak 50%, dan apabila melebihi
jenuh, dianjurkan asupan target (Hb naik > 2.5 mg/dL dan
Hct > 8%), maka dosis
kolesterol < 300 mg/hari
diturunkan 25%
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 Tatalaksana
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Indikasi hemodialisa
Hipervolemi
BUN > 100-150 cepat dalam waktu pendek
Creatinin > 10
Hiperkalemia K > 5 yang sulit dikoreksi secara konservatif
biasanya dengan injeksi bikarbonat
Prekoma
Terima
kasih