Acute Kidney Injury

(AKI)

Departemen Penyakit Dalam

 Objectives

• Defininition and classification of AKI

• Epidemiology of AKI
• Etiology and common cause of AKI
• Pathophysiology of AKI
• Clinical manifestation of AKI
• Management and treatment of AKI
DEFINITION & CLASSIFICATION OF AKI
 Definitions

Acute Renal Failure

Acute Kidney Injury

Brivet et al (1996) Increase in SCr > 2.0 mg/dl = (“AKI”)
Increase in SCr >3.5 mg/dl and / or increase BUN > 100 mg/dl
(“Severe AKI”)
de Medonca et al (2000), Increase in SCr more than 0,5 mg/dl in 48 hour
Tepel et al (2000)

Agrawal dan Swartz (2000) Increase in SCr > 0,5 mg/dl/day with urine production < 400 cc/hari

Ricci et al (2006) Increase in SCr varied between 1,5 – 10 mg/dl

Decrease in urine production varied between 0-900 cc/day
GFR decrease more than > 50 % with a decrease in urine production
lasts several hours to several days

Mehta et al (2007) An abrupt (within 48 hours) reduction in kidney function defined as an

absolute increase in serum creatine of more than or equal to 0,3
mg/dl, a percentage increase in serum creatine of more than or equal
to 50% (1,5-fold from baseline), or a reduction in urine output
(documented oliguria of less than 0,5 ml/kg per hour for more than six
hours)

Keterangan : Scr= Serum Creatinin. BUN = Blood Urea Nitrogen. GFR = Glomeruli Filtration Rate
 Estimated serum creatinine levels by age group and race

MAN MAN WOMAN WANITA

AGE
(black) (white) (black) (white)
(year)
(mg/dL) (mg/dL) (mg/dL) (mg/dL)

20-24 1.5 1.3 1.2 1.0

25-29 1.5 1.2 1.1 1.0

30-39 1.4 1.2 1.1 0.9

40-54 1.3 1.1 1.0 0.8

55-65 1.3 1.1 1.0 0.8

>65 1.2 1.0 0.9 0.8

 Elevated levels of serum creatinine (mg / dl)
according to RIFLE criteria

Baseline 0.5 1.0 1.5 2.0 2.5 3.0

Risk 0.75 1.5 2.25 3.0 3.75 -

Injury 1.0 2.0 3.0 - - -

Failure 1.5 3.0 4.0 4.0 4.0 4.0

 RIFLE criteria based on urine output (UO) and body weight

Criteria Body weight (kg)

RIFLE
40 50 60 70

RIFLE - R UO= <120 cc UO= <150 cc UO= <180 cc UO= <210 cc

(in 6 hour) (in 6 hour) (in 6 hour) (in 6 hour)

RIFLE - I UO = <240 cc UO = <300 cc UO = <360 cc UO = <420 cc

(in 12 hour) (in 12 hour) (in 12 hour) (in 12 hour)

RIFLE - F UO = < 288 cc UO = < 360 cc UO = < 432 cc UO = < 504 cc

(in 24 hour) (in 24 hour) (in 24 hour) (in 24 hour)
ANURI ANURI ANURI ANURI
(in 12 hour) (in 12 hour) (in 12 hour) (in 12 hour)

Roesli R. 2007
EPIDEMIOLOGY
 AKI: A Common, Serious Problem

• AKI is present in 5% of all hospitalized patients,

and up to 50% of patients in ICUs
• The incidence is increasing -globally
• Mortality rate 50 - 80% in dialyzed ICU patients–
4 Million die each year of AKI
• AKI requiring dialysis is one of the most
important independent predictors of death in
ICU patients
• 25% of ICU dialysis survivors progress to ESRD
within 3 years
 AKI: A Common, Serious Problem

• 5% of hospital patients
• Up to 50% of ICU admissions
• AKI with clincal manifestation and
requiring renal replacement therapy;
survival = 90%
• AKI with multi-organ failure; survival =
10%
Natural History of AKI
ETIOLOGY or COMMON
CAUSES OF AKI
 AKI: Common Causes

• Ischemia (60%): cardiovascular disease, cardiac

surgery, abdominal surgery, shock, sepsis
• Nephrotoxins(30%): antibiotics, contrast,
chemotherapy, anti-rejection, NSAIDs

These causes also frequently lead to

sub-clinical renal injury,a vastly
underestimated problem
 Causes of AKI

 Pre-renal (35-40%)
 Intrarenal (55-60%)
ATN accounts for 85%
interstitial nephritis
glomerulonephritis
renal vascular disease
 Post-renal (2-5%)
Singri N. JAMA 2003;289:747-51
Etiology of AKI
 Pre – renal failure
• Hypovolemia
– Hemorrhage, GI fluid loss (diarrhea, vomiting,
NG suction), 3rd spacing (pancreatitis, bowel
disease), renal loses (diuretics, glycosuria),
trauma, surgery, burns
• Relative hypovolemia (effective volume)
– Sepsis, hepatic failure, anaphylaxis,
vasodilator drugs, nephrotic syndrome,
anesthetic agents
N Engl Med 1998;338:671- 675
 Pre – renal failure
• Myocardial failure
– Myocardial infarction, pulmonary embolism,
congestive heart failure, tamponade,
mechanical ventilation
• Disruption of renal autoregulation
– Angiotensin-converting-enzyme
• Renal artery or vein occlusion
– Thrombosis, thromboembolism, severe
stenosis, dissecting aneurysm
N Engl Med 1998;338:671- 675
 Intrinsic Renal Failure
• Small vessel vasculitis or acute
glomerulonephritis
– Connective tissue disease (SLE, scleroderma)
– Malignant hypertension
– Toxemia of pregnancy
– Microscopic polyarteritis
– Poststreptococcal glomerulonephritis
– Rapidly progressive glomerulonephritis
N Engl Med 1998;338:671- 675
 Intrinsic Renal Failure
• Interstitial nephritis
– Drugs (e.g methicillin)
– infection
– Cancer (lymphoma, leukemia, sarcoidosis)

N Engl Med 1998;338:671- 675

 Intrinsic Renal Failure
 Acute tubular necrosis
Ischemia (secondary to pre – renal events)
Nephrotoxic antibiotics (gentamicin, kanamycin)
Heavy metals (mercury, cisplatin)
Solvents (carbon tetrachloride, ethylene, glycol)
Radiographic contrast agents
Intratubular crystals (uric acid or oxalate)
Intratubular pigments (myoglobinuria)
 Post – renal Failure
• Upper urinary tract obstruction
– Ureteral obstruction of one or both kidneys
• Lower urinary tract obstruction
– Bladder – outlet obstruction (more common)

N Engl Med 1998;338:671- 675

COMMON CAUSES/ETIOLOGY OF AKI
PATHOPHYSIOLOGY
 Pathophysiology of AKI

• Functional alterations lead to injury

 Failure of autoregulation
• Injury precedes functional change
 Direct Nephrotoxicity
 Ischemia Reperfusion
 Inflammation
• Injury and functional change are concurrent
 Complete vascular occlusion
Etiology of AKI
 CLINICAL
MANIFESTATION
 Acute Kidney Injury
potential – life threatening
complications
• Hyperkalemia
– Muscle weakness and paralysis
– ECG changes
• Metabolic acidosis
– Kussmaul’s respiration, hypotension,
hyperreflexia
• Salt and water retention
– Pulmonary edema, ascites, pleural effusion
N Engl Med 1998;338:671- 675
 Complications of acute oliguria
• Cardiovascular
– Congestive heart failure, pulmonary oedema,
hypertension (25%), arrhytmia, pericarditis
• Infections
– Occur in 30 – 70% of patients
– A leading cause of morbidity and mortality

N Engl Med 1994;331:1416 – 20

 Complications of acute oliguria
• Neurological
– Confusion, somnolence, seizures
• Gastrointestinal
– Anorexia, nausea, vomiting, ileus
– Gastrointestinal bleed in 10 – 30% of patients
– Anemia (decreased erythropoiesis, GI bleed
and frequent blood sample)

N Engl Med 1994;331:1416 – 20

MANAGEMENT
 Management of AKI
• Search for a cause

• DO NOT give furosemide or dopamine

unless definite fluid overload
 Diagnostic evaluation
• History
• Examination
• Urine
• Blood tests
• Radiological investigations
• Renal biopsy
Identifying the cause of oliguria
Pre – renal (common)
Has the patient got an aduquate BP and
cardiac output?
Renal (less common)
Have we poisoned the kidney?
Is there a primary renal cause?
Post – renal (common)
Is there obstruction to the urine flow?
Rules for the management of oliguria (1)

• Maximize treatment before referral to ICU

• Close observation of vital signs
• Regular serum U&E
• Don’t let out of less than 0.5 mls/kg/hour
continue for more than 2 hours
Rules for the management of oliguria (2)

• Exclude obstruction to urine outflow

(particularly if absolute anuria)
– Bladder washout to exclude blocked catheter
– Renal ultrasound scan
• Fluid resuscitation
– Consider central line If appropriate
– Close monitoring of vital signs
 Vital signs assessment
(observations)
• Monitor vital signs appropriately
– RR, oxygen requirement, and chest
auscultation during fluid resuscitation
– Use CVP line for trend information

• Parameter for review

– Use Early Warning Score
– Monitor urea and electrolytes
Renal rescue - avoid risk factors
Nephrotoxic drugs

• NSAIDs inhibit synthesis of renal

prostaglandins - needed for afferent
arteriolar dilatation during low states
• ACE inhibitors - reduce production of
angiotensin II (normally constricts efferent
arterioles)
• Gentamicin - once daily dosing safer
 Renal replacement therapy -
indications

• Anuria • Metabolic acidosis

• Hyperkalaemia (pH < 7.1)
• Urea > 200 mg/dl • Uraemia causing:
• Creatinine > 4 mg/dl – encephalopathy
– pericarditis
• Pulmonary oedema
– neuropathy
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