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Ketut Suwitra
Division of Nephrology Department of Medicine
Faculty of Medicine Udayana University – Sanglah Hospital
DENPASAR
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Definition
Acute Kidney Injury (AKI)
a. abrupt of kidney function (< 7 days)
b. changes in blood chemistry (rise in serum creatinine)
c. decrease of urine out put
d. or both (b and c)
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Risk of renalDysfunction
Serum creatinine increased1.5 fold (1.5 – 2. mg/dL) or
GFR decreased by morethan 25%
Less than 0.5 ml/kg/h ofurine for 6 hours
Serum cretainine increased2 fold (2 – 4 mg/dL) or
GFR decreased than 50%
Less than 0.5 ml/kg/hof urine for 12 hoursInjury to the
Kidney
Failure ofKidneyFunction
Serum cretainine increased3 fold or An Acute rise inceratenine of greater than
44 mol/L so that newcreatinine is greater than
350 mol/L(>4 mg/dL)GFR decreased more than
75%
Less than 0.3 ml/kg/h ofurine for 24 hours oranuria for 12 hours
Loss of Kidneyfunction Complete loss of kidney for longer than 4 weeks
End-stage renal
Disease
The need for dialysis for longer than 3 months
GFR criteria Urine output criteriaAND/OR
Goldsmith D, 2007. ABC of Kidney Disease
RIFLE Criteria
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Aetiology
Acute Kidney Injury
Pre-renal Renal (intrinsic) Post-renal
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Pre-renal (40- 80% of cases)
Pre renal
Hypotension Hypovolaemia(reduced intravascular volume)
Low cardiac output
Total loss Volume redistribution
Reduced effectivecirculating volume
(Ascites, oedema, “3rd spacing”,
congestive cardiac failure)
Altered vascularcapacitance
(Sepsis: shunting, vasodilatation.Hepatorenal syndrome HRS)
GI loss(Vomiting, diarrhea, surgical
fistulae)
Haemorrhage(Visible and occult)
Renal loss(Diuretics, polyuria)
Skin loss(Exessive sweating, burns)
Blakeley S, 2008. Renal Failure and replacement Therapy
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Renal (Intrinsic) (20- 40% of cases)
Intrinsic
Glomerular(Glomerulonephritis)
Tubular Interstitial
(Autoimmune, toxic, infectious)Vascular
Toxic
Ischaemic(Extreme pre renal,sepsis, pancreatitis)
Large vessel
(Renovascular disease,atheroembolic)
Small vessel
(Vasculitis, HRS,renovascular, malignanthypertension)
Intrinsic toxins(Rhabdomyolysis, massive
aemolysis tumour lysis, myeloma)
Extrinsic toxins (Radio contrast, drugs, antibiotics)
Blakeley S, 2008. Renal Failure and replacement Therapy
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Post-renal (10- 20% of cases)
Intrinsic Extrinsic
Intra-luminal: e.g. stone, blood
cloth, papillary necrosis
Pelvic malignancy
Intra-mural: e.g. urethral stricture,
prostatic hypertophy or
malignancy, bladder tumour,
radiation fibrosis
Retroperitoneal fibrosis
Goldsmith D, 2007. ABC of Kidney Disease
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Causes of AKI
Pre-renal (volume responsive) Intrinsic Post-renal
Hypovolaemia
• Vomiting and diarrhoea
• Hemorrhage
Decrease in effectivecirculating volume
• Cardiac failure
• Septic shock
• Cirrhosis
Drugs• ACE inhibitors
Glomerular
• Glomerulonephritis
Glomerular endothelium
• Vasculitis
• HUS
• Malignant hypertension
Tubular
• Acute tubular necrosis
• Rhabdomyolysis• Myeloma
Interstitial
• Intersitial nephritis
Obstruction
• Renal calculi
• Retroperitoneal fibrosis
• Prostatic hypertrophy
• Carcinoma
• Cervical carcinoma
• Urethral stricture
• Bladder neoplasm
• Pelvic neoplasm
• Retroperitoneal neoplasm
Davenport A, 2008. Clinical Practice Guidelines; Module 5: Acute Kidney Injury.
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Prerenal
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Renal
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Postrenal
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Investigation of the causes
A. History
1. Presence of risk factors
- hemorrhage, water loss
- DM, advanced age, hypertension, heart disease
2. Previous episodes of renal disease (stone, cystic disease)
3. History of medication (anti TB, NSAID, aminoglycoside)
4. Systemic disease (SLE, hyperuricemia)
5. Family history
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B. Physical Finding 1. Blood pressure
2. Volaemic state
3. Loan pain 4. Ballotment
5. Retensio urinae
6. Prostate hyperthropy
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C. Laboratory finding
1. Oligouria
2. Anemia
3. Elevated serum urea and creatinine
4. Elevated serum cystatin C (?)
5. Hyperkalemia
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D. Imaging
1. Plain foto abdomen
2. Ultrasound
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Diagnostic step
1. Is this acute or chronic
renal failure ?
• history & examination
• Anemia
• hypertension
• Edema
• previous Sc
• small kidney in USG
2. Present a sign of
obstruction ?
• complete anuria
• ballotment/palpable blader
• USG
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3. Volaemic state ? Blood pressure, pulse
JVP/CVP
Urea/SC >20
heart failure
Urine Na < 20 mmol/L
4. Renal parenchymal
disease ?
history and examination
urine dipstic & microscopic
- proteinuria
- hematuria
- cast
Diagnostic step
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MANAGEMENT OF AKI
A. Conservative management
1. Exclude reversible/treatable causes of AKI 2. Obtain and maintain euvolemic state
3. Attempt to establish a urine output if patients oligouric
4. Provide adequate nutrition
5. Minimize use of invasive lines and procedures 6. Monitor drug usage, carefully, and modify dosage or
interval appropriately
7. Monitor and treat for clinical and biochemical
complications
B. Active management
• Renal Replacement Therapy
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Use of Diuretic and Renal vasodilators in AKI
1. success for converting an oligouric to an nonoligouric stateoccurs when the duration of oliguric was brief
2. respond more readly to a continuous infusion rather than abolus of loop diuretic
3. a small controlled study suggest dopamine may be synergistic
with lop diuretic in conversion an oligouric to nonoligouricstate , but this issue still controversy
4. the complication rate of low-dose dopamine and continuousinfusion of loop diuretic appears to be low
Important : obstructive uropathy must be excluded and prerenal factors corrected
Schrier, 2007
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Other Pharmacologic Agents :
Inotropic support (norapenephrine)
Some studies suggest that in patients with septic shock,
norepinephrine induces a diuresis more effectively than
other vasoactive agents as dopamine
Atrial Natriuretic Peptide
No consistent evidence for a beneficial role of ANP in the
treatment of AKI
Insulin like growth factor 1
No beneficial effect
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Nutritional support in AKIThe goal of nutritional support :
1. Restoration of metabolic homeostasis with
maintenance of fluid, electrolyte, and acid-base
balance
2. Preservation of lean body mass
3. Maximization of protein synthesis
4. Prevention of vitamin, mineral, and trace element
depletion
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Recommendation of nutrition in AKI : • 35 kcal/kg body weight/day
in sepsis, energy requirement can be increased by 25%
• 0.8 gm protein/kg body weight
• ratio between glucose and fat 70/30
Careful attention to electrolyte (Potassium & Sodium )
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RENAL REPLACEMENT THERAPY
The issues regarding renal replacement therapy in AKI
are currently the source of much debate and
investigations
• when to start ?
• what modality to use
• how much is enough ?
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When to start ?
earlier renal replacement therapy
“prophylactic” to keep BUN 90-100 mg/dl,creatinine 9-10 mg/dl
Schier, 2007
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Indications and criteria for initiating
renal replacement therapy in the intensive care unit
Bellomo R, Ronco C : Kidney int 1998;53 (66):S106-109
1. Oliguria (urine output < 200 ml/12 hr)
2. Anuria/extreme oliguria (urine output < 50 ml/12 hr)
3. Hyperkalemia ([K+] > 6.5 mmol/liter)
4. Severe acidemia (pH < 7.1)
5. Azotemia (urea) > 30 mmol/liter)
6. Clinically significant organ (especially lung) edema
7. Uremic enchepalopathy
8. Uremic pericarditis
9. Uremic neuropathy/myopathy
10. Severe dysnatremia ([Na] > 160 or < 115 mmol/liter)
11. Hyperthermia/Hypothermia
12. Drug overdose with dialysable toxin
The presence of :• one of the above criteria is sufficient to initiate renal replacement therapy in a critically ill
patients• two of these criteria makes renal replacement urgent and mandatory.• combined derangements suggest initiation of renal replacement therapy even before the
above mentioned limits have been reached.
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Dialysis modalities for acute kidney injury
Intermittent therapies
(up to 12 hours)
Continuous therapies
(24 hours)
Hemodialysis
intermittent
daily
Hemodiafiltration
Slow Continuous Ultra-Filtration
Extended Daily Dialysis
Sustained Low Efficiency Dialysis
Peritoneal dialysis
Ultrafiltration (SCUF)
Hemofiltration (CAVH, CVVH)
Hemodialysis (CAVHD, CVVHD)
Hemodiafiltration (CAVHDF,
CVVHDF)
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.
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ADVANTAGES DISADVANTAGES
Intermittent
hemodialysis
Efficient and rapid removal of
volume and small molecules
Cost effective
Readily available
Central venous access required
Anticoagulation may be required
May not be tolerated by
hemodynamically unstable
patients
Continuoushemofiltration
Excellent control of volumeenabling liberal use of
hyperalimentation, blood
products, etc.
Good removal of larger
molecules
Can be used in relatively
hypotensive patients
Central venous access requiredAnticoagulation may be required
Labor intensive and expensive
Peritoneal dialysis No need for anticoagulation
Cost-effective
Slow removal of uremic toxins
Risk of peritonitis
May be tolerated poorly in patients
with splanchnic hypo perfusion
The advantages and disadvantages of intermittent versus
continuous renal replacement therapies
Nephrology Secret, 2006
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NATURAL HISTORY OF AKI
INSULT1 – FULL RECOVERY
2 – AKI TO CKD
3 – ACUTE-ON-CHRONICKIDNEY DISEASE
4 – AKI TO ESRD
100
0
TIME
Clin J Am Soc Nephrol 3: 881-886, 2008
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SUMMARY
ACUTE KIDNEY INJURY
• A common critical condition with high mortality
• The classification depends on site of position and
etiology
• Loss of autoregulation, vasoconstriction,
glomerulotubular damage, and inflammation is a main
pathogenesis
• Some modality of treatments with a different result
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Treatment Evidence of benefit Comment
Loop diuretics No difference in renal revovery or mortality compared with placebo
May promote diuresis inoliguric AKI, but may be
ototoxic in high doses
Dopamine No difference in mortality or need for
dialysis compared with placebo
Potential adverse effects
include tachycardia,
extravasation necrosis
and peripheral gangrene
Natriuretic peptides No difference in dialysis-free survival
compared with placebo
Renal replacementtherapy
No significant difference in dialysis-dependency or mortality between
continuous and intermittent renal
replacement therapy
Continuous renalreplacement therapy is
less likely to ptovoke
haemodynamic
instability
Summary of Treatment
Goldsmith D, 2007. ABC of Kidney Disease
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