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ACUTE KIDNEY
INJURY IN CHILDREN
LE THANH BINH,MD
DEFINITIONS
DEFINITIONS
14,220 children from 24 studies worldwide
from 2004 to 2012
Studies used KDIGO definition for AKI
Most studies originated from N America,
Europe, and East Asia, from high income
countries and from nations that spent ≥5% of
the gross domestic product on total health
expenditure
Pooled incidence of AKI was 33.7% in
hospitalized children (95% CI 26.9-41.3)
DEFINITIONS
 Abrupt loss of kidney function(GFR): An
elevated or a rise in serum creatinine from
baseline
 Retention of urea and other nitrogenous waste
products.
 Dysregulation of extracellular volume and
electrolytes.
RIFLE Classification of AKI
AKIN classification of AKI
Serum creatinine criteria Urine output criteria
Stage 1 Increase in serum creatinine ≥0.3
mg/dL (≥26.4 umol/L) or
increase to ≥150-200% (1.5-2
fold) from baseline
<0.5 ml/kg/hour for 6
hours
Stage 2 Increase to >200-300% (>3 fold)
from baseline
<0.5 ml/kg/hour for 12
hours
Stage 3 Increase in serum creatinine to
>300% (>3 fold) from baseline
or serum creatinine ≥4 mg/dL
(≥354 umol/L) with acute
increase of at least 0.5 mg/dL
(45.5 umol/L)
<0.3 ml/kg/hour for 24
hours or anuria for 12
hours
Criteria for the Kidney Disease Improving
Global Outcomes (KDIGO) AKI in children
Serum creatinine Urine output
Stage 1 Increase to 1.5-1.9 times baseline within
the prior 7 days OR
Increase of serum creatinine ≥0.3 mg/dL
(≥26.5 umol/L) within 48 hours
<0.5 ml/kg/hour
for 6-12 hours
Stage 2 Increase to 2-2.9 times baseline <0.5 ml/kg/hour
for ≥12 hours
Stage 3 Increase >3 times baseline OR
Serum creatinine ≥4 mg/dL (≥353.6
umol/L) OR
Initiation of renal replacement therapy
OR
eGFR <35 ml/min/1.73m2 (<18 years)
<0.3 ml/kg/hour
for 24 hours or
anuria for 12 hours
The 3 different criteria resulted in
different incidences and staging
26.9
13.4
10.8
48.9
Stage 1 Stage 2
Stage 3 No AKI
19.4
11.2
6.7
62.7
18.2
10.4
11.7
59.7
Stage 1
Stage 2
Stage 3
No AKI
pRIFLE AKIN KDIGO
All 3 definitions correlate highly with outcomes
in terms of mortality and length of stay
1720
6
5406
427
15
3
0
0
pRIFLE
KDIGO
AKI
N
n Mortality LOS
AKI by all three 5406 2.7% 10 (5-21)
No AKI any 6146 0.8% 4 (2-6)
AKI pRIFLE 1720 1.5% 5 (3-9)
AKI AKIN 0 n/a n/a
AKI KDIGO 6 0 6 (3-8)
Not diagnosed
by pRIFLE
153 0 5 (4-8)
Not diagnosed
by AKIN
427 0.7% 12 (7-18)
Not diagnosed
by KDGIO
0 0 n/a
CLASSIFICATION
URINE OUTPUT
Anuria no urine output
Oliguria Infant: <1 mL/kg per hour
Children and adults: <0.5 mL/kg per hour for greater than six
hours
Nonoliguria Infant: >1 mL/kg per hour for greater than six hours
Children and adults: >0.5 mL/kg per hour for greater than six
hours
Polyuria Urine output of greater than 3 mL/kg per hour
Less frequently use
CLASSIFICATION
Prerenal diseases: reduced renal perfusion
Hypovolemia: blood loss, dehydration
Sepsis
Congenital heart disease: cardiac failure, Cardiac
surgery
Renal artery stenosis
Hepatorenal syndrome
Drugs: IV radiocontrast agents, indomethacin
Hypoalbuminemia: Congenital nephrotic syndrome
CLASSIFICATION
Intrinsic renal diseasses: Renal pathology
Acute tubular necrosis
Cortical necrosis
CAKUT
ARPKD
Congenital nephrotic syndrome
Acute pyelonephritis
Renal arterial or venous thrombosis
Acute tubulointerstitial nephritis
CLASSIFICATION
Postrenal diseases: Obstructive uropathy
Urethral obstruction:
Posterior urethral valves
Urethral stricture
Neurogenic bladder
Bilateral or solitary kidney with
Vesicoureteric junction obstruction
Pelviureteric junction obstruction
Causes of AKI in children
in Asia
 Infections: post-infectious GN,
pneumococcus associated HUS
 Animal toxins: snake-bite
 Plant toxins: “Djenkol” bean
 Pigment-induced: G6PD-deficiency
associated hemolysis
 Calculi obstruction: melamine
Shift in etiology of Pediatric
AKI to ischemic/toxic injury
CLINICAL FINDINGS
 SIGNS AND SYMPTOMS:
 Edema
 Decreased or no urine output
 Gross hematuria ( or microscopic )
 Hyperetension
 Etiologic causes
 Laboratory monitoring:
 serum Creatinin/ Ure and UA.
 Tests related to disoders and
complications.
 Etiology finding tests.
DIAGNOSIS TESTS
Using serum creatinine, diagnosis of AKI is made 24-72 hours
following the event that precipitated the reduction in GFR
long past the window of potential reversibility
Tests to distinguish between
prerenal and intrinsic ATN ?
Fractional excretion of sodium
UNa x SCr
FENa, percent = ——————— x 100
SNa x Ucr
- A FENa < 1% suggests prerenal AKI
- A FENa > 2% suggests ATN
Limitations
- Previous fluid administration
- Diuretic therapy
- AKI due to contrast nephropathy
Tests to distinguish between
prerenal and intrinsic ATN ?
Diagnostic fluid challenge
- Infuse 10 to 20 mL/kg of normal saline
Indications
- Suspected prerenal AKI but the duration is unknown.
- An increase in serum creatinine with unclear cause.
Contraindicated in patients with obvious volume overload
or heart failure.
MANAGEMENT OF AKI
- Specific treatment of the underlying cause
- Fluid management
- Electrolyte management
- Nutritional support
- Adjustment of drug dosing
- Renal replacement therapy
- Specific pharmacologic therapies
FLUID MANAGEMENT
Hypovolemia clinical history and physical exam
- Normal saline bolus (10 to 20 mL/kg over 30 minutes,
repeated twice as needed)
Euvolemia
- Ongoing fluid losses (insensible fluid [300 to
500 mL/m2 per day], urine, and gastrointestinal losses)
Hypervolemia
- Furosemide
- A single high-dose bolus (2 to 5 mg/kg/dose) (oliguria of less than
24 hours’ duration),
 If effective, then a continuous infusion of furosemide (0.1 to
0.3 mg/kg per hour)
 If not response within 2 hours, should be promptly discontinued
ELECTROLYTE MANAGEMENT
Hyperkalemia
Metabolic acidosis
Hyperphosphatemia and hypocalcemia
HYPERTENSION
Nicardipin:
Initial 0.5 to 1 mcg/kg per minute, increased every 15
to 30 minutes; maximum dose: 4 to 5 mcg/kg per
minute
Labetatol:
Initial bolus of 0.2 to 1 mg/kg per dose (maximum
dose: 40 mg) followed by an infusion of 0.25 to
3 mg/kg per hour
NUTRITIONAL SUPPORT
Adequate nutrition
Enteral route/Parenteral route
DRUG MANAGEMENT
Avoidance of nephrotoxic drugs
Dosing adjustment of renally excreted drugs
- if AKI is in an early stage and Cr is rising ( Injury), assume GFR is
<10 mL/min 1.73 m2.
Drug levels should be routinely monitored
- Vancomycin
- Digoxin
RENAL REPLACEMENT THERAPY
RENAL REPLACEMENT THERAPY
RENAL REPLACEMENT THERAPY
RENAL REPLACEMENT THERAPY
RENAL REPLACEMENT THERAPY
AKI PREVENTION
Fluid administration
Prerenal AKI due to hypovolemia: normal saline 10 to
20 mL/kg over 30 minutes may prevent more severe
intrinsic AKI
AKI PREVENTION
Nephrotoxin management
- AMINOGLYCOSIDE
AKI PREVENTION
Nephrotoxin management
- CONTRAST INDUCED AKI: defined as
- A rise in SCr of X 0.5 mg/dl (X44 mmol/l) or
- A 25% increase from baseline value
Assessed at 48 hours after a radiological procedure.
AKI PREVENTION
Nephrotoxin management
- Contrast induced AKI
AKI PREVENTION
Nephrotoxin management
- Contrast induced AKI prevention
-Isotonic crystaloid fluid should be started 3 hours and
continued 6 hours after contrast-media administration at the
dose of 1.5-3 ml/kg/h, to maintain UO at least 150 ml/h.
THANKS FOR YOUR ATTENTION

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ACUTE KIDNEY INJURY IN CHILDREN - LE THANH BINH.pptx

  • 1. ACUTE KIDNEY INJURY IN CHILDREN LE THANH BINH,MD
  • 4. 14,220 children from 24 studies worldwide from 2004 to 2012 Studies used KDIGO definition for AKI Most studies originated from N America, Europe, and East Asia, from high income countries and from nations that spent ≥5% of the gross domestic product on total health expenditure
  • 5. Pooled incidence of AKI was 33.7% in hospitalized children (95% CI 26.9-41.3)
  • 6. DEFINITIONS  Abrupt loss of kidney function(GFR): An elevated or a rise in serum creatinine from baseline  Retention of urea and other nitrogenous waste products.  Dysregulation of extracellular volume and electrolytes.
  • 8. AKIN classification of AKI Serum creatinine criteria Urine output criteria Stage 1 Increase in serum creatinine ≥0.3 mg/dL (≥26.4 umol/L) or increase to ≥150-200% (1.5-2 fold) from baseline <0.5 ml/kg/hour for 6 hours Stage 2 Increase to >200-300% (>3 fold) from baseline <0.5 ml/kg/hour for 12 hours Stage 3 Increase in serum creatinine to >300% (>3 fold) from baseline or serum creatinine ≥4 mg/dL (≥354 umol/L) with acute increase of at least 0.5 mg/dL (45.5 umol/L) <0.3 ml/kg/hour for 24 hours or anuria for 12 hours
  • 9. Criteria for the Kidney Disease Improving Global Outcomes (KDIGO) AKI in children Serum creatinine Urine output Stage 1 Increase to 1.5-1.9 times baseline within the prior 7 days OR Increase of serum creatinine ≥0.3 mg/dL (≥26.5 umol/L) within 48 hours <0.5 ml/kg/hour for 6-12 hours Stage 2 Increase to 2-2.9 times baseline <0.5 ml/kg/hour for ≥12 hours Stage 3 Increase >3 times baseline OR Serum creatinine ≥4 mg/dL (≥353.6 umol/L) OR Initiation of renal replacement therapy OR eGFR <35 ml/min/1.73m2 (<18 years) <0.3 ml/kg/hour for 24 hours or anuria for 12 hours
  • 10. The 3 different criteria resulted in different incidences and staging 26.9 13.4 10.8 48.9 Stage 1 Stage 2 Stage 3 No AKI 19.4 11.2 6.7 62.7 18.2 10.4 11.7 59.7 Stage 1 Stage 2 Stage 3 No AKI pRIFLE AKIN KDIGO
  • 11. All 3 definitions correlate highly with outcomes in terms of mortality and length of stay 1720 6 5406 427 15 3 0 0 pRIFLE KDIGO AKI N n Mortality LOS AKI by all three 5406 2.7% 10 (5-21) No AKI any 6146 0.8% 4 (2-6) AKI pRIFLE 1720 1.5% 5 (3-9) AKI AKIN 0 n/a n/a AKI KDIGO 6 0 6 (3-8) Not diagnosed by pRIFLE 153 0 5 (4-8) Not diagnosed by AKIN 427 0.7% 12 (7-18) Not diagnosed by KDGIO 0 0 n/a
  • 12. CLASSIFICATION URINE OUTPUT Anuria no urine output Oliguria Infant: <1 mL/kg per hour Children and adults: <0.5 mL/kg per hour for greater than six hours Nonoliguria Infant: >1 mL/kg per hour for greater than six hours Children and adults: >0.5 mL/kg per hour for greater than six hours Polyuria Urine output of greater than 3 mL/kg per hour Less frequently use
  • 13. CLASSIFICATION Prerenal diseases: reduced renal perfusion Hypovolemia: blood loss, dehydration Sepsis Congenital heart disease: cardiac failure, Cardiac surgery Renal artery stenosis Hepatorenal syndrome Drugs: IV radiocontrast agents, indomethacin Hypoalbuminemia: Congenital nephrotic syndrome
  • 14. CLASSIFICATION Intrinsic renal diseasses: Renal pathology Acute tubular necrosis Cortical necrosis CAKUT ARPKD Congenital nephrotic syndrome Acute pyelonephritis Renal arterial or venous thrombosis Acute tubulointerstitial nephritis
  • 15. CLASSIFICATION Postrenal diseases: Obstructive uropathy Urethral obstruction: Posterior urethral valves Urethral stricture Neurogenic bladder Bilateral or solitary kidney with Vesicoureteric junction obstruction Pelviureteric junction obstruction
  • 16. Causes of AKI in children in Asia  Infections: post-infectious GN, pneumococcus associated HUS  Animal toxins: snake-bite  Plant toxins: “Djenkol” bean  Pigment-induced: G6PD-deficiency associated hemolysis  Calculi obstruction: melamine
  • 17. Shift in etiology of Pediatric AKI to ischemic/toxic injury
  • 18.
  • 19. CLINICAL FINDINGS  SIGNS AND SYMPTOMS:  Edema  Decreased or no urine output  Gross hematuria ( or microscopic )  Hyperetension  Etiologic causes  Laboratory monitoring:  serum Creatinin/ Ure and UA.  Tests related to disoders and complications.  Etiology finding tests.
  • 21. Using serum creatinine, diagnosis of AKI is made 24-72 hours following the event that precipitated the reduction in GFR long past the window of potential reversibility
  • 22.
  • 23. Tests to distinguish between prerenal and intrinsic ATN ? Fractional excretion of sodium UNa x SCr FENa, percent = ——————— x 100 SNa x Ucr - A FENa < 1% suggests prerenal AKI - A FENa > 2% suggests ATN Limitations - Previous fluid administration - Diuretic therapy - AKI due to contrast nephropathy
  • 24. Tests to distinguish between prerenal and intrinsic ATN ? Diagnostic fluid challenge - Infuse 10 to 20 mL/kg of normal saline Indications - Suspected prerenal AKI but the duration is unknown. - An increase in serum creatinine with unclear cause. Contraindicated in patients with obvious volume overload or heart failure.
  • 25. MANAGEMENT OF AKI - Specific treatment of the underlying cause - Fluid management - Electrolyte management - Nutritional support - Adjustment of drug dosing - Renal replacement therapy - Specific pharmacologic therapies
  • 26. FLUID MANAGEMENT Hypovolemia clinical history and physical exam - Normal saline bolus (10 to 20 mL/kg over 30 minutes, repeated twice as needed) Euvolemia - Ongoing fluid losses (insensible fluid [300 to 500 mL/m2 per day], urine, and gastrointestinal losses) Hypervolemia - Furosemide - A single high-dose bolus (2 to 5 mg/kg/dose) (oliguria of less than 24 hours’ duration),  If effective, then a continuous infusion of furosemide (0.1 to 0.3 mg/kg per hour)  If not response within 2 hours, should be promptly discontinued
  • 28. HYPERTENSION Nicardipin: Initial 0.5 to 1 mcg/kg per minute, increased every 15 to 30 minutes; maximum dose: 4 to 5 mcg/kg per minute Labetatol: Initial bolus of 0.2 to 1 mg/kg per dose (maximum dose: 40 mg) followed by an infusion of 0.25 to 3 mg/kg per hour
  • 30. DRUG MANAGEMENT Avoidance of nephrotoxic drugs Dosing adjustment of renally excreted drugs - if AKI is in an early stage and Cr is rising ( Injury), assume GFR is <10 mL/min 1.73 m2. Drug levels should be routinely monitored - Vancomycin - Digoxin
  • 36. AKI PREVENTION Fluid administration Prerenal AKI due to hypovolemia: normal saline 10 to 20 mL/kg over 30 minutes may prevent more severe intrinsic AKI
  • 38. AKI PREVENTION Nephrotoxin management - CONTRAST INDUCED AKI: defined as - A rise in SCr of X 0.5 mg/dl (X44 mmol/l) or - A 25% increase from baseline value Assessed at 48 hours after a radiological procedure.
  • 40. AKI PREVENTION Nephrotoxin management - Contrast induced AKI prevention -Isotonic crystaloid fluid should be started 3 hours and continued 6 hours after contrast-media administration at the dose of 1.5-3 ml/kg/h, to maintain UO at least 150 ml/h.
  • 41. THANKS FOR YOUR ATTENTION