PEDIATRIC ACUTE KIDNEY INJURY

MOHAMED KHALED
PCICU SPECIALIST
 AKI

Clinical Prevention &

features & Management
Diagnosis
Definition

AKI is defined as a decrease in glomerular filtration rate (GFR), which

traditionally is manifested by an elevated or a rise in serum creatinine from
baseline, and/or a reduction in urine output .

Validated definitions for pediatric AKI include the Pediatric Risk, Injury, Failure,
Loss, End-Stage Renal Disease (pRIFLE) , and Kidney Disease Improving Global
Outcomes (KDIGO) classifications .

Other definitions : AKIN criteria (Acute Kidney Injury Network), pROCK criteria
(Pediatric reference change value optimized for AKI in children) .
 pRIFLE
Modification of the adult RIFLE classification and consists of three graded
levels of injury (Risk, Injury, and Failure), and two outcome measures (Loss of
kidney function and End-stage kidney disease)
estimated creatinine clearance is based on the original Schwartz formula
Original Schwartz Equations: eGFR = k x (height in cm) ÷ serum Cr
k = 0.33 in preemie infants
k = 0.45 in term infants to 1 year of age
k = 0.55 in children to 13 years of age
k = 0.70 in adolescent males (females remain at 0.55 after age 13 years)
 Estimated creatinine
pRIFLE stage Urine output
clearance (eCCl)

R = Risk for renal dysfunction eCCl decreased by 25 percent <0.5 mL/kg per hour for 8 hours

I = Injury to the kidney eCCl decreased by 50 percent <0.5 mL/kg per hour for 16 hours

eCCl decreased by 75 percent

<0.3 mL/kg per hour for 24 hours or
F = Failure of kidney function or anuria for 12 hours
eCCl <35 mL/min per 1.73 m2

L = Loss of kidney function Persistent failure >4 weeks

E = End-stage renal disease Persistent failure >3 months

Pediatric RIFLE (pRIFLE)

Stage Serum creatinine (SCr) Urine output
1 Increase to 1.5 to 1.9 times baseline, OR increase of ≥0.3
mg/dL (≥26.5 mcmol/L) <0.5 mL/kg per hour for 6 to 12 h

2 Increase to 2 to 2.9 times baseline

<0.5 mL/kg per hour for ≥12 h
3 Increase greater than 3 times baseline, OR <0.3 mL/kg per hour for ≥24 h, OR
SCr ≥4 mg/dL (≥353.6 mcmol/L), OR Anuria for ≥12 h
Initiation of renal replacement therapy, OR
eGFR <35 mL/min per 1.73 m2 (<18 years)

The time frames for the increases in serum creatinine are:

Increase of SCr ≥0.3 mg/dL (≥26.5 mcmol/L) within 48 hours
Increase in SCr >1.5 times the baseline within the prior seven days
eGFR: estimated glomerular filtration rate; h: hours.

Criteria for the Kidney Disease Improving Global Outcomes (KDIGO)

Risk factors

1. Critical illness
2.

3. Neonates (congenital heart disease (CHD) , very low birth weight (VLBW;
birth weight <1500 g) , sepsis , low gestational age and perinatal asphyxia) .
4.

5. Nephrotoxin use ; most commonly

(aminoglycosides, vancomycin, piperacillin-tazobactam, antiviral agents,
radiocontrast agents, angiotensin-converting enzyme inhibitors, calcineurin
inhibitors, and nonsteroidal anti-inflammatory drugs (NSAIDs)
6.

7. Comorbid conditions (CHD, Cancer, Nephrotic syndrome, sickle cell vaso-

occlusive pain crisis .. )
Classifications (Etiology &
Pathogenesis)
Several AKI classification schemas have been
developed.

1- According to anatomic location of the initial injury :

1. Prerenal disease
2. Intrinsic kidney disease
3. Post renal disease

2- Clinical setting or circumstance :

4. Community-acquired AKI
5. Hospital-acquired AKI
Classifications (Etiology &
Pathogenesis) cont’d

3- Urine output :

1. Anuria – No urine output

2. Oliguria – Urine output <1 mL/kg per hour in infants, and in children and
adults, urine output <0.5 mL/kg per hour for greater than six hours.
3. Nonoliguria – Urine output for greater than six hours of >1 mL/kg per hour for
infants and >0.5 mL/kg per hour for children and adults.
4. Polyuria – Urine output of greater than 3 mL/kg per hour.
Mechanism Etiology
Prerenal causes
Dehydration, hemorrhage, diuretics, burns, shock,
Decreased intravascular volume
nephrotic syndrome
Decreased cardiac function Heart failure, arrhythmias
Peripheral vasodilatation Sepsis, anaphylaxis, antihypertensive medication
Sepsis, nonsteroidal antiinflammatory drugs, ACE
Renal vasoconstriction
inhibitor
Intrinsic causes

Tubular injury (acute tubular necrosis) Prolonged ischemia, nephrotoxins, hypotension, sepsis
Renal vascular diseases Hemolytic uremic syndrome, vasculitides, thrombosis
Renal vascular diseases Interstitial nephritis, infections, malignant infiltrations
Post-infectious glomerulonephritis, rapidly progressive
Glomerulonephritides
glomerulonephritis, Henoch-Schönlein purpura

ACE: angiotensin converting enzyme.

Causes of prerenal and intrinsic pediatric acute kidney

injury
Clinical presentation

1. Volume overload, heart failure

2. Electrolyte imbalance ( Hyperkalemia,Metabolic acidosis, Hyponatremia,
Hypocalcemia, Hyperphosphatemia )
3. Hematuria
4. Hypertension
5. Signs & symptoms of the original disease
Diagnosis

Signs & Symptoms

Laboratory findings :
1. Serum creatinine (depends on age, gender, muscle mass, diet and hydration status of the child)

2. Urinalysis
3. serum cystatin C (more accurate, more expensive, can be altered by thyroid dysfunction, administration of
corticosteroids, inflammatory diseases )

4. Novel biomarkers :
Neutrophil gelatinase-associated lipocalin (NGAL) , kidney injury molecule-1 (KIM-1) ,
interleukin-18 (IL-18) , fibroblast growth factor 23 (FGF23) , insulin growth factor binding
protein 7 (IGFBP-7) and tissue inhibitor of metalloproteinases 2 (TIMP-2)
IDENTIFYING THE UNDERLYING CAUSE
History
Physical examination
1. Signs on intravascular volume depletion
2. Signs of volume overload
3. Renal disease due to systemic causes
4. Palpable enlarged kidney
5. Signs of obstruction
History of fluid loss
Diarrhea, vomiting
Burns
Surgery
Shock
Exposure to nephrotoxic agents
Nonsteroidal antiinflammatory drugs
Aminoglycosides
Contrast agents
Factors associated with glomerular diseases
Streptococcal infection: Poststreptococcal glomerulonephritis
Bloody diarrhea: Hemolytic uremic syndrome
Joint symptoms, rash, or purpura: Henoch-Schönlein purpura
Signs of obstruction
Complete anuria
Poor urinary stream

Potential historical findings in children with acute kidney

injury
Palpable purpura in IgA vasculitis (Henoch-Schönlein purpura). Multiple
papules and plaques on the buttocks and legs.
Acute cutaneous lupus erythematosus
IDENTIFYING THE UNDERLYING CAUSE
cont’d

Laboratory and imaging evaluation

1. Urinalysis
2. Fractional sodium excretion to differentiate between pre- and intrinsic AKI
3. Kidney ultrasound
Diagnostic fluid challenge
Additional laboratory measurements : CBC, Complement studies,
Elevated serum levels of aminoglycosides are associated with ATN
Kidney imaging
Kidney biopsy
PREVENTIO MANAGEME
FLUID N
ADMINSTRATION NT
FLUID MANAGEMENT

NEPHROTOXIN ELECTROLYTE
MANAGEMENT MANAGEMENT

UNPROVEN HYPERTENSION
PHARMACOLOGIC
AGENTS
NUTRITIONAL SUPPORT

DRUG MANAGEMENT

REPLACEMENT THERAPY
 Prevention
1- Fluid administration :
Prerenal AKI due to hypovolemia, intravenous (IV) fluid bolus with normal saline (10 to 20 mL/kg
over 30 minutes)
contraindicated in patients with obvious volume overload or heart failure

2- Nephrotoxin management
drug level (if possible) is important
adjustment of drug dosing

3- Unproven pharmacologic agents :

- mannitol , loop diuretics , low-dose dopamine , fenoldopam , atrial natriuretic peptide
, and N-acetylcysteine have been studied in the prevention of AKI . However , none of
these agents have been shown to be of proven benefit !!
 Management

1- Fluid management :

A. Hypovolemia : (as mentioned before)

B. Euvolemia : (insensible fluid [300 to 500 mL/m2 per day], urine, and
gastrointestinal losses)
C. Hypervolemia : furosemide, renal replacement therapy
2- ELECTRLYTES MANAGEMENT

a) Hyperkalemia : most common electrolyte complication, most serious

Agent Dose Onset of ¶ Calcium should be
administered in a
action larger vein or central
Stabilization of line preferably
cardiac myocardial (irritant), and sodium
membrane in bicarbonate should
setting of not be introduced into
the line because of
hyperkalemia-
potential
associated precipitation.
abnormal ECG or Continuous ECG
arrhythmia monitoring should be
Calcium 0.5 to 1 mL/kg IV over 5 to 15 min (50 to 100 mg/kg calcium Immediate performed during
gluconate¶ gluconate, maxiumum dose 3 grams) Repeat after 10 administration.
minutes, if needed
Movement of Treatment
extracellular
potassium into the of
cells*
hyperkalemi
Glucose and insulin IV administration of glucose 2 mL/kg of a 25 percent 30 minutes
dextrose solution IV administration of insulin 0.1 units/kg a in children
over 30 min
Inhaled beta- 0.1 to 0.3 mg/kg 30 minutes
agonists (albuterol)
IV: intravenous administration; PO: oral administration; PR: rectal administration; ECG: electrocardiogram.

Sodium bicarbonate IV administration of 1 mEq/kg over 10 min (maximum dose 15 minutes

of 50 mEq per hour)
Removal of
potassium
b) Metabolic acidosis :
IV fluids, NaHCO3 reserved for life threatening conditions

3- Hypertension :
Several contributing factors may cause an elevation in blood pressure including fluid
overload and renin-mediated hypertension, often seen in children with
glomerulonephritis. Initial management is typically administration of a diuretic

4- Nutritional support :
- AKI is associated with marked catabolism.
- No validated guidelines for the nutritional management of the critically-ill child with
AKI are currently available. infants should receive at least 120 Kcal/kg per day, and in
older children, nutritional intake should be at least 150 percent of maintenance needs.
5- Drug management :
Avoidance of nephrotoxic drugs
Dosing adjustment of renally excreted drugs
Glomerular filtration rate estimate for children by Schwartz formula
Dose reductions are generally necessary for renally excreted drugs when GFR falls
below 50 mL/min per 1.73 m2
Drug levels should be routinely monitored

6- Kidney replacement therapy :

Hemodialysis (HD) , peritoneal dialysis (PD) , and continuous RRT (CRRT)
RRT choice depends on the clinical status of the patient, the expertise of the clinician,
and the availability of appropriate resources
Peritoneal dialysis
GOALS

AT THE END OF THIS LECTURE YOU WILL BE ABLE TO :

1- DEFINE PD
2- KNOW INDICATIONS AND CONTRINDICATIONS OF PD
3- PD PRESCRIPRITON
4- COMPLICATIONS OF PD
Definition

Peritoneal dialysis is the use of patient’s own body

tissue-peritoneal membrane inside the abdominal
cavity as a filter to :
(Indications of PD) :
1. Remove extra fluid “Ultrafiltration” .
2. Restore balance of blood chemistries .
3. Filter waste products . (uremia, lactic acidosis .. Etc)
PHYSIOLOGY

1.Osmosis : movement of water across membrane from

area of
low “solute” to area of high “solute” .
2.

3.Diffusion : movement of molecules across membrane

from area of
“high concentration” to area of “low concentration” .
Molecules eg ; ( electrolytes , urea ,
creatinine , medications , toxins )
CONTRAINDICATIO Recent abdominal surgery ‘relative’ , open abdomen
‘absolute’
NS Fungal peritonitis ‘absolute’

Paralytic ileus

Open chest post cardiac surgery

Abdominal compartment syndrome

Difficulty ventilating the patient

Pleuroperitoneal connection allowing dialysate in the chest

Diaphragmatic hernia

Inguinal hernia

Abdominal wall cellulitis or burn

TECHNIQUE

Procedure :
1- Blind placement using guide wire
2- Surgical placement

Site :
1- Midline : 3cm below umbilicus
2- Lateral : halfway between
umbilicus and ant superior iliac
spine , left side is preferred
COMPLICATIONS

1. Bowel perforation
2. Injury to abdominal organ “Liver , Spleen”
3. Bleeding
4. Leakage
Suggested prescription modulation to achieve
outcomes
COMPLICATIONS
1. Peritonitis :
Organism : staphylococci (60%), enterococci, and gram-negative intestinal bacteria
(eg; pseudomonas , E-coli)(20%), fungi (< 5%)
Signs & Symptoms : fever , abdominal pain , nausea , vomiting , cloudy PD fluid
“fibrin” , slow flow of PD “in or out”
Diagnosis : PD fluid analysis “>100 leukocytes/μL , >50% neutrophils “
Treatment : Antibiotics (systemic and intraperitoneal) : Vancomycin 30 mg/L ,
Ceftazidime 125 mg/L
Antifungals (systemically only): – Amphotericin B not intraperitoneally (damages
the peritoneum)
refer to ISPD “International Society Of Peritoneal Dialysis“ for more details
COMPLICATIONS

2. Mechanical Complications :
A. Leakage : “infection , poor efficacy , dialysate fluid harms the skin , dextrose (energy
source for bacteria)
B. Obstruction
C. Pleural effusion : Drains
D. Ventilation problem (increased intraabdominal pressure)
3. Decreased U.F :Catheter block (blood , fibrin , omentum)
4. Protein loss
5. Hyperglycemia due to high glucose concentration in PD
fluid
Advantages of PD over HD

1. Easy to use without sophisticated equipements

2. No need for vascular access
3. More suitable in hemodynamic instability
TAKE HOME MESSAGE

1. Be aware of nephrotoxins
2. When possible measure antibiotics level
3. GFR , when below 50 , you need to adjust
4. Use fluids wisely
5. PD is a very effective mean of RRT
6. Always look for the hidden cause behind AKI
References
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Curr Pediatr Rep 2013; 1:34.
Akcan-Arikan A, Zappitelli M, Loftis LL, et al. Modified RIFLE criteria in critically ill children with
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its application and association with measures of mortality and morbidity. Kidney Int 2012; 81:791.
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO
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Joyce EL, Kane-Gill SL, Priyanka P, et al. Piperacillin/Tazobactam and Antibiotic-Associated Acute
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19:59.
References
Perazella MA. Drug use and nephrotoxicity in the intensive care unit. Kidney Int 2012; 81:1172.
Li Y, Tang X, Zhang J, Wu T. Nutritional support for acute kidney injury. Cochrane Database Syst Rev
2012; :CD005426.
Nkoy AB, Ndiyo YM, Matoka TT, et al. A promising pediatric peritoneal dialysis experience in a
resource-limited setting with the support of saving young lives program. Perit Dial Int 2020;
40:504.
McCulloch M, Luyckx VA, Cullis B, et al. Challenges of access to kidney care for children in low-
resource settings. Nat Rev Nephrol 2021; 17:33.
Reznik VM, Griswold WR, Peterson BM, et al. Peritoneal dialysis for acute renal failure in children.
Pediatr Nephrol 1991; 5:715.
Warady BA, Bakkaloglu S, Newland J, et al. Consensus guidelines for the prevention and treatment
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2014; 34:494.
Dr. Henry Tenckhoff ( 1930 –
2017 )
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