Overview
Definition:
Acute Kidney Injury (AKI) in children is a sudden decline in kidney function, characterized by an inability to maintain fluid and electrolyte balance, excrete nitrogenous wastes, and the presence of urine abnormalities
It is defined by a rapid increase in serum creatinine or a decrease in urine output
The KDIGO (Kidney Disease: Improving Global Outcomes) guidelines define AKI based on creatinine rise or urine output criteria over 7 days.
Epidemiology:
AKI affects approximately 10-40% of critically ill children, with higher incidence in neonatal intensive care units (NICUs) and pediatric intensive care units (PICUs)
Prerenal AKI is the most common cause, accounting for up to 50-70% of cases
Intrinsic AKI, though less common, is associated with higher morbidity and mortality
Incidence varies by age, with neonates having unique risk factors.
Clinical Significance:
AKI in children is associated with increased mortality, prolonged hospitalization, and a higher risk of developing chronic kidney disease (CKD) later in life
Prompt recognition and management are crucial to prevent irreversible kidney damage and systemic complications
Understanding the distinction between prerenal and intrinsic AKI guides appropriate diagnostic workup and therapeutic interventions, especially fluid management, which is paramount.
Clinical Presentation
Symptoms:
Decreased urine output (oliguria or anuria)
Lethargy and irritability
Poor feeding or vomiting
Signs of dehydration
In older children: flank pain
In severe cases: seizures, altered mental status, respiratory distress.
Signs:
Decreased urine output
Signs of dehydration: dry mucous membranes, decreased skin turgor, sunken fontanelles (infants), tachycardia
Signs of fluid overload: edema (periorbital, peripheral), hypertension, crackles on auscultation, ascites
Pallor
Abdominal distension.
Diagnostic Criteria:
KDIGO AKI Classification: Stage 1: Serum creatinine increase by >= 0.3 mg/dL within 48 hours, or urine output < 0.5 mL/kg/hr for 6 hours
Stage 2: Serum creatinine increase by 1.5-2x baseline, or urine output < 0.5 mL/kg/hr for 12 hours
Stage 3: Serum creatinine increase by >= 3x baseline, or urine output < 0.3 mL/kg/hr for 24 hours or anuria for 12 hours.
Diagnostic Approach
History Taking:
Recent fluid intake and losses (vomiting, diarrhea, insensible losses)
Urinary symptoms (frequency, dysuria, hematuria)
Medications (nephrotoxic drugs)
Recent infections, particularly those with dehydration or sepsis
History of congenital anomalies of the kidney and urinary tract (CAKUT)
Previous renal function
Family history of renal disease.
Physical Examination:
Assess hydration status: skin turgor, mucous membranes, capillary refill time
Evaluate for edema
Auscultate for pulmonary congestion
Check blood pressure for hypertension or hypotension
Palpate abdomen for organomegaly or distension
Perform a thorough genitourinary examination, including external genitalia.
Investigations:
Laboratory tests: Serum creatinine and BUN (baseline and serial monitoring)
Electrolytes (Na+, K+, Cl-, bicarbonate)
Urinalysis: specific gravity, pH, protein, glucose, ketones, blood, presence of casts (hyaline, granular, RBC, WBC)
Urine electrolytes (FENa, FEUrea) to differentiate prerenal from intrinsic AKI
Complete blood count (CBC)
Blood gas analysis
Imaging: Renal ultrasonography to assess kidney size, structure, and rule out obstruction (hydronephrosis).
Differential Diagnosis:
Prerenal AKI (hypovolemia, decreased cardiac output)
Intrinsic AKI (acute tubular necrosis, acute interstitial nephritis, glomerulonephritis, hemolytic uremic syndrome, vasculitis)
Postrenal AKI (obstruction: posterior urethral valves, ureteropelvic junction obstruction, stones).
Prerenal Vs Intrinsic Differentiation
Prerenal Features:
Typically characterized by decreased renal perfusion
Urine specific gravity > 1.015
Urine sodium < 20 mEq/L
Fractional excretion of sodium (FENa) < 1%
Response to fluid challenge (urine output increases)
Serum BUN:Creatinine ratio > 20:1.
Intrinsic Features:
Damage to the renal tubules, glomeruli, or interstitium
Urine specific gravity may be low or normal
Urine sodium > 40 mEq/L (in ATN)
FENa > 2% (in ATN)
Urine may contain cellular casts (e.g., RBC casts in glomerulonephritis, WBC casts in AIN)
Poor or no response to fluid challenge
BUN:Creatinine ratio typically < 10:1.
Fluid Challenges:
Indicated when hypovolemia is suspected as a cause of AKI
Gradual intravenous infusion of isotonic crystalloids (e.g., Normal Saline or Lactated Ringer's)
Monitor urine output, heart rate, blood pressure, and signs of fluid overload
A brisk diuresis in response to fluid administration strongly suggests prerenal AKI
Hesitation in fluid administration is crucial if signs of fluid overload are present.
Management
Initial Management:
Address the underlying cause
Restore adequate renal perfusion
Fluid resuscitation if hypovolemic, cautiously if at risk of overload
Discontinue nephrotoxic agents
Correct electrolyte abnormalities (hyperkalemia is an emergency).
Fluid Management Strategy:
The cornerstone of AKI management in children is judicious fluid management
If prerenal, administer isotonic fluids (e.g., Normal Saline, Lactated Ringer's) at 10-20 mL/kg per bolus, repeated as needed, while closely monitoring for fluid overload
If intrinsic AKI with fluid overload, fluid restriction and diuretics (e.g., furosemide) may be considered
Daily weights, intake/output charting, and frequent clinical assessment are essential.
Medical Management:
Correction of hyperkalemia: calcium gluconate, insulin/dextrose, sodium polystyrene sulfonate, sodium bicarbonate, dialysis
Management of metabolic acidosis: sodium bicarbonate
Nutritional support: adequate caloric intake, protein restriction if severe azotemia
Management of hypertension
Treatment of underlying intrinsic causes: immunosuppressants for glomerulonephritis/vasculitis, removal of offending agent for AIN.
Renal Replacement Therapy:
Indications include refractory hyperkalemia, severe metabolic acidosis, fluid overload refractory to diuretics, uremic symptoms (encephalopathy, pericarditis), and severe azotemia
Modalities include hemodialysis, peritoneal dialysis, and continuous renal replacement therapy (CRRT), with CRRT often preferred in hemodynamically unstable children.
Supportive Care:
Close monitoring of vital signs, urine output, fluid balance, electrolytes, and renal function
Respiratory support if pulmonary edema develops
Seizure precautions if encephalopathy is present
Prompt treatment of infections.
Complications
Early Complications:
Hyperkalemia
Metabolic acidosis
Fluid overload (pulmonary edema, heart failure)
Hyponatremia
Uremic encephalopathy
Uremic pericarditis
Hypertension.
Late Complications:
Progression to chronic kidney disease (CKD)
End-stage renal disease (ESRD)
Growth failure
Bone mineral disorder
Cardiovascular complications.
Prevention Strategies:
Maintain adequate hydration
Avoid nephrotoxic drugs where possible, or monitor renal function closely if used
Promptly treat underlying conditions leading to AKI
Judicious use of contrast agents
Early recognition and management of sepsis.
Prognosis
Factors Affecting Prognosis:
Severity of AKI (KDIGO stage)
Underlying cause of AKI (sepsis, HUS vs
nephrotoxic exposure)
Presence of multi-organ dysfunction syndrome (MODS)
Age at onset (neonates and younger children may have poorer outcomes)
Degree of renal recovery.
Outcomes:
Approximately 50-70% of children with AKI experience full recovery of renal function
However, a significant proportion (10-30%) may develop CKD
Mortality rates vary widely, from <10% for mild AKI to >50% for severe AKI associated with MODS
Early and appropriate fluid management significantly impacts outcomes.
Follow Up:
Children who have experienced AKI require long-term follow-up to monitor renal function (serum creatinine, eGFR, urinalysis)
Screening for hypertension and proteinuria is essential
Regular assessment of growth and development is also critical, especially if CKD develops.
Key Points
Exam Focus:
Distinguishing prerenal from intrinsic AKI using FENa, urine sodium, urine specific gravity, and response to fluid challenges
KDIGO criteria for AKI staging
Management of hyperkalemia and fluid overload in pediatric AKI
Indications for RRT in children.
Clinical Pearls:
Always check baseline renal function before administering potentially nephrotoxic agents
A good urine output response to fluid bolus is a strong indicator of prerenal AKI
Fluid management in pediatric AKI is a delicate balance
aggressive resuscitation can be dangerous in intrinsic AKI or in children with pre-existing cardiac or renal compromise.
Common Mistakes:
Over-resuscitation leading to fluid overload in intrinsic AKI
Delayed recognition of AKI in non-critically ill children
Inadequate monitoring of fluid balance and electrolytes
Misinterpretation of FENa in the context of diuretic use or dehydration
Failure to consider postrenal causes of AKI.