Overview
Definition:
Acute Kidney Injury (AKI) in pediatrics is a sudden, rapid decline in kidney function, characterized by an increase in serum creatinine and/or a decrease in urine output
It is a syndrome with diverse causes and significant morbidity and mortality.
Epidemiology:
Incidence varies widely depending on the clinical setting, ranging from 1-10% in general pediatric hospital admissions and up to 60% in pediatric intensive care units (PICUs)
Premature infants, neonates with congenital anomalies, and critically ill children are at higher risk.
Clinical Significance:
AKI in children is associated with short-term complications such as fluid overload, electrolyte imbalances, and metabolic acidosis, and long-term sequelae including chronic kidney disease (CKD) and increased risk of cardiovascular events
Timely recognition and appropriate nephrology consultation are crucial for optimal outcomes.
Indications For Consultation
Oliguria Or Anuria:
Persistent decrease in urine output (oliguria < 1 mL/kg/hr in infants, < 0.5 mL/kg/hr in older children) or complete absence of urine (anuria) for >6-12 hours, especially in the absence of clear dehydration.
Rising Serum Creatinine:
A significant and unexplained increase in serum creatinine, exceeding baseline or expected age-related values
A 50% increase from baseline or reaching stage 2-3 AKI by KDIGO criteria warrants consideration.
Electrolyte And Acid Base Abnormalities:
Severe hyperkalemia (>6.5 mEq/L, especially if symptomatic), hyponatremia, hypernatremia, metabolic acidosis (bicarbonate < 17 mEq/L), or other significant electrolyte derangements not responsive to initial management.
Fluid Overload:
Signs of volume overload, such as pulmonary edema, peripheral edema, hypertension, or weight gain, particularly in the context of decreased urine output.
Suspected Intrinsic Renal Disease:
Clinical suspicion of primary kidney disease (glomerulonephritis, interstitial nephritis, hemolytic uremic syndrome) based on hematuria, proteinuria, edema, or systemic symptoms.
Medication Induced AKI:
Use of nephrotoxic agents (e.g., aminoglycosides, vancomycin, NSAIDs, contrast media) in a patient with deteriorating renal function.
Sepsis And Shock:
Development of AKI in the setting of sepsis or septic shock, as renal hypoperfusion is a common complication.
Pediatric Aki Workup
History Taking:
Detailed birth history (prematurity, congenital anomalies)
Recent illnesses (diarrhea, vomiting, fever, rash)
Medication history (nephrotoxic drugs, recent NSAID use)
Family history of kidney disease
Fluid intake and output
Symptoms of uremia (lethargy, poor feeding, vomiting).
Physical Examination:
General appearance (lethargy, distress)
Hydration status (mucous membranes, skin turgor)
Vital signs (BP, HR, RR, temperature)
Assess for edema (periorbital, peripheral)
Abdominal examination (palpable kidneys, ascites)
Auscultation of lungs for signs of fluid overload
Examine for rash or signs of systemic illness.
Laboratory Investigations:
Serum creatinine and BUN: baseline and serial monitoring
Electrolytes (Na, K, Cl, HCO3)
Complete blood count (CBC): assess for anemia, thrombocytopenia
Urinalysis: specific gravity, pH, protein, glucose, ketones, blood, WBCs, RBCs, casts (hyaline, granular, RBC, WBC, waxy)
Urine electrolytes (Na, K), fractional excretion of sodium (FeNa), fractional excretion of urea (FeUrea): to differentiate pre-renal from intrinsic AKI
Serum albumin and total protein: assess for nephrotic syndrome
Calcium, phosphate, uric acid
Blood gas analysis: assess for acidosis.
Imaging Studies:
Renal ultrasound: assess kidney size, echogenicity, corticomedullary differentiation, presence of hydronephrosis, and ruling out structural anomalies or obstruction
Doppler ultrasound may be used to assess renal blood flow
Other imaging may be indicated based on suspected etiology (e.g., abdominal CT for masses, MRI for congenital anomalies).
Specialized Tests:
If specific causes are suspected: autoimmune markers (ANA, anti-dsDNA, ANCA, anti-GBM), complement levels (C3, C4), viral serologies (e.g., HUS-associated pathogens, hepatitis B/C, HIV), hemoglobin electrophoresis (sickle cell), bone marrow biopsy (malignancy), renal biopsy (for definitive diagnosis of intrinsic renal disease when indicated).
Differential Diagnosis
Prerenal Aki:
Most common cause
due to decreased renal perfusion (hypovolemia, dehydration, shock, sepsis, cardiac failure)
Typically responds to fluid resuscitation.
Intrinsic Renal Aki:
Damage to the glomeruli (glomerulonephritis), tubules (acute tubular necrosis - ATN from ischemia or toxins), interstitium (acute interstitial nephritis - AIN from drugs or infections), or vasculature.
Postrenal Aki:
Obstruction of the urinary tract (e.g., posterior urethral valves, stones, tumors, neurogenic bladder)
Often suggested by bladder distension or bilateral hydronephrosis on ultrasound.
Neonatal Specific Causes:
Congenital anomalies of the kidney and urinary tract (CAKUT), perinatal asphyxia, congenital heart disease, sepsis, hemolytic uremic syndrome (HUS).
Management Principles
Identify And Treat Underlying Cause:
Crucial first step
address dehydration, sepsis, obstruction, or specific intrinsic renal disease.
Supportive Care:
Fluid and electrolyte management: careful fluid balance, correction of electrolyte abnormalities (especially hyperkalemia), manage acidosis
Nutritional support: adequate caloric intake, protein restriction if uremic symptoms are severe.
Monitoring:
Close monitoring of urine output, vital signs, daily weights, serum creatinine, electrolytes, and acid-base status.
Renal Replacement Therapy:
Indicated for severe refractory hyperkalemia, fluid overload refractory to diuretics, severe metabolic acidosis, uremic complications (pericarditis, encephalopathy), or failure to thrive in chronic settings
Modalities include hemodialysis, peritoneal dialysis, and continuous renal replacement therapy (CRRT).
Key Points
Exam Focus:
KDIGO criteria for AKI staging, differentiation between pre-renal, intrinsic, and post-renal AKI using clinical data and urine indices (FeNa, FeUrea), indications for renal biopsy, common nephrotoxic agents in pediatrics.
Clinical Pearls:
Always check baseline creatinine if available
Ultrasound is key to rule out obstruction
Monitor urine output religiously
Early nephrology consultation improves outcomes significantly
Suspect HUS in children with bloody diarrhea and AKI.
Common Mistakes:
Delaying consultation, aggressive fluid resuscitation in cases of intrinsic AKI with fluid overload, misinterpreting FeNa in diuretic-treated patients, failure to consider rare causes of AKI.