11.1 Pediatric Acute Kidney Injury: KDIGO Staging, Prerenal vs. Intrinsic vs. Postrenal Differentiation
Key Takeaways
Apply the higher of creatinine and urine output stages in the issued KDIGO pediatric framework. Use neonatal criteria and the lowest previous neonatal creatinine in the NICU.
The bedside CKiD estimate uses height and standardized creatinine. During evolving AKI, interpret it alongside serial labs and urine output, and use drug-specific guidance and levels for dosing.
Calculate fractional excretion from paired samples with matching units. Diuretics, sepsis, CKD and developmental differences limit interpretation. Neither fractional index is a stand-alone diagnosis.
Use urine sediment, clinical volume status and exposure history to distinguish hypoperfusion, tubular injury and glomerular disease. Anemia with schistocytes, thrombocytopenia and AKI after bloody diarrhea suggests STEC-HUS.
Drain a suspected lower urinary tract obstruction with urology support. Ultrasound raises suspicion for posterior urethral valves and voiding cystourethrography helps confirm the diagnosis.
Pediatric acute kidney injury
Recognize and stage AKI
Use the issued 2012 KDIGO criteria for the pediatric staging below. The 2026 AKI/AKD public-review draft proposes separate creatinine, urine output and damage-biomarker categories. It has not replaced the issued staging. Older studies may use pRIFLE or AKIN. Check the definition before comparing results. Issued KDIGO guideline · KDIGO update status
Identify AKI with a creatinine rise of at least 0.3 mg/dL (about 26.5 µmol/L) within 48 hours, a rise to at least 1.5 times baseline known or presumed to have occurred within seven days, or urine output below 0.5 mL/kg/h for six hours. Use the higher stage when creatinine and urine output differ.
| Stage | Creatinine or other filtration criterion | Urine output criterion |
|---|---|---|
| 1 | 1.5 to 1.9 times baseline or rise of at least 0.3 mg/dL | Below 0.5 mL/kg/h for 6–12 hours, with the higher stage applying at 12 hours |
| 2 | 2.0 to 2.9 times baseline | Below 0.5 mL/kg/h for at least 12 hours |
| 3 | At least three times baseline, a rise to at least 4.0 mg/dL, initiation of kidney replacement therapy (KRT), or in patients younger than 18 years a decrease in estimated GFR to below 35 mL/min/1.73 m² | Below 0.3 mL/kg/h for at least 24 hours or anuria for at least 12 hours |
Track both measurements. Oliguria can identify injury when creatinine has not yet risen, and AKI can occur with preserved output. Check collection duration, weight used to index the measurement, and catheter patency when relevant. Use a stable pre-illness creatinine if available. If it is missing, document how the baseline was estimated and revisit staging as trends emerge. Assuming a GFR of 120 mL/min/1.73 m² may misclassify patients, particularly young infants or those with CKD. Positive balance can dilute measured creatinine. Research adjustments use measured creatinine × (1 + cumulative balance/estimated total body water), with both volumes in liters. The estimate depends on reliable balance and body-water assumptions and does not replace KDIGO staging. AWARE cohort · PODIUM baseline assessment · Creatinine dilution study
Apply neonatal criteria in the NICU
Early neonatal creatinine reflects maternal creatinine and then changes with postnatal age and gestation. The neonatal modification compares with the lowest previous creatinine. Stage 1 uses a rise of at least 0.3 mg/dL within 48 hours or 1.5–1.9 times the reference within seven days. Stage 2 uses a rise to 2.0–2.9 times reference. Stage 3 uses at least three times reference, creatinine at least 2.5 mg/dL or KRT. Neonatal urine-output implementations vary. The AWAKEN cohort used 24-hour increments on postnatal days 2–7 and an AKI detection threshold around 1 mL/kg/h. Other neonatal protocols use time-based thresholds closer to the pediatric table. Use the specified NICU method, confirm output reliability and interpret the creatinine trajectory even when a single criterion misses concern. NIDDK neonatal workshop · AWAKEN cohort · Example neonatal guideline
Estimate filtration and review medication exposure
The 2009 bedside CKiD Schwartz equation uses standardized creatinine. It was derived in children with CKD aged 1–16 years and provides a quick estimate.
The result is indexed to 1.73 m². In a child 110 cm tall with stable creatinine of 0.60 mg/dL, the estimate is 75.7 mL/min/1.73 m². At a body surface area of 0.80 m², the nonindexed estimate is about 35 mL/min (75.7 × 0.80/1.73). Use the units and method required by the drug-specific reference. NIDDK prefers CKiD U25 for routine estimates in ages 1–25. During evolving AKI, creatinine lags changes in filtration, and a steady-state estimate can overstate filtration during deterioration or understate it during recovery. Cystatin C is a filtration marker. NGAL is studied as a marker of tubular injury. Interpret adjunct biomarkers in their clinical setting. Original Schwartz cohort · CKiD U25 study · NIDDK equations · Pediatric cystatin C study · PODIUM consensus
Reassess nephrotoxins and renally cleared medicines with pharmacy. Use serial creatinine, urine output, drug concentrations when available and the current KRT prescription. A single eGFR during a creatinine rise cannot determine the maintenance dose. Check aminoglycoside exposure with protocol-directed levels. For serious MRSA infection, the U.S. vancomycin consensus favors AUC-guided monitoring. The 400–600 mg·h/L target assumes an MIC of 1 mg/L. Vancomycin plus piperacillin/tazobactam has been associated with creatinine-defined AKI in pediatric cohorts. The combination and a creatinine rise alone cannot establish the mechanism. NSAIDs can reduce prostaglandin-dependent renal perfusion during volume depletion and can cause interstitial nephritis. With amphotericin B deoxycholate, monitor kidney function, potassium and magnesium. Assess risk and alternatives for contrast imaging while accounting for the urgency of the diagnostic question. KDIGO medication stewardship · Vancomycin consensus · Pediatric antibiotic cohort · Gentamicin label · Pediatric NSAID cohort · Amphotericin B label · Pediatric contrast cohort
Integrate perfusion, urine findings and imaging
- Hemodynamic (prerenal): Gastrointestinal losses, shock or low effective circulating volume can reduce perfusion. Venous congestion can also impair kidney function. Use the examination, balance and response to treatment to decide whether fluids, vasoactive support or decongestion address the problem. Prolonged hypoperfusion can coexist with tubular injury.
- Intrinsic: Tubular epithelial cells and muddy brown granular casts support acute tubular injury. Dysmorphic erythrocytes, red cell casts, proteinuria, edema or hypertension suggest glomerular disease. Pyuria can occur with interstitial disease. Interpret sediment with the clinical findings.
- Postrenal: Check for retention, catheter obstruction or upper tract obstruction. Consider posterior urethral valves in an infant boy with poor stream, a distended bladder or bilateral hydroureteronephrosis. Bilateral upper tract obstruction and neurogenic bladder are other causes. Ultrasound can identify dilation and bladder distension, but early obstruction may have little dilation and the keyhole sign is not specific. Drain suspected lower tract obstruction promptly with appropriate urologic support. Avoid forcing a catheter against resistance. Urology can arrange alternative drainage, voiding cystourethrography for suspected valves and definitive treatment after stabilization. Monitor for postobstructive diuresis and electrolyte loss. KDIGO evaluation · Urine microscopy study · EAU pediatric obstruction guideline
Calculate fractional excretion when it can inform the differential
Use paired urine () and plasma () samples. Match units for each analyte across the two specimens. For urea, use urine urea nitrogen with plasma urea nitrogen (BUN), or use urea in both specimens.
A low sodium fraction, often below 1% in the classic oliguric setting without confounders, can support renal sodium conservation. Loop diuretics can raise it. Sepsis, CKD, developmental tubular immaturity, sodium intake and glomerular disease also limit its use. Neonatal values vary with gestational and postnatal age. A urea fraction below 35% has been studied as an adjunct, but later studies found limited performance and changes with loop diuresis. Specific gravity, osmolality and the BUN-to-creatinine ratio are context-dependent clues. Use the history, exam, sediment and response to treatment when deciding whether hypoperfusion, tubular injury or obstruction predominates. Original sodium study · Urea threshold study · Diagnostic comparison · Loop diuretic study
Worked example. After furosemide, an oliguric child with diarrheal fluid loss has urine and plasma sodium of 120 and 138 mEq/L, urine and plasma creatinine of 40 and 1.20 mg/dL and urine and plasma urea nitrogen of 430 and 52 mg/dL. Sodium fractional excretion is . Urea fractional excretion is . These discordant results do not establish a mechanism. Clinical hypovolemia supports careful restoration of perfusion with reassessment of output, creatinine and congestion.
Recognize glomerular and microvascular patterns
Poststreptococcal glomerulonephritis can follow pharyngitis or a skin infection. Look for hematuria, edema, hypertension and low C3 with evidence of recent group A streptococcal infection. Treat complications and eradicate residual group A streptococci as indicated. Consider lupus nephritis when systemic findings, proteinuria or active sediment suggest it. Complement and anti-dsDNA are supportive. Consult nephrology for evaluation and possible biopsy. CDC poststreptococcal guidance · ACR lupus nephritis guideline
After bloody diarrhea, microangiopathic hemolytic anemia with schistocytes, thrombocytopenia and AKI suggests Shiga toxin-producing E. coli HUS (STEC-HUS). Send stool testing for Shiga toxin or its genes and culture for O157. Avoid antimotility agents and antibiotics directed at O157, Shiga toxin 2-producing or toxin-genotype-unknown STEC. An independent infection indication requires separate assessment. Individualize fluids to perfusion and renal function. Early hydration during diarrhea differs from fluid management once oligoanuria or edema develops. Manage electrolytes, blood pressure and anemia, and use KRT for clinical indications. Avoid routine prophylactic platelet transfusion and individualize decisions for bleeding or procedures. If the clinical pattern is atypical, evaluate urgently with specialists for other thrombotic microangiopathies, including complement-mediated HUS and TTP. For complement-mediated HUS, C5 inhibition is specialist-directed and requires meningococcal precautions. Eculizumab has a U.S. indication for aHUS with a limitation for STEC-HUS. CDC STEC guidance · IDSA infectious diarrhea guideline · Pediatric hydration cohort · Pediatric procedural cohort · Eculizumab label
Treat life-threatening electrolyte, acid-base or fluid complications while involving nephrology. A stage alone does not mandate KRT. After AKI, arrange follow-up to reassess renal recovery and screen for persistent disease. KDIGO recommends reassessment at three months, with earlier review when recovery is incomplete or the clinical course warrants it. KDIGO evaluation and follow-up
A 14-month-old child weighing 10 kg and measuring 75 cm has septic shock. Urine output is 24 mL over eight hours, and serum creatinine rises from a known baseline of 0.30 mg/dL to 0.70 mg/dL within 24 hours. No KRT has started. Which pairing gives the issued KDIGO stage and the numeric bedside CKiD estimate, recognizing that creatinine is changing?
Stage 2, with a formula result of approximately 44 mL/min/1.73 m².
Stage 1, with a formula result of approximately 44 mL/min/1.73 m².
Stage 3, with a formula result of approximately 28 mL/min/1.73 m².
Stage 1, with a formula result of approximately 75 mL/min/1.73 m².
A 7-year-old with gastroenteritis, delayed capillary refill and dry mucous membranes remains oliguric three hours after receiving furosemide at another hospital. Paired urine and plasma sodium are 120 and 138 mEq/L. Urine and plasma creatinine are 40 and 1.20 mg/dL. Urine and plasma urea nitrogen are 430 and 52 mg/dL. Which interpretation best combines the calculated values and clinical findings?
FENa is about 2.61%, which establishes acute tubular injury and makes volume restoration inappropriate.
FENa is about 2.61% and FEUrea about 24.81%. Neither proves the cause after furosemide. The clinical volume depletion supports restoring perfusion and reassessing.
The differing values diagnose outflow obstruction and require suprapubic drainage.
FEUrea is about 49.6%, which establishes drug-induced interstitial nephritis.
A 3-year-old girl is admitted to the pediatric critical care unit with lethargy, extreme pallor, and oliguria. Five days ago, she developed severe abdominal cramping and bloody diarrhea after attending a petting zoo. Physical examination reveals petechiae on the trunk and periorbital edema. Laboratory investigations demonstrate: Hemoglobin , Platelet count , Serum Creatinine , Total Bilirubin , Lactate Dehydrogenase (LDH) , and peripheral blood smear displaying numerous schistocytes. Which diagnostic conclusion and therapeutic principle are most accurate?
The child has immune thrombocytopenic purpura (ITP) complicated by sepsis, requiring immediate high-dose intravenous immunoglobulin (IVIG) and systemic corticosteroids.
The child has acute post-streptococcal glomerulonephritis complicated by DIC, requiring broad-spectrum intravenous ampicillin and fresh frozen plasma transfusions.
Suspect STEC-HUS, send stool testing and manage perfusion, electrolytes and kidney complications. Avoid antimotility agents and empiric antibiotics directed at the suspected STEC.
The child has Henoch-Schönlein purpura (IgA vasculitis), requiring immediate therapeutic plasma exchange and oral aspirin therapy to prevent renal infarction.
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