Acute Kidney Injury


  • Characterized by elevated serum creatinine, blood urea nitrogen, electrolyte abnormalities, metabolic disturbances, acidosis, and difficulties with fluid management. (1)
  • Classically defined as an acute decrease in glomerular filtration rate which is followed by increase in serum creatinine. This has limitations as rise in serum creatinine may not occur for 48 hours following the injury.
  • RIFLE and Acute Kidney Injury Network (AKIN) criteria are the most commonly used criteria for diagnosing and grading kidney injury.



  • AKI occurs in 3.9/1000 pediatric hospitalizations. (3)
  • In the US at tertiary care centers, the most common cause of AKI in hospitalized children include sepsis, nephrotoxins, congenital heart disease, and renal ischemia. (4) In critically sick children, often one aspect of multiorgan failure.
  • In developing countries, the most prevalent causes are acute tubular necrosis secondary to dehydration with gastroenteritis or sepsis, or primary renal diseases such as hemolytic uremic syndrome or post streptococcal glomerulonephritis. (5)



  • Patients may or may not present with oliguria.
  • History provides important clues as to the etiology of AKI.
    • Vomiting, diarrhea, poor PO intake, bleeding, edema, sepsis, heart disease all increase likelihood of pre-renal cause.
    • Recent viral illness or sore throat (post-streptococcal glomerulonephritis); joint swelling and rashes (systemic diseases such as SLE); hematuria (glomerulonephritis); or medication exposures may all suggest intra-renal causes.
    • History of enlarged bladder or hydronephrosis on fetal ultrasound or oligohydramnios may be suggestive of a post-renal or obstructive etiology.



  • As with adult AKI, the overall approach involves determining etiology to be pre-renal, intra-renal, or post-renal.
  • Initial lab work to differentiate between these etiologies involves:
    • Basic metabolic panel including serum creatinine and blood urea nitrogen
    • Urinalysis
    • Urine electrolytes including urine Na, urine urea, and urine urea
    • Renal ultrasound study



  • Urine and blood studies should be able to differentiate between pre-renal and intrinisic, or intra-renal, AKI and drive further evaluation.


  • Once a pre-renal cause is suggested, history, physical, and preliminary labs will drive further workup of specific pre-renal etiology
    • Reduced blood volume
      • GI losses
      • Renal losses (DI, diuretics)
      • Hemorrhage
      • Increased insensible losses (burn patients)
    • Blood volume redistribution
      • Decreased oncoctic pressure
        • Cirrhosis
        • Nephrotic syndrome
        • Malnutrition
      • Increased vacular leak
        • Sepsis
    • Systemic vasodilation
      • Sepsis
      • Anaphylaxis
    • Reduced flow to kidneys
      • Heart disease
      • Renal artery stenosis



  • Urinalysis findings such as muddy brown granular casts (acute tubular necrosis); red blood cells casts, proteinuria, or hematuria (glomerulonephritis); or absence of red cell casts in presence of positive urine dipstick for blood (hemoglobinuria or myoglobinuria) may be suggestive of specific intra-renal causes.
    • Glomerulonephritis: Diagnosis of post-infectious glomerulonephritis in correct clinical setting may not require biopsy. Renal biopsy is necessary to differentiate between other etiologies.
      • Etiologies that REDUCE complement:
        • Post streptococcal glomerulonephritis: Low C3 and normal C4. Diagnosis can be supported with anti-streptolysis O antibody or anti-DNAse B antibody titers.
        • Systemic lupus erythematous (SLE): Low C3 and low C4 and presence of suggestive symptoms such as rash or arthralgias. Warrants testing ANA and anti-dsDNA Abs.
        • Membranoproliferative glomerulonephritis (MPGN): Low C3 and low or normal C4. Less common in children and diagnosed on renal biopsy.


  • Etiologies with NORMAL complement levels:
    • IgA nephropathy: Normal complement levels; may present during or 2-3 days after viral upper respiratory infection.
    • Goodpasture syndrome: Hemoptysis and anti-glomerular basement membrane antibody.
    • Granulomatosis with polyangiitis: Upper airway and lung involvement with cANCA.
    • Microscopic polyangiitis: Lung involvement and pANCA.
    • Eosinophilicgranulomatosis: Associated with sinusitis, asthma, peripheral eosinophilia, and pANCA.


  • Acute tubular necrosis (ATN): Muddy brown granular casts on urinalysis.
    • Transformation of pre-renal AKI.
    • Drugs: Includes aminoglycosides, amphotericin, chemotherapy agents, and IV contrast.
    • Toxin mediated: Due to myoglobinuria, hemoglobinuria and heavy metal toxicity.


  • Acute interstitial nephritis: Fever, eosinophilia, and rash make up the classic triad, but the complete triad only occurs in 15% of cases. UA may demonstrate eosinophils, WBC casts, or RBC casts.
    • Drug induced: Antibiotics, proton pump inhibitors.
    • Systemic disease:Sarcoidosis, Sjogren disease, renal transplant rejection.


  • Hemolytic uremic syndrome: Diagnosed by microangiopathic hemolytic anemia with schistocytes on the peripheral smear. Classically occurs with Shiga toxin producing E. coli 0:157-H7 or with non-intestinal infections.



May demonstrate hydronephrosis on renal US. Can cause AKI if occurs in solitary kidney, occurs in ureters bilaterally, or if there is a urethral obstruction. Management of all etiologies involves promptly relieving the obstruction.

  • Posterior urethral valves
  • Bilateral uretropelvic junction obstruction
  • Bilateral kidney stones
  • Tumor obstructing both ureters or the urethra



  1. Selewski DT, Symons JM. Acute kidney injury.Pediatr Rev Am AcadPediatr. 2014 Jan;35(1):30–41.
  2. Andreoli SP. Acute kidney injury in children. PediatrNephrolBerl Ger. 2009 Feb;24(2):253–63.
  3. Sutherland SM, Ji J, Sheikhi FH, Widen E, Tian L, Alexander SR, et al. AKI in hospitalized children: epidemiology and clinical associations in a national cohort. Clin J Am SocNephrolCjasn. 2013 Oct;8(10):1661–9.
  4. Hui-Stickle S, Brewer ED, Goldstein SL. Pediatric ARF epidemiology at a tertiary care center from 1999 to 2001. Am J Kidney Dis Off J Natl Kidney Found. 2005 Jan;45(1):96–101.
  5. Van Biljon G. Causes, prognostic factors and treatment results of acute renal failure in children treated in a tertiary hospital in South Africa. J Trop Pediatr. 2008 Aug;54(4):233–7.