Acute Kidney Injury (AKI)


  • Increase in creatinine by 1.5 x baseline OR
  • Increase in creatinine by 0.3 mg/dL from baseline OR
  • Urine output < 0.5 mL/kg/hour for 12+ hours



  • Etiologies
    • Cardiorenal Syndrome
    • Hepatorenal Syndrome
    • Hypovolemia (Dehydration, Diarrhea, Diuresis, Vomiting)
    • Arterial insufficiency (Renal Artery Stenosis, Fibromuscular Dysplasia)
  • Work-Up
    • History and Physical Exam: Determine volume status
    • Urinalysis: Increased specific gravity and hyaline casts
    • FENa (Fractional Excretion of Sodium): <1%
    • FEUrea (Fractional Excretion of Urea) <35% (if patient is on diuretics)
      • Tubules are still working, trying to absorb as much solute as possible, so less of a fraction of solute is excreted through the urine
    • BUN/Cr ratio > 20
      • Since the tubules are still working, urea may still be reabsorbed and a small amount of creatinine may still be secreted
  • Management
    • Cardiorenal Syndrome: Diuresis (to move leftward on the Frank-Starling curve)
    • Hepatorenal Syndrome: Octreotide, midodrine, norepinephrine, and eventually a liver transplant is usually necessary
    • Hypovolemia (Dehydration, Diarrhea, Diuresis, Vomiting): IV fluid resuscitation
    • Arterial insufficiency (Renal Artery Stenosis, Fibromuscular Dysplasia): Vascular Surgery intervention may be necessary


  • BUN/Creatinine <20
    • When the tubules are injured, they are unable to reabsorb urea, so a higher percentage is excreted
  • FENa >1% and FEUrea >35%
    • When the renal tubules are injured, they are unable to reabsorb solute, so a larger fraction of solute is excreted through the urine
  • Etiologies
    • Nephrotic Syndrome
      • 3.5+ g/day of proteinuria (or random urine protein:urine creatinine ratio of 3.5+), hypoalbuminemia, edema
      • May require renal biopsy
    • Nephritic Syndrome
      • UA with large hematuria, hypertension
      • May require renal biopsy
    • Acute Interstitial Nephritis
      • Fever, eosinophilia or WBC casts, rash
    • Acute Tubular Necrosis
      • May be secondary to ischemia or toxins (such as myoglobin, aminoglycosides, cisplatin, iodinated contrast, etc)
      • “Muddy brown” AKA “granular” casts AKA amorphous crystals


  • Work-Up
    • History of incontinence, prostate disease, kidney stones, trauma
    • Post-void residual for urinary retention
    • Ultrasound kidneys and bladder for hydronephrosis
    • Consider CT scan for renal stones or neoplasm
  • Etiologies
    • BPH, prostate cancer
    • Cervical cancer (less common)
      • History, CT pelvis can diagnose
    • Nephrolithiasis (typically would need to be bilateral to cause AKI)
      • CT scan (without contrast) is most sensitive, may be able to use ultrasound or abdominopelvic radiography to diagnose
    • Neuropathy
      • Spinal cord injury
      • Diabetes Mellitus
    • Medications
      • Anticholinergics are generally the biggest offender
  • Management
    • Foley catheter may be necessary (except for in the case of nephrolithiasis), but definitive treatment is to treat the underlying cause

Initial Workup:

  • History and physical (volume status, history of heart failure, cirrhosis, spinal trauma, etc)
  • Urinalysis + microscopy
  • Basic Metabolic Panel
  • Urine creatinine, urine sodium, urine urea nitrogen
  • Bladder scan
  • Consider retroperitoneal ultrasound to assess for hydronephrosis


  1. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012; 2:8.

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