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Acute Tubular Necrosis

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Topic updated on 07/28/17 9:12pm

Snapshot
  • A 44-year-old woman with no significant past medical history presents to the emergency room with toxic ingestion of ethylene glycol. She answers appropriately but requires frequent redirection. Physical exam reveals bilateral flank pain. Her serum creatinine, previously normal, is now increased at 3 mg/dL. Urinalysis with sediment analysis reveals granular casts and significant hematuria. Fomepizole is given.
Introduction
  • Clinical definition
    • intrinsic acute kidney injury (AKI) to the kidneys from ischemia and/or toxins
  • Epidemiology
    • incidence
      • US incidence
        • 38% of hospitalized patients with AKI
        • 76% of ICU patients with AKI
        • most common cause of AKI in hospitalized patients
    • risk factors
      • pre-existing kidney disease
      • exposure to nephrotoxin
  • Etiology
    • ischemia
      • hypovolemia
      • sepsis
    • nephrotoxic injury
      • drugs
        • aminoglycosides
        • cisplatin
        • contrast for imaging
        • heavy metals
        • calcium oxalate crystals from ethylene glycol
        • urate crystals from tumor lysis syndrome
        • myoglobinuria (from crush injury)
        • hemoglobinuria
  • Pathogenesis
    • decreased renal blood flow results in ischemia
      • this results in death of renal tubular cells
      • in particular proximal convoluted tubule and thick ascending limb are affected
    • nephrotoxicity leads to damage in renal tubules
      • in particular proximal convoluted tubule is affected
  • Prognosis
    • 3 stages of disease
      • inciting event
      • oliguric (maintenance) phase
        • 1-3 week duration
        • risk of electrolyte abnormalities
          • hyperkalemia
          • metabolic acidosis
          • uremia
      • polyuric (recovery) phase
        • BUN and creatinine return back to normal
        • re-epithelialization of tubules
        • risk of hypokalemia
    • prognostic variable
      • negative
        • pre-existing renal disease
        • requiring dialysis
    • survival with treatment
      • over half of patients fully recover
      • 5-11% require long-term dialysis
        • 50% mortality in those needing dialysis
 
Classification of Acute Renal Failures
Urinary Indices Pre-Renal Intrinsic Renal Post-Renal
Urine osmolality (mOsm/kg)
  • > 500
  • < 350
  • < 350
Urine Na (mEq/L)
  • < 20
  • > 40
  • > 40
Serum BUN:creatinine
  • > 20
  • < 15
  • < 15
FENa (%)
(fractional excretion of Na)
  • < 1%
  • > 2%
  • > 2%
FEUrea (%) (fractional excretion of urea)
  • < 35%
  • 50-65 %
-
 
 
Presentation
  • Symptoms
    • primary symptoms
      • signs of acute renal failure
        • vomit
        • diarrhea
        • blood loss
        • shock
        • altered mental status
      • oliguria or polyuria
  • Physical exam
    • signs of volume overload
      • edema
      • jugular venous distention
      • decreased breath sounds in pulmonary edema
Imaging
  • Ultrasound
    • indications
      • if an obstruction needs to be ruled out (post-renal cause of AKI)
      • best initial test
    • findings
      • can see hydronephrosis or stones
Studies
  • Labs
    • serum potassium
      • hyperkalemia during oliguric phase
      • hypokalemia during polyuric phase
    • anion gap metabolic acidosis
    • ↑ BUN
    • ↑ creatinine
      • BUN:creatinine ratio < 15
  • Urinalysis with microscopy and sediment analysis
    • granular casts
      • “muddy brown” from sloughing of tubular cells
  • Diagnostic criteria
    • diagnosis of AKI
      • ↑ serum creatinine of 0.3 mg/dL within 48 hours
      • ↑ serum creatinine of 1.5 fold from baseline
    • signs of acute tubular necrosis
      • urine osmolality < 350-500 mOsm/kg
      • muddy brown casts on urine sediment analysis
      • fractional excretion of sodium > 2%
      • decreased BUN:creatinine ratio
Differential
  • Prerenal azotemia
    • BUN:creatinine ratio > 20
  • Post-renal azotemia
    • source of obstruction found on imaging
      • e.g., stones or congenital abnormality
Treatment
  • Conservative
    • supportive care
      • remove nephrotoxic agent
      • intravenous hydration
      • close electrolyte and fluid level monitoring
      • anitbiotics if infection is suspected
      • indications
        • for all with suspected acute tubular necrosis
  • Medical
    • renal replacement therapy (dialysis)
      • indications
        • signs of fluid overload
        • toxic electrolyte levels
        • acid-base imbalance
        • uremia
Complications
  • Electrolyte abnormalities
    • hypokalemia
    • hyperkalemia
  • Volume overload
  • Uremia


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