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Acute tubular necrosis
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Acute tubular necrosis

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Contributors: Casey Silver MD, Catherine Moore MD, Abhijeet Waghray MD
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Synopsis

Acute tubular necrosis (ATN) is renal tubule epithelial cell destruction resulting in acute kidney injury. It is most often caused by nephrotoxins and renal ischemia (impaired oxygenation of kidneys) and is characterized by elevated creatine and blood urea nitrogen (BUN). Other common signs and symptoms include nausea, vomiting, edema, oliguria, anuria, dehydration, malaise, and decreased consciousness (delirium, drowsiness, seizures, coma). Risk factors include prolonged hypotension (more than 30 minutes), major surgery, reaction to blood transfusion, traumatic damage to muscles, radiation contrast dye, nephrotoxic drugs, and diabetic nephropathy.

Management first targets rehydration and cessation of any causative agent. Prognosis is typically favorable due to the kidney's mechanism for replacement of tubular cells in approximately 1-3 weeks. In cases of severe kidney injury and complications (for example, extremely elevated serum potassium), dialysis may be necessary for supportive care.

Codes

ICD10CM:
N17.0 – Acute kidney failure with tubular necrosis

SNOMEDCT:
35455006 – Acute tubular necrosis

Look For

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Diagnostic Pearls

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Differential Diagnosis & Pitfalls

  • Prerenal azotemia – Look for an elevated BUN:creatinine ratio > 20, bland urine sediment, and resolution of acute kidney injury with fluid resuscitation.
  • Acute interstitial nephritis – Look for onset of kidney injury 4-7 days after exposure to a new agent, particularly penicillin, cephalosporins, or long-term proton pump inhibitor use. Urinalysis may have WBCs and eosinophils.
  • Obstructive uropathy – Renal ultrasound with bladder outlet obstruction or bilateral hydronephrosis. Note that hydronephrosis may not be evident in chronic obstruction.
  • Nephritic syndrome (see glomerulonephritis) – Look for hypertension, microscopic and/or macroscopic hematuria, proteinuria 1-2 grams.
  • Nephrotic syndrome – Look for proteinuria > 3 grams per day, edema, hyperlipidemia.
  • Renal atheroembolic disease – Look for onset of acute kidney injury 2-4 weeks after cardiac catheterization, endovascular instrumentation, or cardioversion. Urine eosinophils may be present and serum complements may be low.
  • Contrast-induced nephropathy – Look for iodinated contrast exposure 1-3 days prior to onset of acute kidney injury.

Best Tests

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Management Pearls

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Therapy

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Drug Reaction Data

Below is a list of drugs with literature evidence indicating an adverse association with this diagnosis. The list is continually updated through ongoing research and new medication approvals. Click on Citations to sort by number of citations or click on Medication to sort the medications alphabetically.

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References

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Last Reviewed: 02/27/2019
Last Updated: 03/06/2019
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Acute tubular necrosis
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Acute tubular necrosis : Nausea, Creatinine elevated, Dehydration, Delirium, Edema, Oliguria, Drowsiness, BUN elevated
Copyright © 2019 VisualDx®. All rights reserved.