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For further information, see CMDT Part 22-06: Acute Tubular Necrosis

Key Features

Essentials of Diagnosis

  • Acute kidney injury

  • Ischemia or toxic insult or underlying sepsis

  • Pigmented granular casts and renal tubular epithelial cells in urine sediment are pathognomonic but not always present

General Considerations

  • Acute kidney injury as a result of tubular damage

  • Accounts for approximately 85% of intrinsic acute kidney injury

  • Two major causes are ischemia and nephrotoxin exposure

  • Renal tubular damage can be caused by low effective arterial blood flow to the kidneys in the setting of prolonged hypotension or hypoxemia, such as volume depletion or shock

  • Underlying sepsis is an independent risk factor for acute tubular necrosis, even in the absence of hemodynamic compromise

  • Prolonged periods of renal hypoperfusion can occur with major surgical procedures, which are exacerbated by vasodilating anesthetic agents

  • Exogenous nephrotoxins more commonly cause damage than endogenous nephrotoxins

Exogenous nephrotoxins

  • Aminoglycosides

  • Vancomycin, intravenous acyclovir, several cephalosporins

  • Radiographic contrast media

  • Antineoplastics, such as cisplatin and organic solvents (eg, etoposides, paclitaxel), and heavy metals (mercury, cadmium, and arsenic)

Endogenous nephrotoxins

  • Myoglobinuria as a consequence of rhabdomyolysis

  • Hemoglobinuria as a consequence of massive intravascular hemolysis

  • Hyperuricemia

  • Bence Jones proteinuria, paraproteins

Clinical Findings

Symptoms and Signs

Differential Diagnosis

  • Prerenal azotemia (eg, dehydration)

  • Postrenal azotemia (eg, benign prostatic hyperplasia)

  • Renal causes of acute kidney injury

    • Acute glomerulonephritis: immune complex (eg, IgA nephropathy), pauci-immune (eg, granulomatosis with polyangiitis), antiglomerular basement membrane disease

    • Acute interstitial nephritis: drugs (eg, β-lactams), infections (eg, Streptococcus), immune (eg, systemic lupus erythematosus)


  • BUN:creatinine ratio < 20:1

  • Hyperkalemia and hyperphosphatemia are commonly present

  • Urine microscopy may show evidence of acute tubular damage

  • Kidney biopsy is sometimes helpful in cases of diagnostic uncertainty

  • Fractional excretion of sodium or FENa = clearance of Na+/GFR = clearance of Na+/creatinine clearance

  • FENa = (urineNa/serumNa)/(urineCr/serumCr) × 100%

  • FENa is high (> 1%) in acute tubular necrosis



  • Stop offending agent and correct ischemia

  • Furosemide

    • Intravenous use can minimize disabling side effects of supranormal dosing

    • Starting dose of 0.1–0.3 mg/kg/h is appropriate

      • Increase to a maximum of 0.5–1 mg/kg/h

      • A bolus of 1–1.5 mg/kg should be administered with each dose escalation

  • Thiazide diuretics can be used to augment urinary output; reasonable choices include

    • Metolazone: 2.5–5 mg orally every 12–24 hours

      • Less expensive than intravenous chlorothiazide

      • Reasonable bioavailability

    • Chlorothiazide at doses of 250–500 mg intravenously every 8–12 hours

  • Phosphate-binding agents

    • Aluminum hydroxide, 500 mg orally with meals

    • Calcium carbonate, 500–1500 mg ...

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