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    Subjects/Pathology/Acute Tubular Necrosis
    Acute Tubular Necrosis
    hard
    microscope Pathology

    A 42-year-old woman with severe sepsis from urosepsis is admitted to the ICU. She has been oliguric (urine output 0.3 mL/kg/hr) for 18 hours despite aggressive fluid resuscitation. Serum creatinine has risen from 1.2 to 4.1 mg/dL. Urinalysis shows muddy brown casts, and fractional excretion of sodium (FENa) is 3.2%. Serum potassium is 6.8 mEq/L. What is the most appropriate next step in management?

    A. Start renal replacement therapy (RRT) and manage hyperkalaemia with calcium gluconate, insulin-dextrose, and sodium bicarbonate
    B. Continue aggressive fluid resuscitation with normal saline and reassess in 24 hours
    C. Perform urgent renal ultrasound to rule out obstructive uropathy
    D. Initiate loop diuretics (furosemide 240 mg IV) to promote urine output

    Explanation

    Clinical Diagnosis: ATN in Sepsis-Induced AKI

    Key Point
    This patient has established acute tubular necrosis (ATN) with sepsis-induced acute kidney injury (AKI). The muddy brown casts, elevated FENa (>2%), and oliguria despite fluid resuscitation confirm intrinsic renal failure, not prerenal azotaemia.

    Diagnostic Criteria for ATN

    Table
    FeatureATNPrerenalPostrenal
    FENa>2%<1%Variable
    Urine castsMuddy brown, granularHyalineNone
    Response to fluidsPoorRapid improvementDepends on obstruction
    Urine osmolality<400 mOsm/kg>500 mOsm/kgVariable

    Management Algorithm for ATN with Hyperkalaemia and Oliguria

    Loading diagram...

    Why RRT is Indicated Now

    High-YieldNEET PG
    RRT is indicated in ATN when:
    1. 1.
      Oliguria persists despite fluid resuscitation (>18 hours)
    2. 2.
      Serum creatinine rises rapidly (>2-fold increase)
    3. 3.
      Life-threatening hyperkalaemia (K+ >6.5 mEq/L with ECG changes)
    4. 4.
      Severe metabolic acidosis (pH <7.15)
    5. 5.
      Pulmonary oedema (fluid overload unresponsive to diuretics)

    This patient meets criteria 1, 2, and 3.

    Immediate Management of Hyperkalaemia

    Clinical Pearl
    Hyperkalaemia in ATN is an emergency because the kidneys cannot excrete potassium. Immediate interventions shift K+ intracellularly and stabilize the myocardium:
    1. 1.
      Calcium gluconate 10% (10 mL IV over 2–5 min) — stabilizes cardiac membrane; does NOT lower K+ but prevents dysrhythmia
    2. 2.
      Insulin 10 units IV + dextrose 25 g IV — shifts K+ into cells; onset 10–20 min; duration 4–6 hours
    3. 3.
      Sodium bicarbonate 50 mEq IV — alkalinizes serum, shifts K+ intracellularly; less effective in acidosis
    4. 4.
      RRT — definitive removal of potassium and correction of acidosis
    Warning
    Loop diuretics are contraindicated in oliguric ATN because:
    • The tubules are damaged and cannot respond to diuretics
    • Diuretics may worsen dehydration and further reduce glomerular filtration rate
    • Furosemide will not increase urine output in established ATN

    Why Fluid Resuscitation Alone Is Insufficient

    Key Point
    The patient has already received aggressive fluid resuscitation for 18 hours with no improvement in urine output or creatinine. Continuing fluids without RRT will cause:
    • Pulmonary oedema
    • Hypertension
    • Worsening hyperkalaemia (K+ cannot be excreted)
    • Metabolic acidosis

    Fluid responsiveness has been exhausted; RRT is now the definitive therapy.

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