Acute Tubular Necrosis (ATN)
ATN is the most common cause of acute kidney injury (AKI) in the hospitalized patient. It is characterized by injury and necrosis of tubular epithelial cells, typically due to ischemia or nephrotoxins.
1. Clinical Phases
- Initiation Phase: Ischemic/toxic insult; slight decrease in GFR.
- Maintenance Phase: Sustained decrease in GFR; oliguria; hyperkalemia; metabolic acidosis.
- Recovery Phase: Polyuria (as tubules regenerate); risk of hypokalemia due to incomplete reabsorption.
2. Pathological Features
| Finding | Description |
|---|---|
| Brown Muddy Casts | The hallmark finding on urinalysis (pathognomonic for ATN). |
| Tubular Findings | Loss of brush border (proximal tubule), epithelial cell necrosis, and sloughing. |
3. Etiologies & Exam Must-Knows
- Ischemic ATN: Decreased perfusion (e.g., hypotension, shock). The proximal tubule and thick ascending limb are most susceptible due to high metabolic demand.
- Nephrotoxic ATN: Aminoglycosides, contrast dye, myoglobinuria (rhabdomyolysis), ethylene glycol, uric acid (tumor lysis syndrome).
- Urinalysis: Fractional excretion of sodium (FeNa) is >2% because the tubules cannot concentrate urine or reabsorb sodium.
Pathology Board Hint: For test questions, always look for the “muddy brown cast” in a patient with a history of recent surgery, sepsis, or exposure to a known toxin (like aminoglycosides). Remember: ATN causes an intrinsic AKI, meaning the urine osmolality will be low (<350 mOsm/kg).