Nephrology · USMLE Step 1 and Step 2

Acute Tubular Necrosis song

Acute Tubular Necrosis - Phases & Casts, as a song. Hear the short teaser here. The full song is on YouTube and Spotify.

Acute Tubular Necrosis

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Key points in this song10

ATN is the most common cause of acute kidney injury (AKI) in hospitalized patients, caused by ischemic or nephrotoxic injury to tubular epithelial cells.
Ischemic ATN follows prolonged prerenal azotemia (shock, sepsis, major surgery), while nephrotoxic ATN is classically caused by aminoglycosides, cisplatin, myoglobin, or IV contrast.
Hallmark urinalysis finding is muddy brown granular casts (pigmented epithelial cell casts), distinguishing ATN from prerenal azotemia.
In ATN, urine sodium is >40 mEq/L and fractional excretion of sodium (FENa) is >2%, reflecting loss of tubular reabsorptive capacity.
Aminoglycoside toxicity causes proximal tubular injury and accumulates in the renal cortex; toxicity correlates with trough levels and is enhanced by concurrent loop diuretics or volume depletion.
Myoglobinuria (rhabdomyolysis-induced ATN) presents with tea-colored urine, elevated CK, and urine dipstick positive for blood with no RBCs on microscopy.
Contrast-induced ATN is prevented with IV isotonic saline hydration before and after contrast; N-acetylcysteine evidence is weak but still tested.
ATN classically progresses through three phases: oliguric phase (days to weeks), diuretic phase (risk of hypokalemia and hypovolemia), and recovery phase.
During the oliguric phase, expect hyperkalemia, metabolic acidosis, hyperphosphatemia, and hyponatremia — indications for emergent dialysis if severe.
Unlike prerenal azotemia, ATN does not improve with IV fluids; BUN-to-creatinine ratio is typically less than 20:1 due to impaired urea reabsorption.