A 58-year-old man with diabetes mellitus presents with acute kidney injury. Urinalysis shows muddy brown casts and proteinuria <1 g/day. Serum creatinine has risen from 1.2 to 3.8 mg/dL over 48 hours. Which single finding best distinguishes acute tubular necrosis (ATN) from prerenal azotemia in this clinical context?

## Distinguishing ATN from Prerenal Azotemia **Key Point:** The fractional excretion of sodium (FENa) is the single most reliable discriminator between ATN and prerenal azotemia. It reflects the kidney's ability to reabsorb filtered sodium. ### Calculation and Interpretation $$FENa = \frac{[Na^+]_u \times Cr_p}{[Cr]_u \times Na^+_p} \times 100$$ Where subscripts u = urine, p = plasma. | Feature | Prerenal Azotemia | ATN | |---------|-------------------|-----| | **FENa** | <1% (usually <0.1%) | >2% (often >3%) | | **Urine osmolality** | >500 mOsm/kg | <350 mOsm/kg | | **BUN:Cr ratio** | >20:1 | <10:1 | | **Urine Na⁺** | <20 mEq/L | >40 mEq/L | | **Muddy brown casts** | Absent | Present | | **Fluid response** | Rapid improvement | Slow or absent | **High-Yield:** In prerenal states, the tubules are intact and avidly reabsorb sodium to conserve intravascular volume → FENa <1%. In ATN, tubular epithelial damage prevents sodium reabsorption → FENa >2%. ### Clinical Context in This Case The presence of **muddy brown casts** (hallmark of ATN) combined with a **rapid rise in creatinine** and **proteinuria <1 g/day** strongly suggests ATN. The FENa >2% would confirm tubular dysfunction rather than prerenal hypoperfusion. **Clinical Pearl:** FENa is most reliable in non-oliguric AKI and when the patient is not on diuretics. In oliguric AKI or with concurrent diuretic use, fractional excretion of urea (FEUrea) may be more reliable. **Warning:** Do not rely on urine osmolality or BUN:Cr ratio alone—these overlap significantly between the two conditions, especially in early ATN.