From the Research
In acute tubular necrosis (ATN), typical laboratory findings include elevated urine sodium (typically >40 mEq/L) and increased fractional excretion of sodium (FENa >2%), reflecting the kidney's inability to conserve sodium due to tubular damage, as supported by the most recent study 1.
Key Laboratory Findings
- Elevated urine sodium: typically >40 mEq/L
- Increased fractional excretion of sodium (FENa): >2%
- Urine specific gravity: typically fixed around 1.010, indicating loss of concentrating ability
- Urinary sediment examination: often reveals muddy brown granular casts, renal tubular epithelial cells, and cellular debris, which are hallmarks of tubular injury These findings occur because ATN causes damage to the tubular epithelium, impairing its normal reabsorptive functions. The damaged tubules cannot properly reabsorb sodium, leading to increased sodium excretion despite the body's need to retain it. Similarly, the kidney loses its ability to concentrate urine, resulting in isosthenuria (fixed specific gravity). The presence of tubular epithelial cells and granular casts in the sediment directly reflects the ongoing tubular cell death and sloughing characteristic of ATN.
Diagnostic Utility
The diagnostic utility of FENa in differentiating ATN from prerenal azotemia is well-established, with a recent systematic review and meta-analysis 1 demonstrating high sensitivity and specificity for this purpose, particularly in oliguric patients without a history of chronic kidney disease or diuretic therapy.
Clinical Implications
These laboratory parameters help distinguish ATN from prerenal azotemia, where sodium conservation would typically be intact, and guide clinical management accordingly. The most recent and highest quality study 1 provides strong evidence for the use of FENa in the diagnosis of ATN, and its findings should be prioritized in clinical decision-making.