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Differences between prerenal azotemia and Acute Tubular Necrosis
How can prerenal azotemia be differentiated from Acute Tubular Necrosis?
It is important to differentiate between prerenal azotemia and intrinsic forms of Acute kidney injury, as prerenal azotemia will generally improve with the correction of the underlying hemodynamic disturbance.
In contradistinction, the volume loading of patients with Acute Tubular Necrosis or other forms of intrinsic Acute kidney injury will not result in improved kidney function and may exacerbate volume overload.
Characteristic laboratory findings that help differentiate between prerenal azotemia and Acute Tubular Necrosis reflect the preservation of tubular function with increased sodium reabsorption and urinary concentration in prerenal azotemia.
Preexisting Chronic Kidney Disease or diuretic use may limit the usefulness of these indices.
Novel biomarkers of tubular injury, such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), have been proposed as candidates for differentiating between prerenal azotemia and intrinsic tubular damage, but are not yet validated for clinical use.
Laboratory Differences Between Prerenal Azotemia and Acute Tubular Necrosis
Prerenal Azotemia | Acute Tubular Necrosis | |
|---|---|---|
| Serum BUN:creatinine ratio | >20:1 | 10:1 |
| Urine specific gravity | >1.015 | ∼1.010 |
| Urine sodium | <20 mmol/L | >40 mmol/L |
| Fractional excretion of sodium | <1% | >2% |
| Fractional excretion of urea | <35% | >50% |
| Urine osmolality | >500 mOsm/kg | ∼300 mOsm/kg |
| Urine sediment | Normal, or hyaline casts | Kidney tubular cells and “muddy brown” granular casts |
| Biomarkers of tubular injury | Negative | Positive |
BUN, blood, urea, nitrogen.
