1FENa Explained — Distinguishing AKI Types
FEUrea (%) = [(Urine Urea × Serum Cr) ÷ (Serum Urea × Urine Cr)] × 100
| Marker | <1% | 1–2% | >2% |
|---|---|---|---|
| FENa | Prerenal AKI | Indeterminate | Intrinsic renal / postrenal |
| FEUrea | <35% = Prerenal | 35–50% | >50% = Intrinsic renal |
When FENa Can Be Misleading
False low FENa (looks prerenal, but isn't):
- Early contrast nephropathy — tubules initially intact, FENa <1% for first 24 hours
- Myoglobinuria / haemoglobinuria — tubular toxin but early FENa low
- Early urinary obstruction
- Acute glomerulonephritis — sodium retention due to inflammation
False high FENa (looks intrinsic, but may be prerenal):
- Diuretics — loop and thiazide diuretics block tubular sodium reabsorption → use FEUrea instead
- Pre-existing CKD — tubular function already impaired
- Adrenal insufficiency
- Bicarbonaturia (high bicarbonate with sodium in urine)
AKI Management by Type
- Prerenal (FENa <1%): IV fluid resuscitation — 500 mL NS over 30 min (adult). Monitor urine output, creatinine. Identify and treat cause (bleeding, sepsis, heart failure, medications)
- Intrinsic renal (FENa >2%): Identify specific cause — ATN (most common), glomerulonephritis, interstitial nephritis, vasculitis. Nephrology referral. Avoid nephrotoxins. Optimise haemodynamics
- Postrenal (obstruction): FENa may be >2% or <1% early. Urinary ultrasound mandatory. Catheterise if urethral obstruction. Nephrostomy if ureteric obstruction
2Frequently Asked Questions
FENa differentiates prerenal azotaemia from intrinsic acute tubular necrosis, guiding whether fluid resuscitation or nephrology-directed conservative management is required.
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