## Differentiating AKI Etiology: Role of Urine Electrolytes **Key Point:** FENa and urine sodium are the gold-standard non-invasive investigations to differentiate prerenal AKI from intrinsic renal (acute tubular necrosis) and postrenal causes. ### Pathophysiology of FENa In **prerenal AKI** (volume depletion, hypoperfusion): - Kidneys attempt to conserve sodium - Tubular reabsorption of sodium increases - FENa **< 1%** and urine sodium **< 20 mEq/L** In **intrinsic renal AKI** (ATN, contrast-induced nephropathy): - Tubular damage impairs sodium reabsorption - FENa **> 2%** and urine sodium **> 40 mEq/L** ### Clinical Application to This Case The patient has **contrast-induced nephropathy (CIN)** — a form of ATN following cardiac catheterization. The investigation must distinguish this from: - Prerenal AKI (if volume-depleted) - Cholesterol embolism (if atheroembolic) FENa and urine sodium will show **FENa > 2%**, confirming intrinsic renal damage and guiding fluid management (avoid aggressive hydration if ATN; consider it if prerenal). ### Formula $$FENa = \frac{[Na^+]_{urine} \times [Cr]_{plasma}}{[Na^+]_{plasma} \times [Cr]_{urine}} \times 100$$ **High-Yield:** FENa is **unreliable in diuretic use, rhabdomyolysis, and contrast nephropathy** — use urine sodium alone in these settings. ### Diagnostic Cutoffs | Parameter | Prerenal AKI | Intrinsic Renal AKI | |-----------|--------------|---------------------| | FENa | < 1% | > 2% | | Urine Na | < 20 mEq/L | > 40 mEq/L | | Urine Osmolality | > 500 mOsm/kg | < 350 mOsm/kg | | BUN:Cr ratio | > 20:1 | < 10:1 | **Clinical Pearl:** In contrast-induced nephropathy, FENa may be low initially due to reflex vasoconstriction, but urine sodium is more reliable.
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