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FeNa significance

Fractional excretion of sodium (FeNa) can be calculated as part of an assessment of acute kidney injury, particularly in oliguric patients. FeNa is a measurement of the ability of the kidney to extract water and sodium from the glomerular filtrate. It is a ratio of the rate of sodium filtration to the overall GFR (estimated by renal creatinine filtration) – in other words how much sodium is excreted into the urine relative to the total amount of sodium passing through the kidney. Traditionally, calculating the FeNa allows one to classify the cause of AKI as “pre-renal” or a hypovolemic state versus intrinsic damage to the kidneys. Intact tubules, such as in “pre-renal” etiologies are still able to reabsorb sodium, whereas damaged tubules (ex. ATN, AIN) will not.

To calculate FeNa, you must have serum sodium, serum creatinine, urine sodium, and urine creatinine.

FeNa = 100 x (Urinary sodium x plasma creatinine)/(plasma sodium x urinary creatinine)

Interpreting FeNa:

  • Low FeNa <1% – Pre-renal etiology: The intact proximal tubules are able to reabsorb sodium resulting in a very low urine sodium concentration. There is also stimulus to conserve or reabsorb sodium, and water with it, suggesting the kidneys sense poor perfusion or decreased arterial volume. Poor perfusion may be the result of hypovolemia, renal vasoconstriction or renal artery stenosis, reduced cardiac function, or decreased glomerular filtration pressure. If the patient is truly hypovolemic, kidney function may improve with fluid resuscitation. Low FeNa can be seen in other states with low urine sodium that are not volume depleted such as acute glomerulonephritis, sepsis, cardiorenal syndrome or CHF, hepatorenal syndrome, contrast induced nephropathy.
  • Healthy euvolemic patients with normal renal function and dietary sodium intake will have a FeNa of approximately 1%.
  • High FeNa >2 or 3% – Intrinsic damage: Damaged tubules, such as in ATN or AIN, do not reabsorb sodium from glomerular filtrate resulting in higher urinary sodium. ATN (acute tubular necrosis) is the most common cause of intrinsic damage, which has resulted from prolonged pre-renal failure, shock, sepsis or a toxin.
  • FeNa should not be used and is less accurate in patients with known chronic kidney disease, obstruction, acute glomerular disease, or those taking diuretics. FeUrea is preferred for patients on diuretics.


  1. Makris K, Spanou L. Acute kidney injury: diagnostic approaches and controversies. Clin Biochem Rev. 2016;37:153–175 PubMed Link

Other References

  1. Lima, C.; Macedo, E. Urinary biochemistry in the diagnosis of acute kidney injury. Dis. Markers 2018. Article ID 4907024, 7 pages, 2018 Link