Bedside Snapshot

Normal (Adult)
No universal normal. Diagnostic cutoffs, not a healthy range: prerenal pattern is FENa under 1% or FEUN 35% or less (untreated patients)
Urine Na⁺ and osmolality: lab-specific
Critical Values
No universal critical value: interpret by trend and clinical context
High Suggests
  • FENa 1% or more with no diuretic: intrinsic injury (ATN), most useful when oliguric
  • Urine Na⁺ above 30 mEq/L: renal sodium loss
  • Urine osmolality above 100 mOsm/kg: ADH activity (SIADH, hypovolemia)
Low Suggests
  • FENa under 1%: prerenal pattern if no diuretic; does not exclude intrinsic AKI
  • Urine Na⁺ 30 mEq/L or less: effective volume loss
  • Urine osmolality 100 mOsm/kg or less: water excess
Act Now If
Seizure, coma, GCS 8 or less, or vomiting with hyponatremia: treat per protocol; do not wait for urine results. Oliguric AKI: pair urine and plasma samples, check volume, call nephrology.
Watch Out For
A diuretic or fluid bolus before the sample. FENa reads high in prerenal AKI after diuretics, so check the medication record first.

Reference & Critical Ranges

Lab-specific ranges: Every lab sets its own urine electrolyte interval, and fluid intake moves it. Use the range on your report. The values below are typical or come from the cited guidance.

Reference ranges

PopulationConventionalSINotes
Adult: FENa
Under 1%
Under 1%
Prerenal pattern when untreated. Less reliable with diuretics or CKD (see Interpretation).
Adult: FEUN
35% or less
35% or less
Prerenal pattern in the original 2002 study. Later meta-analyses are mixed.
Adult: urine sodium
30 mEq/L or less (effective volume loss); above 30 mEq/L (renal loss)
30 mmol/L or less; above 30 mmol/L
Random spot sample with a paired plasma sodium. Thresholds apply to hyponatremia work-up.
Adult: urine osmolality
Lab-specific; 100 mOsm/kg or less (water excess); above 100 mOsm/kg (ADH activity)
Same (mOsm/kg)
Use with serum osmolality. Dilute urine with high serum osmolality points away from ADH excess.
Children
Pediatric lab interval
Pediatric lab interval
Adult cutoffs are not established for children. Discuss with pediatric nephrology.

Severity & critical values

LevelConventionalSIWhat it means
Prerenal pattern
FENa under 1%
Under 1%
Kidney is retaining sodium; usually low effective perfusion in an untreated patient.
Intrinsic pattern
FENa 1% or more
1% or more
Tubular injury is likely in an oliguric patient with no diuretic and no CKD.
Effective volume loss
Urine Na⁺ 30 mEq/L or less
30 mmol/L or less
Low effective arterial volume: hypovolemia, heart failure or cirrhosis.
Renal sodium loss
Urine Na⁺ above 30 mEq/L
Above 30 mmol/L
Diuretics, SIADH, adrenal insufficiency or cerebral salt wasting.
ADH activity
Urine osmolality above 100 mOsm/kg
Same
Hypotonic hyponatremia with ADH present: SIADH, hypovolemia, hypothyroidism, adrenal insufficiency, heart failure.
Critical values: There is no universal critical value for urine electrolytes. Severe hyponatremia symptoms come first. Do not wait for urine results.

Conversion: Sodium in mEq/L equals mmol/L because sodium is monovalent. FENa and FEUN are percentages, so the units cancel out of the formulas.

Fractional excretion of sodium (FENa)
(Urine Na⁺ × Plasma creatinine) ÷ (Plasma Na⁺ × Urine creatinine) × 100

Under 1% in an untreated patient points toward a prerenal pattern.

Fractional excretion of urea nitrogen (FEUN)
(Urine urea nitrogen × Plasma creatinine) ÷ (Plasma BUN × Urine creatinine) × 100

35% or less points toward a prerenal pattern. The formula takes BUN (urea nitrogen). It does not take a serum urea value in another unit.

Calculated total osmolality
2 × Na⁺ + glucose ÷ 18 + BUN ÷ 2.8

The BUN term adds an ineffective osmole. That is why total osmolality overestimates tonicity in uremia.

Effective osmolality (tonicity)
2 × Na⁺ + glucose ÷ 18 (BUN excluded)

Under 275 mOsm/kg of effective osmolality means a hypotonic state. When the calculated value does not fit the patient, measure osmolality.

Causes of Abnormal Results

High (intrinsic injury or renal sodium loss)

MechanismCommon causesBedside clue
Tubular injury (ATN)
Ischemia, sepsis, nephrotoxins such as contrast or aminoglycosides
Oliguria, rising creatinine, muddy-brown granular casts on microscopy
Diuretic effect
Furosemide, bumetanide, thiazides, mannitol
Recent diuretic dose; FENa reads high even when the cause is prerenal
Renal sodium loss
Diuretics, adrenal insufficiency, cerebral salt wasting
Urine Na⁺ above 30 mEq/L; check cortisol when hyponatremia is present
SIADH (ADH excess)
SSRIs, carbamazepine, cyclophosphamide, CNS disease, lung disease, pain, nausea
Urine osmolality above 100 mOsm/kg with euvolemia and urine Na⁺ above 30 mEq/L
Osmotic diuresis
Hyperglycemia, mannitol
Large urine volume; glucose in urine
Diuretic trap: Furosemide can make FENa read high on its own. Before you call it ATN, find every diuretic dose and when it was given.

Low (prerenal pattern or water excess)

MechanismCommon causesBedside clue
Effective volume loss (prerenal)
Hemorrhage, vomiting, diarrhea, burns, third spacing
FENa under 1%, urine Na⁺ 30 mEq/L or less, low blood pressure, tachycardia
Low effective arterial volume
Heart failure, cirrhosis with ascites, nephrotic syndrome
Edema, ascites, raised JVP; urine studies are less reliable with kidney disease
Water excess
Polydipsia, beer potomania, very low solute intake
Urine osmolality 100 mOsm/kg or less; ask about water, beer and tea intake
Diabetes insipidus
Central: pituitary injury or surgery. Nephrogenic: lithium, hypercalcemia
Dilute urine with high serum osmolality and polyuria
Check osmolality first: Dilute urine with a low serum sodium is not automatically water excess. Hyperglycemia really does lower serum sodium by dilution. Lipids or protein lower the measured value only on indirect ISE. Check serum osmolality before you act.

Interpretation & Bedside Approach

Step-by-step approach

  1. Is it real? Pair the urine sample with a plasma sample drawn at the same time. Note any diuretic, fluid bolus or catheter problem before you read the result.
  2. How sick is the patient? Assess severity first. Seizure, coma, GCS 8 or less, vomiting or cardiorespiratory distress is treated per protocol without waiting for urine studies.
  3. Acute vs chronic and the trend: One urine sample is a snapshot of the last few hours. Repeat after volume restoration, a diuretic or a change in fluids.
  4. Calculate derived values: FENa, FEUN and calculated serum osmolality (formulas in Reference & Critical Ranges).
  5. Classify with named criteria: For hypotonic hyponatremia, apply the ESE 2014 SIADH criteria below. For acute kidney injury, use FENa and FEUN with the limits in the next section.
  6. Escalate or dispose: Severe symptoms or oliguric AKI need the receiving team now. Hand off the urine and plasma values with the times they were drawn.

Decision table

PatternSuggests
Serum osmolality under 275, urine osmolality 100 mOsm/kg or less
Water excess (polydipsia, beer potomania)
Serum osmolality under 275, urine osmolality above 100, urine Na⁺ above 30 mEq/L, euvolemic, normal intake
SIADH (ESE 2014 criteria; diagnosis of exclusion)
Urine Na⁺ 30 mEq/L or less with edema, ascites or volume loss
Effective volume loss (prerenal or hypervolemic)
FENa under 1%, no diuretic
Prerenal pattern. Does not exclude intrinsic AKI (contrast, pigment, glomerular injury, early sepsis); use with microscopy, history and trend
FENa 1% or more, oliguric, no diuretic, no CKD
Intrinsic AKI (ATN) likely
Dilute urine with high serum osmolality
Diabetes insipidus (central or nephrogenic)
Diuretic within hours of the sample
FENa and urine Na⁺ unreliable; interpret with the clinical picture

SIADH criteria from the 2014 ESE guideline

SIADH is a diagnosis of exclusion. All of these ESE 2014 essential criteria must be met:

  1. Effective serum osmolality (2 × Na⁺ + glucose ÷ 18, without the BUN term) below 275 mOsm/kg
  2. Urine osmolality above 100 mOsm/kg at some level of reduced effective osmolality
  3. Clinical euvolemia
  4. Urine sodium above 30 mmol/L with normal sodium and water intake
  5. No adrenal, thyroid, pituitary or renal insufficiency; no recent diuretic use

Look for supporting findings too. Serum uric acid below 0.24 mmol/L (4 mg/dL), serum urea below 3.6 mmol/L (21.6 mg/dL urea, about 10 mg/dL BUN), and a sodium that fails to correct after a 0.9% saline infusion all support the picture.

How well FENa performs

A 2022 systematic review and meta-analysis of adults with AKI tested the 1% threshold. Here is how it performed:

SettingFENa (sensitivity / specificity)
Studies using the 1% threshold (15 studies, 872 patients)
90% / 82%
CKD or diuretic subgroup (6 studies, 511 patients)
83% / 66%
Diuretic-only subgroup (5 studies, 238 patients)
80% / 54%
Oliguric, no CKD or diuretic (8 studies, 264 patients)
95% / 91%

The authors concluded that FENa adds little in CKD or with diuretics. It is most useful when oliguria is present.

In the original 2002 study, FENa under 1% showed up in 92% of untreated prerenal patients. Only 48% of prerenal patients on diuretics had it. FEUN of 35% or less appeared in 89% of the diuretic-treated prerenal group. FEUN ran higher in ATN.

FEUN is contested: A 2024 meta-analysis found FEUrea no better than FENa, even in patients on diuretics. A 2026 meta-analysis reported moderate accuracy with low certainty. Treat FEUN as a second opinion. It does not replace the bedside picture.

Special Populations

PopulationWhat changesClinical implication
Neonates & infants
Tubular function is immature at birth, especially in preterm infants, so FENa is normally higher than the adult cutoff
A neonatal FENa above 1% does not by itself mean intrinsic injury. Use neonatal-specific references and discuss with pediatric nephrology.
Children & adolescents
Hyponatremia work-up and treatment follow pediatric protocols
Hypertonic saline dosing is weight-based in many pediatric protocols. Follow the pediatric protocol and medical direction.
Pregnancy
Pregnancy physiologically lowers serum sodium and osmolality
A mildly low value may be normal for gestation. Interpret in context and do not treat the number alone.
Older adults
Diuretic use is common
Ask about diuretics first; FENa and FEUN both move with diuretic use.
CKD / dialysis
Baseline tubular handling is altered
FENa has a limited role. Interpret with the baseline creatinine and the trend.
Liver disease
Ascites with low effective volume lowers urine Na⁺
Read low urine sodium with the ascites exam and creatinine trend; it does not by itself mean kidney injury.
Diuretics and CKD: Both move FENa and FEUN. The same urine values mean something different in these patients. Check the medication list and the baseline creatinine before you interpret.

Interfering Factors & Pitfalls

Collection & handling

FactorEffectWhyAvoid / fix
Urine and plasma drawn at different times
False ↑ or ↓ FENa
The ratio needs both values from the same time point
Draw paired urine and plasma together
Diluted or delayed specimen
Lower urine Na⁺ and osmolality
Dilution lowers concentration
Use a fresh sample; follow lab handling
Specimen after a fluid bolus
Changes the urine picture
Volume restoration alters sodium handling
Note the bolus time and repeat after it

Medications & treatments

FactorEffectWhyAvoid / fix
Loop or thiazide diuretics (furosemide, bumetanide, thiazides)
False ↑ FENa
Diuretics block tubular sodium reabsorption
Check the dose time; FEUN is less affected in one study, but this is contested
Mannitol
False ↑ FENa
Osmotic diuresis increases sodium excretion
Treat the result as diuretic-affected
SSRIs, carbamazepine, cyclophosphamide
Urine Na⁺ and osmolality ↑
ADH release or renal sodium loss
Review the medication list before calling SIADH

Physiologic & biologic

FactorEffectWhyAvoid / fix
CKD
FENa unreliable
Altered tubular handling at baseline
Interpret with baseline creatinine
Heart failure or cirrhosis
Low urine Na⁺ with edema
Effective volume loss despite high total body sodium
Read with the exam and creatinine trend
Hyperglycemia
True ↓ serum Na⁺ (dilutional)
Glucose draws water out of cells, diluting plasma sodium; this is not an assay error
Correct Na⁺ for glucose before judging tonicity or using urine values

Assay & device-specific

FactorEffectWhyAvoid / fix
High lipids or protein
False ↓ measured Na⁺ (pseudohyponatremia)
Non-aqueous volume displaces plasma water; occurs with indirect ISE, not direct ISE
Check serum osmolality; ask the lab which ISE method is used
Lab method and reporting units
Ranges differ by lab
Osmolality and electrolyte methods vary
Confirm the reported unit and the reference range on your report

Common misinterpretations

  • A low FENa (under 1%) does not rule out intrinsic AKI or ATN. Contrast, pigment (rhabdomyolysis), glomerular injury and early sepsis can all push it down. Pair it with microscopy, history and trend.
  • A high FENa or urine Na⁺ does not prove ATN. It does not rule out hypovolemia either. Diuretics, bicarbonaturia (for example vomiting with metabolic alkalosis) and glucosuria all push urine sodium up. In vomiting-related alkalosis, urine chloride is the better volume marker.
  • One urine sample shows the last few hours. It does not show the trend.
  • Dilute urine does not always mean water excess. Check serum osmolality first.

Physiology & Test Basics

What it measures

This page is the urine half of the sodium and kidney work-up. It covers urine sodium, urine osmolality, and the fractional excretion indices FENa and FEUN. The serum value lives on the sodium page. Here, the question is how the kidney handled sodium and water.

Physiology & regulation

  • The kidney filters sodium and takes back nearly all of it. FENa compares what gets excreted with what got filtered.
  • Low renal perfusion makes the kidney hold on to sodium. Urine sodium falls. That is the basis of the prerenal pattern.
  • ADH (vasopressin) tells the collecting duct to take back water. High ADH makes concentrated urine.
  • Dilute urine shows up when ADH is low, as in water excess or diabetes insipidus.
  • Tubular injury makes it harder for the kidney to take sodium back. FENa rises.
  • Urea moves mostly by passive forces. That is why FEUN was less thrown off by diuretics in the 2002 study.

How it is measured

Collect a spot urine sample and draw plasma at the same time. Measure urine sodium, creatinine, urea nitrogen and osmolality. Measure plasma sodium, creatinine, BUN and osmolality too. Write down the time of the last diuretic dose, any fluid bolus and recent urine output. Container, turnaround and reference ranges depend on the lab.

Why it matters

Urine studies tell you whether a kidney is responding to low perfusion or has been injured. They also help classify hyponatremia. In emergency and critical care they come second. The bedside picture and the trend come first.

Clinical Pearls

EMS: You can't run urine studies in the field. Don't hold treatment for them. Note the time of any diuretic dose and the time of the last void, and pass both to the receiving team.
Nursing: Chart strict intake and output, and time every void. A urine result means little without the fluid balance behind it.
Diuretic timing: Check the medication record before you read FENa. A furosemide dose in the hours before the sample can make prerenal AKI look intrinsic.
Water excess: Urine osmolality of 100 mOsm/kg or less with low serum osmolality points to water intake. Before you call it SIADH, ask about water, beer and tea.
Oliguria matters: Eight studies looked at oliguric patients with no CKD and no diuretic. Pooled, FENa had a sensitivity of 95% and a specificity of 91%. That is the setting where FENa earns its place.
Trend beats a single value: Overcorrecting chronic hyponatremia risks osmotic demyelination. Recheck plasma sodium after each bolus or change in therapy. Follow the protocol's correction limit. ESE 2014 suggests no more than 10 mmol/L in the first 24 h, and 8 mmol/L in each later 24 h (Adrogué 2022 also cites the 10 mEq/L first-24-hour limit).
Dilute diuresis: After volume repletion or stopping a thiazide, a brisk water diuresis can raise sodium fast and cause overcorrection. Watch urine output and urine osmolality together. A sudden high output of dilute urine during hyponatremia treatment calls for an immediate sodium recheck.

References

  1. Carvounis CP, et al. Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure. Kidney International. 2002 Dec. https://doi.org/10.1046/j.1523-1755.2002.00683.x
  2. Abdelhafez M, et al. Diagnostic performance of fractional excretion of sodium for the differential diagnosis of acute kidney injury: a systematic review and meta-analysis. Clinical Journal of the American Society of Nephrology. 2022 Jun. https://doi.org/10.2215/CJN.14561121
  3. Abdelhafez MO, et al. Utility of fractional excretion of urea in acute kidney injury with comparison to fractional excretion of sodium: a systematic review and meta-analysis. The American Journal of the Medical Sciences. 2024 Sep. https://doi.org/10.1016/j.amjms.2024.04.021
  4. Pan HC, et al. Assessing the utility of fractional excretion of urea in distinguishing intrinsic and prerenal acute kidney injury in hospitalised patients: a systematic review and meta-analysis. BMJ Open. 2026 Jan. https://doi.org/10.1136/bmjopen-2025-100875
  5. Spasovski G, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. European Journal of Endocrinology. 2014;170(3):G1–G47. https://doi.org/10.1530/EJE-13-1020
  6. Adrogué HJ, Tucker BM, Madias NE. Diagnosis and management of hyponatremia: a review. JAMA. 2022;328(3):280–291. https://doi.org/10.1001/jama.2022.11176
  7. Neonatal renal function: evaluation of glomerular and tubular functional and structural integrity in neonates. American Journal of the Medical Sciences. 2002;324(5):261–266. https://pubmed.ncbi.nlm.nih.gov/12449447/

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