What are the causes of low urinary sodium (<20 mEq/L)?

Causes of Low Urinary Sodium (<20 mEq/L)

Low urinary sodium (<20 mEq/L) indicates the kidneys are avidly retaining sodium, which occurs in three primary clinical scenarios: hypovolemic states (true volume depletion), hypervolemic states with reduced effective arterial blood volume (heart failure, cirrhosis), and occasionally in SIADH when diuresis is very low. 1

Hypovolemic States (True Volume Depletion)

The most common cause of low urinary sodium is true volume depletion, where the body appropriately conserves sodium to maintain intravascular volume. 1

• Extrarenal sodium losses result in urinary sodium typically <20 mEq/L, including gastrointestinal losses (vomiting, diarrhea), third-spacing (burns, pancreatitis), and excessive sweating 2, 3
• Dehydration triggers activation of the renin-angiotensin-aldosterone system (RAAS) as a protective mechanism, leading to enhanced proximal nephron sodium reabsorption and low urinary sodium 3, 2
• Hemorrhage or blood loss causes decreased effective circulating volume, prompting the kidneys to conserve sodium with urinary sodium <30 mEq/L 2, 1
• A urinary sodium <30 mmol/L has a positive predictive value of 71-100% for response to 0.9% saline infusion in hypovolemic hyponatremia 4, 1

Hypervolemic States with Reduced Effective Arterial Blood Volume

Despite total body sodium overload, these conditions present with low urinary sodium due to perceived arterial underfilling triggering sodium retention. 2

• Advanced cirrhosis with ascites demonstrates urinary sodium typically <10 mEq/L due to systemic vasodilation, portal hypertension, and activation of RAAS causing excessive sodium and water reabsorption 2, 4
• Congestive heart failure leads to low urinary sodium (<50-70 mEq/L) reflecting heightened renal sodium avidity and persistent effective hypovolemia despite total body fluid overload 2, 4
• Nephrotic syndrome causes urinary sodium retention due to decreased oncotic pressure and perceived hypovolemia 4
• In cirrhosis, recent diuretic use may elevate urinary sodium above 10 mEq/L, but baseline values remain low 2

SIADH with Low Diuresis

While SIADH typically presents with urinary sodium >20-40 mEq/L, patients with very low urine output can have urinary sodium <20 mEq/L, creating diagnostic confusion. 5, 6

• SIADH patients with high urinary to plasma creatinine ratio (U/P creat >180) demonstrate fractional excretion of sodium (FENa) values <0.5%, overlapping with salt depletion 5
• When diuresis is severely reduced (U/P creat >140), SIADH patients may have FENa as low as 0.3 ± 0.2%, though still higher than salt-depleted patients (0.1 ± 0.04%) 5
• Combined use of FENa and fractional excretion of urea (FEurea) remains reliable for discrimination: in SIADH with low diuresis, FENa >0.15% and FEurea >45% distinguish it from salt depletion where both are lower 5, 2

Acute Kidney Injury (Prerenal Azotemia)

Low urinary sodium in the setting of acute kidney injury suggests prerenal causes that are potentially reversible with volume repletion. 7, 2

• Prerenal azotemia typically presents with FENa <1% and urinary sodium <20 mEq/L, indicating intact tubular function and appropriate sodium conservation 7, 2
• Hepatorenal syndrome in cirrhosis shows urinary sodium <10 mEq/L and FEurea <28.16% (75% sensitivity, 83% specificity for HRS) 2
• Important caveat: FENa <1% can also occur in acute glomerulonephritis, contrast nephrotoxicity, pigment nephropathy, and early obstruction—none of which are volume-responsive 7

Diagnostic Approach and Pitfalls

Physical examination alone has poor accuracy (sensitivity 41.1%, specificity 80%) for determining volume status in hyponatremic patients, making urinary sodium measurement essential. 1, 4

• A spot urine sodium <30 mEq/L clearly separates hypovolemic (mean 18.4 ± 3.1 mEq/L) from euvolemic patients (mean 72 ± 3.7 mEq/L) in hyponatremia 1
• Diuretic use confounds interpretation: patients on loop diuretics may have FENa >1% despite true volume depletion, making FEurea more reliable 2, 7
• In cirrhosis, FENa <1% has 100% sensitivity but only 14% specificity for prerenal causes of AKI, limiting its diagnostic utility 2
• Recent diuretic administration can elevate urinary sodium above expected values in otherwise volume-depleted states 2, 7

Special Populations

• Neonates and preterm infants (<34 weeks gestation) have deficient tubular sodium reabsorption, making low urinary sodium less reliable as a marker of volume status 4
• Patients with chronic kidney disease may have FENa >1% despite volume depletion due to impaired tubular function 7
• Cerebral salt wasting presents with urinary sodium >20 mEq/L despite clinical hypovolemia, distinguishing it from typical hypovolemic states 4