What Is Low Sodium Called? Hyponatremia Explained

Low sodium is medically called hyponatremia. It’s diagnosed when blood sodium drops below 135 milliequivalents per liter (mEq/L), which is the standard threshold used by healthcare providers. Sodium helps regulate water balance, nerve signaling, and muscle function, so even a modest drop can cause noticeable symptoms.

How Severity Levels Break Down

Not all hyponatremia is the same. Clinicians classify it by how far sodium has fallen:

  • Mild: 125 to 133 mEq/L
  • Moderate: 115 to 125 mEq/L
  • Severe: below 115 mEq/L

Mild cases often go unnoticed or cause vague symptoms like fatigue. Severe cases are medical emergencies that can lead to seizures, coma, or death. The speed of the drop matters too. When sodium falls gradually over more than 48 hours (chronic hyponatremia), the brain has time to adapt, and symptoms tend to be more moderate. When it plunges rapidly in under 48 hours (acute hyponatremia), the brain swells quickly, which is far more dangerous.

What It Feels Like

Early symptoms of hyponatremia are easy to dismiss or blame on something else. You might notice nausea, headaches, fatigue, or a general sense of sluggishness. As sodium drops further, muscle cramps and weakness become more common, along with irritability and restlessness.

At dangerously low levels, the condition becomes neurological. Confusion sets in, followed by seizures and, in the most extreme cases, coma. Because these symptoms overlap with dehydration, heat exhaustion, and other conditions, hyponatremia often gets missed until a blood test reveals the real problem.

Common Causes

Hyponatremia isn’t simply about not eating enough salt. It reflects an imbalance between sodium and water in the body. There are three main patterns, depending on your overall fluid status.

Too Much Water, Normal Sodium Intake

This is the most common pattern in everyday life. Your body holds onto more water than it should, diluting the sodium that’s already there. A major driver is a condition called SIADH (syndrome of inappropriate antidiuretic hormone secretion), where the body produces too much of the hormone that tells your kidneys to retain water. Thyroid problems and adrenal insufficiency can also trigger this pattern. Many medications fall into this category too, which is covered below.

Losing Both Sodium and Water

Prolonged vomiting, diarrhea, or heavy sweating can deplete both sodium and water, but sodium losses outpace fluid losses. Burns, pancreatitis, and kidney diseases that impair sodium retention can do the same. Certain diuretics (especially thiazide-type water pills) are a well-known culprit here, forcing the kidneys to dump sodium.

Excess Fluid Retention

Conditions like heart failure, liver cirrhosis, and kidney disease cause the body to retain large volumes of fluid. The total amount of sodium in the body may actually be normal or even high, but it’s so diluted by excess water that blood levels read as low.

Medications That Lower Sodium

Drug-induced hyponatremia is surprisingly common, particularly with two classes of medication: thiazide diuretics and antidepressants.

A large Danish population study found that nearly all commonly prescribed antidepressants were significantly associated with hyponatremia. Citalopram carried the strongest link, with roughly an eightfold increase in risk shortly after starting the drug. Other SSRIs like sertraline, paroxetine, and escitalopram also raised risk, as did SNRIs like venlafaxine and duloxetine, though to a lesser degree. The risk was highest in the first two weeks after starting treatment, then gradually declined as the body adjusted.

Anti-seizure medications, opioids, and NSAIDs (common over-the-counter painkillers) can also contribute. If you’re starting a new medication and experience unusual fatigue, nausea, or confusion in the first few weeks, it’s worth having your sodium levels checked.

Overhydration During Exercise

Endurance athletes and people exercising in hot weather face a specific risk called exercise-associated hyponatremia. The usual cause is straightforward: drinking too much water or sports drinks during prolonged activity. Despite marketing that encourages aggressive hydration, sports drinks are still hypotonic, meaning they contain far less sodium than your blood does. Drinking large volumes dilutes your blood sodium the same way plain water would.

Pain, stress, nausea, and intense exercise all increase antidiuretic hormone levels, which makes your kidneys hold onto even more water. Taking NSAIDs like ibuprofen before a race, a common practice, amplifies this effect. The best prevention guideline is also the simplest: drink when you’re thirsty, not on a fixed schedule. Studies have shown that limiting fluid availability at aid stations during distance events actually reduces hyponatremia rates.

How Hyponatremia Is Corrected

Treatment depends entirely on how quickly sodium dropped and how severe it is. For acute cases under 48 hours old, faster correction is considered safe because the brain hasn’t had time to fully adapt to the lower sodium level. For chronic hyponatremia, or any case where the timeline is unknown, correction has to be slow and carefully controlled.

The general safety limit for chronic cases is raising sodium by no more than 8 mEq/L in 24 hours. Correcting too fast risks a rare but serious complication called osmotic demyelination syndrome, where nerve cells in the brain are damaged by the rapid fluid shift. This is why doctors often assume hyponatremia is chronic when they can’t confirm when it started, erring on the side of slower correction.

Mild chronic cases are sometimes managed by simply restricting fluid intake or adjusting medications. Moderate to severe cases typically require treatment in a hospital setting where sodium levels can be monitored with frequent blood draws throughout the correction process.