Lab result explainedMetabolic panelLast updated November 8, 2026

Sodium blood test: what low sodium (hyponatremia) and high sodium mean

Sodium (serum) (Na) · Basic or comprehensive metabolic panel (BMP/CMP), electrolyte panel · reported in mEq/L (identical to mmol/L for sodium)

Sodium is the main electrolyte in the fluid outside your cells, and a sodium blood test measures its concentration in the liquid part of your blood. Normal is 135 to 145 mEq/L (the same number in mmol/L). Despite the name, the result is far more about water than about salt: your kidneys and the hormone vasopressin (antidiuretic hormone) adjust how much water you keep so that sodium stays in that narrow band, so an abnormal value nearly always means the body is holding too much water (low sodium) or has lost too much (high sodium).

Low sodium, or hyponatremia, is the most common electrolyte problem in medicine, found in roughly 15 to 20 percent of people admitted to hospital and in a large share of older adults on water tablets. Thiazide diuretics, heart failure, cirrhosis, kidney disease, under-active adrenal glands and a long list of medicines that make the body hold water (SSRIs, carbamazepine, some painkillers) are the usual causes. Drinking more water than the kidneys can excrete, as can happen in endurance events or with heavy beer intake on little food, does it too.

High sodium, or hypernatremia, is less common and almost always means not enough water is being drunk to replace what is lost. It is seen in frail older people whose sense of thirst is blunted, in infants, in people with fever, diarrhoea or uncontrolled diabetes, and in the rare condition diabetes insipidus. Mild shifts in either direction usually cause no symptoms; values below 125 or above 155 mEq/L affect the brain and are medical emergencies.

Na at a glance

What it is: the concentration of sodium in blood plasma, which reflects the balance of water to salt in the body, not how much salt you eat.
Normal: 135–145 mEq/L (mmol/L); labs vary slightly, some use 136–145.
Low (hyponatremia): below 135. Mild 130–134, moderate 125–129, severe below 125. Below 120 with confusion or seizures is life-threatening.
High (hypernatremia): above 145. Symptoms usually start above 155 to 160 and almost always mean a water deficit.
Most common causes of low sodium: thiazide diuretics, SIADH (from lung or brain disease, cancer, or drugs such as SSRIs), heart failure, cirrhosis, kidney disease, adrenal insufficiency and excess water intake.
Next step: a repeat test, blood and urine osmolality, urine sodium, thyroid and cortisol checks, a review of medicines and fluid intake; correction is deliberately slow (no more than about 8 to 10 mEq/L in 24 hours).

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What Na measures

Sodium is measured with an ion-selective electrode on serum or plasma and reported in milliequivalents per litre (mEq/L), which for sodium equals millimoles per litre (mmol/L). Because sodium is the dominant particle outside cells, it largely determines plasma osmolality, the concentration of dissolved particles that pulls water into or out of cells. The brain is the organ most sensitive to this: when sodium falls quickly, water moves into brain cells and they swell; when it rises quickly, they shrink.

The body defends sodium concentration by regulating water. Thirst and vasopressin (ADH) are released when osmolality rises, and the kidneys then concentrate urine and conserve water; when osmolality falls, vasopressin switches off and the kidneys can excrete up to 15 to 20 litres of dilute urine a day. Hyponatremia therefore almost always means vasopressin is active when it should not be (SIADH, heart failure, cirrhosis, pain, nausea, certain drugs) or that water intake has overwhelmed even normal kidneys. Hypernatremia means water is being lost or not drunk, since a healthy, conscious person with access to water will drink before sodium climbs far.

Two artefacts matter. In pseudohyponatremia, very high blood triglycerides or paraproteins (as in myeloma) take up space in the sample and make the reported sodium falsely low on some analysers; a direct ion-selective electrode (blood gas machine) gives the true value. In hyperglycaemia, glucose pulls water out of cells and genuinely dilutes sodium, so clinicians add back about 1.6 to 2.4 mEq/L for every 100 mg/dL of glucose above 100 to get a corrected sodium.

Normal range for Na

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (mEq/L (identical to mmol/L for sodium))	Notes
Adults, normal	135–145 mEq/L	Some labs use 136–145 or 135–147. Values at the edges are usually repeated before being acted on.
Mild hyponatremia	130–134 mEq/L	Often no symptoms. Common in older adults on thiazides. Linked to a higher rate of falls, poor concentration and fractures even at this level.
Moderate hyponatremia	125–129 mEq/L	Nausea, headache, confusion and unsteadiness are more likely, especially if the fall was fast.
Severe (profound) hyponatremia	Below 125 mEq/L	Risk of seizures, coma and brain swelling, particularly below 120 or when the drop happened within 48 hours. Hospital treatment.
Mild hypernatremia	146–155 mEq/L	Usually thirst and a dry mouth only. Points to a water deficit; check intake, fever, diarrhoea, glucose and diuretics.
Severe hypernatremia	Above 155–160 mEq/L	Lethargy, irritability, muscle twitching, seizures. Carries high mortality in frail older adults and needs urgent correction.
Corrected sodium in high blood sugar	Add 1.6–2.4 mEq/L per 100 mg/dL glucose above 100	A sodium of 130 with a glucose of 500 is a corrected sodium of about 136 to 140; the problem is the glucose, not the sodium.
Safe correction rate for chronic low sodium	No more than 8–10 mEq/L in 24 hours	Faster correction of long-standing hyponatremia can cause osmotic demyelination, a serious brain injury. This is why hospitals raise sodium slowly.

High sodium (hypernatremia)

A sodium above 145 mEq/L means there is too little water relative to sodium in your body. In nearly every case the water was lost (through urine, sweat, breath, fever or diarrhoea) or was never drunk, rather than too much salt having been eaten. Because thirst is such a powerful protective reflex, significant hypernatremia in an adult who is awake and can reach water is unusual; it tends to occur in infants, in people with dementia or a stroke who cannot ask for or get to fluids, in hospital patients on tube feeds or ventilators, and in anyone with uncontrolled diabetes whose high glucose is pulling water out through the kidneys.

Mildly high values (146 to 150) are usually a sign of simple dehydration and correct with drinking. Higher values point to a specific water-losing problem: diabetes insipidus, in which the body cannot make or respond to vasopressin and passes 3 to 20 litres of dilute urine a day; osmotic diuresis from high glucose or mannitol; large losses from diarrhoea (especially lactulose or osmotic laxatives), burns or heavy sweating; or, rarely, too much sodium given as hypertonic saline, sodium bicarbonate or accidental salt ingestion. Primary hyperaldosteronism produces a sodium at the top of the normal range rather than frank hypernatremia.

The brain shrinks as blood becomes more concentrated, which is why the symptoms are neurological: irritability, lethargy, muscle twitching, then seizures and coma. As with low sodium, the speed of change matters more than the number, and chronic hypernatremia is corrected slowly (no faster than about 10 to 12 mEq/L a day) to avoid brain swelling as water re-enters cells.

Common causes

Not drinking enough water
The leading cause. Older adults have a blunted thirst response, and people with dementia, after a stroke, or who are bed-bound or sedated may not be able to get a drink. Infants depend on carers for fluid.
Fever, sweating, burns and rapid breathing
Water is lost through skin and lungs (insensible loss) at 0.5 to 1 litre a day normally and much more with fever, heat exposure, hard exercise or extensive burns.
Diarrhoea and vomiting
Watery diarrhoea, particularly from osmotic laxatives such as lactulose or from infections, loses more water than sodium and concentrates the blood if it is not replaced.
Uncontrolled diabetes (osmotic diuresis)
Glucose spilling into urine drags water with it. In hyperosmolar hyperglycaemic state the corrected sodium is often high even when the measured value looks normal or low.
Diabetes insipidus
Central DI (pituitary damage from surgery, trauma or tumour) or nephrogenic DI (lithium, high calcium, low potassium, inherited) prevents the kidneys from concentrating urine, producing litres of dilute urine and intense thirst.
Loop diuretics and mannitol
Furosemide and similar drugs cause the kidneys to excrete urine that is dilute relative to blood, so water loss outpaces sodium loss if intake does not keep up.
Excess sodium intake or infusion
Hypertonic saline, sodium bicarbonate during resuscitation, concentrated infant formula, salt-water ingestion and sea-water drowning raise sodium directly. Dietary salt alone does not, because thirst and the kidneys compensate.
Hospital and tube-feeding situations
High-protein tube feeds without enough free water, ventilation without humidification and sedation that removes the thirst drive are common causes of hypernatremia in intensive care.

Symptoms that can go with it

Intense thirst, dry mouth and tongue, reduced skin turgor (mild cases)
Passing very large volumes of pale urine, day and night (diabetes insipidus)
Lethargy, weakness and irritability
Confusion or drowsiness, particularly in older adults
Muscle twitching, increased reflexes, tremor
Seizures or coma when sodium rises above about 160 or rises quickly
In infants: restlessness, high-pitched cry, fewer wet nappies, sunken fontanelle

Low sodium (hyponatremia)

A sodium below 135 mEq/L means your blood is too dilute: there is too much water relative to sodium. The body can lose sodium (vomiting, diarrhoea, diuretics, adrenal failure), but in most cases the main fault is that the kidneys are holding on to water because vasopressin is being released when it should not be. Clinicians sort hyponatremia by fluid status. In hypovolaemic hyponatremia, both salt and water have been lost and the patient is dry (diuretics, gut losses, Addison's disease). In euvolaemic hyponatremia the patient looks normal and the cause is usually SIADH, hypothyroidism or excess water intake. In hypervolaemic hyponatremia the patient is swollen with fluid from heart failure, cirrhosis or kidney failure, yet the sodium is diluted.

How it feels depends on how far and how fast sodium has fallen. A gradual drift to 128 over months may cause nothing more than mild tiredness, poor concentration and unsteadiness, although even this mild chronic hyponatremia is associated with about four times the rate of falls in older adults and roughly double the fracture risk. A fall to the same level within a day or two, as can happen with marathon over-drinking, MDMA use or after surgery, causes headache, vomiting, confusion and can progress to seizures as the brain swells inside the skull.

The work-up is logical rather than exotic: a repeat sodium, blood and urine osmolality, urine sodium, glucose, thyroid function, a morning cortisol and a careful medication history identify the cause in most people. Thiazide diuretics are the single most common drug cause, particularly in older women, and SIADH from a chest infection, brain disorder, cancer or a drug such as an SSRI or carbamazepine is the most common euvolaemic cause.

Common causes

Thiazide diuretics
Hydrochlorothiazide, chlorthalidone and indapamide impair the kidney's ability to dilute urine while increasing thirst. The most common drug cause of hyponatremia, most often in women over 65, usually within weeks of starting but possible at any time.
SIADH (syndrome of inappropriate antidiuretic hormone)
Vasopressin released without a proper trigger by pneumonia or other lung disease, stroke, head injury, meningitis, small-cell lung cancer and other tumours, pain, nausea and surgery. Urine is inappropriately concentrated and the patient looks neither dry nor swollen.
Medicines that raise vasopressin or mimic it
SSRIs and other antidepressants (especially in older adults), carbamazepine and oxcarbazepine, antipsychotics, NSAIDs, cyclophosphamide, vincristine, desmopressin and the recreational drug MDMA (ecstasy).
Heart failure, cirrhosis and nephrotic syndrome
Reduced effective blood flow to the kidneys triggers vasopressin and salt retention. Total body sodium is high but water is retained even more, so blood sodium falls. A sodium below 130 in heart failure or cirrhosis marks advanced disease.
Kidney disease
Damaged kidneys cannot excrete a large water load. In advanced CKD or acute kidney injury, ordinary fluid intake can be enough to lower sodium.
Vomiting, diarrhoea and sweating with water-only replacement
Losing salty fluids and replacing them with plain water or tea lowers sodium, particularly in infants and endurance athletes.
Excess water intake
Exercise-associated hyponatremia (about 13 percent of finishers in one Boston Marathon study, driven by drinking beyond thirst), psychogenic polydipsia and beer potomania or a 'tea and toast' diet, where very low solute intake limits how much water the kidneys can excrete.
Adrenal insufficiency (Addison's disease)
Lack of cortisol and aldosterone causes salt loss and water retention; low sodium with high potassium, low blood pressure and fatigue is the classic picture and a morning cortisol is essential in unexplained hyponatremia.
Hypothyroidism
Severe, untreated hypothyroidism reduces water excretion and can lower sodium modestly; a TSH is part of the standard work-up.
Pseudohyponatremia and high blood glucose
Very high triglycerides or paraproteins make some analysers read sodium falsely low. High glucose genuinely dilutes sodium, but the problem is the glucose; correct the sodium before worrying about it.

Symptoms that can go with it

Often none when sodium is 130 to 134 and has fallen slowly
Tiredness, low energy and difficulty concentrating
Nausea, loss of appetite and headache
Unsteadiness, slowed thinking and falls, especially in older adults
Muscle cramps or weakness
Confusion, irritability or personality change
Vomiting, drowsiness, seizures or collapse when sodium falls below about 120 or falls quickly

Read it alongside

Potassium — low sodium with high potassium suggests Addison's disease; low potassium with low sodium points to diuretics, vomiting or diarrhoea.
Glucose — every low sodium should be corrected for glucose; a high glucose can explain the whole result.
Chloride and CO2 (bicarbonate) — sodium and chloride usually move together; a disproportionate chloride helps sort acid-base problems and vomiting from diuretic effects.
BUN and creatinine — a high BUN-to-creatinine ratio supports dehydration in hypernatremia; low BUN and uric acid are typical of SIADH.
Serum and urine osmolality — confirm the blood is genuinely dilute and show whether the kidneys are concentrating urine when they should not be (SIADH) or diluting it appropriately (excess water intake).
Urine sodium — below 20–30 mEq/L suggests the kidneys are conserving salt (dehydration, heart failure, cirrhosis); above 30–40 suggests SIADH, diuretics or adrenal insufficiency.
TSH and morning cortisol — rule out hypothyroidism and adrenal insufficiency before SIADH is diagnosed.
Triglycerides and total protein — very high values can produce a falsely low sodium on some analysers.

What usually happens next

A sodium of 130 to 134 with no symptoms is usually repeated within days to weeks, with a review of fluid intake and any new medicine, particularly thiazides, SSRIs and anti-seizure drugs, before anything else is done.
Below 130, or any abnormal sodium with symptoms, expect same-day blood and urine osmolality, urine sodium, glucose, kidney function, TSH and cortisol, and an assessment of whether you are dry, normal or fluid-overloaded, because the treatment differs completely for each.
If SIADH is diagnosed, the usual approach is to find and treat the trigger (a chest infection, a drug, a tumour) and to limit fluid intake under supervision; some people are prescribed salt tablets, oral urea or, less often, a vasopressin-blocking drug.
For high sodium, the questions are how much water you have been drinking, how much urine you are passing, whether there has been fever, diarrhoea or high blood sugar, and whether you take lithium; a water deprivation test or a copeptin level is used when diabetes insipidus is suspected.
Chronic abnormalities are corrected gradually, by no more than about 8 to 10 mEq/L in 24 hours for low sodium and 10 to 12 for high, so do not expect or push for a rapid return to normal.
Ask what your sodium was on previous tests: a stable 133 over years is a very different situation from a fall from 140 to 133 in a month.

Diet, lifestyle and natural levers with evidence

What can move Na once the cause is known. Nothing here replaces finding the cause.

Drink to thirst, not to a schedule, during endurance exercise

Strong evidence

Over-drinking is the cause of exercise-associated hyponatremia. In a study of 488 Boston Marathon finishers, 13 percent had a sodium of 135 or below and 0.6 percent were below 120; weight gain during the race, a direct sign of drinking more than was sweated out, was the strongest predictor. International consensus statements since 2015 recommend drinking according to thirst and avoiding weight gain during events, which has cut hospital admissions where adopted.

Sports drinks contain too little sodium (10 to 20 mEq/L) to prevent hyponatremia if drunk to excess; salt tablets do not fully protect against over-drinking either.

Supervised fluid restriction for SIADH

Moderate evidence

In the first randomised trial of fluid restriction for chronic SIADH, limiting intake to about 1 litre a day raised sodium by a median of roughly 3 mEq/L by day 3 and 4 by day 4, compared with about 1 mEq/L with no treatment, and about one in five patients reached a clinically useful rise of 5 or more. It is first-line treatment in most guidelines but works slowly and fails when urine is very concentrated.

Only appropriate once SIADH is confirmed; restricting fluids in someone whose low sodium comes from dehydration, vomiting or adrenal insufficiency makes things worse. Follow your clinician's limit.

Adequate dietary solute: enough protein and salt

Moderate evidence

The kidneys need dissolved solute (mainly urea from protein and sodium from salt) to excrete water. Older adults on a low-solute 'tea and toast' diet and heavy beer drinkers who eat little can only excrete 2 to 4 litres of water a day before sodium falls. Raising solute intake with normal protein portions and unrestricted salt, or with prescribed oral urea (15 to 30 g a day, which raised sodium by about 5 to 7 mEq/L within a week in SIADH studies), restores water excretion.

Extra salt is inappropriate in heart failure, cirrhosis or kidney failure, where the low sodium reflects fluid overload. Oral urea is prescribed and monitored, not self-started.

Scheduled fluid intake for older adults and people with reduced thirst

Moderate evidence

Healthy men in their 70s drink about half as much as young men after the same degree of dehydration, and in a UK cohort 37 percent of adults over 65 arriving at hospital were already dehydrated by serum osmolality, with higher mortality. Offering about 1.5 to 2 litres of fluid a day on a schedule, more in hot weather or with fever, is the most practical protection against hypernatremia in frail or cognitively impaired people.

People with heart failure, kidney failure or SIADH may have a prescribed fluid limit that takes priority; check before increasing intake.

Limit alcohol, particularly large volumes of beer on little food

Preliminary evidence

Beer potomania, hyponatremia from drinking several litres of beer a day while eating little, is well described in case series and reflects the combination of a large water load and very low solute intake. Alcohol also blunts judgement about fluid intake and is a common co-factor in exercise-associated and MDMA-related hyponatremia. Reducing intake and eating normally resolves the problem within days in reported cases, though no controlled trials exist.

When to see a clinician promptly

A sodium below 125 mEq/L, or any low sodium with confusion, vomiting, severe headache, drowsiness or a seizure: go to an emergency department. Below 120 with symptoms is life-threatening.
A sodium above 155 mEq/L, or any high sodium with confusion, lethargy, twitching or inability to keep fluids down.
Low sodium with low blood pressure, dizziness on standing, weight loss, salt craving or darkening skin: possible Addison's disease, which can become a crisis.
Low sodium in anyone who has recently started a thiazide diuretic, an SSRI or carbamazepine, so the medicine can be reviewed before the level falls further.
Passing more than 3 litres of urine a day with intense thirst, or new confusion in an older relative who has been drinking little, has had a fever or diarrhoea, or takes lithium.
A sodium between 125 and 134 that is falling on repeat testing, or that comes with repeated falls, unsteadiness or new cognitive change in an older adult.

Frequently asked questions

What is a normal sodium level in a blood test?

Normal serum sodium is 135 to 145 mEq/L, which is the same as 135 to 145 mmol/L. Some labs use 136 to 145. Values of 133 or 134 are only slightly low and are often repeated before anything is done; values below 130 or above 150 generally need a cause found and treated.

Is a sodium level of 134 or 133 something to worry about?

Usually not on its own. A sodium of 133 or 134 is mild hyponatremia, often with no symptoms, and frequently traces back to a thiazide water tablet, an antidepressant, drinking a lot of water or a recent illness. It does deserve a repeat test and a medication review, because even mild chronic hyponatremia is linked to more falls and fractures in older adults, and because a falling trend matters more than a single value.

What level of sodium is dangerous?

A sodium below 125 mEq/L is classed as severe hyponatremia and below 120 carries a real risk of seizures, coma and brain swelling, especially if it fell within the previous 48 hours. Above 155 to 160 is dangerous at the other end. Speed matters as much as the number: a sodium of 128 that has been stable for years is far less dangerous than a sodium of 128 reached in a day.

What causes low sodium levels in the elderly?

Thiazide diuretics (hydrochlorothiazide, chlorthalidone, indapamide) are the most common single cause, followed by SIADH from chest infections, strokes or drugs such as SSRIs and carbamazepine, heart failure, kidney disease and a low-solute diet with high fluid intake. Ageing kidneys are less able to excrete water and thirst regulation changes, so older adults are more vulnerable to all of these. Hypothyroidism and adrenal insufficiency are checked in anyone whose cause is not obvious.

Can drinking too much water cause low sodium?

Yes. Healthy kidneys can excrete around 15 to 20 litres of dilute urine a day, so it takes extreme intake to overwhelm them, but it happens in endurance events, in psychiatric polydipsia and in people whose solute intake is very low (beer potomania, 'tea and toast' diets), where the limit drops to a few litres. Drinking to thirst rather than to a target volume prevents it in sport.

Does eating salt raise your blood sodium?

Not in a healthy person. Extra salt makes you thirsty and your kidneys excrete the surplus, so blood sodium stays within 135 to 145 regardless of a salty meal. High sodium almost always means a water deficit, not salt excess. In heart failure, cirrhosis and kidney disease, extra salt causes fluid retention and swelling rather than a high sodium reading, and in those conditions limiting salt is still advised.

Why is my sodium low if I have high blood sugar?

High glucose pulls water out of cells into the blood and dilutes the sodium. Clinicians add about 1.6 to 2.4 mEq/L to the measured sodium for every 100 mg/dL of glucose above 100 to get the corrected value; a sodium of 128 with a glucose of 600 is really a corrected sodium of about 136 to 140. Bringing the glucose down fixes the sodium.

How fast can low sodium be corrected?

Deliberately slowly in most cases. Raising a chronically low sodium by more than about 8 to 10 mEq/L in 24 hours risks osmotic demyelination, a serious and sometimes permanent brain injury, so hospitals aim for 4 to 8 mEq/L a day and check levels every few hours. The exception is someone having seizures or at risk of brain herniation, who is given a small, rapid rise of 4 to 6 mEq/L with hypertonic saline and then slowed down.

References

Sodium blood test. MedlinePlus, US National Library of Medicine (2023)View source
Hyponatremia. Mayo Clinic (2022)View source
Hyponatremia. Merck Manual Professional Version (2023)
Adrogué HJ, Madias NE. Hyponatremia. New England Journal of Medicine (2000)
Adrogué HJ, Madias NE. Hypernatremia. New England Journal of Medicine (2000)
Spasovski G, Vanholder R, Allolio B, et al.. Clinical practice guideline on diagnosis and treatment of hyponatraemia. European Journal of Endocrinology (2014)
Verbalis JG, Goldsmith SR, Greenberg A, et al.. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. American Journal of Medicine (2013)
Almond CS, Shin AY, Fortescue EB, et al.. Hyponatremia among runners in the Boston Marathon. New England Journal of Medicine (2005)
Hew-Butler T, Rosner MH, Fowkes-Godek S, et al.. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference. Clinical Journal of Sport Medicine (2015)
Renneboog B, Musch W, Vandemergel X, Manto MU, Decaux G. Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. American Journal of Medicine (2006)
Garrahy A, Galloway I, Hannon AM, et al.. Fluid restriction therapy for chronic SIAD: results of a prospective randomized controlled trial. Journal of Clinical Endocrinology and Metabolism (2020)
El-Sharkawy AM, Watson P, Neal KR, et al.. Hydration and outcome in older patients admitted to hospital (The HOOP prospective cohort study). Age and Ageing (2015)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.