High sodium levels in the blood, a condition called hypernatremia, almost always result from losing too much water relative to sodium or, less commonly, from taking in too much salt. Normal blood sodium falls between 136 and 145 mmol/L. Levels above 145 mmol/L are considered elevated, and levels above 160 mmol/L are classified as severe, with significantly higher risks of neurological damage and death.
Understanding the cause matters because the condition carries mortality rates between 20% and 60% in hospitalized patients, depending on severity and underlying health. In most cases outside the hospital, though, the cause is straightforward: not drinking enough water to keep up with what the body is losing.
Water Loss Is the Most Common Cause
The vast majority of cases come down to the body losing more water than it takes in. When water leaves the body without a proportional loss of sodium, the remaining sodium becomes more concentrated. This can happen through several routes.
Gastrointestinal losses are among the most familiar triggers. Prolonged vomiting, severe diarrhea, and nasogastric drainage all pull fluid out of the body faster than most people can replace it. Burns and heavy sweating do the same through the skin. Even rapid breathing during illness (especially with fever) increases water loss through the lungs, a route people rarely think about.
The kidneys can also be responsible. Certain kidney diseases reduce the organ’s ability to hold onto water. Osmotic diuresis, where high concentrations of substances like glucose pull extra water into the urine, is particularly common in people with uncontrolled diabetes. When blood sugar runs very high, the kidneys flush out large volumes of water trying to clear the excess glucose, dragging sodium levels upward in the process.
Diabetes Insipidus and Hormone Problems
Despite the similar name, diabetes insipidus has nothing to do with blood sugar. It’s a disorder of water balance controlled by a hormone called vasopressin (also known as ADH), which tells the kidneys how much water to reabsorb. When vasopressin is missing or the kidneys can’t respond to it, the body produces enormous volumes of dilute urine, sometimes several liters a day, and dehydration follows quickly.
In the central form, the brain doesn’t produce or release enough vasopressin. This can result from head injuries, brain tumors, or surgery near the pituitary gland. In the nephrogenic form, the brain releases vasopressin normally, but the kidneys don’t respond to the signal. Genetic mutations can cause this from birth, or it can develop later from medications or kidney damage. Either way, the result is the same: the kidneys can’t concentrate urine, water pours out, and sodium climbs.
Medications That Raise Sodium
Several drugs interfere with the kidney’s ability to retain water. Lithium, commonly prescribed for bipolar disorder, is the single most reported drug cause of high sodium. Nearly 50% of people on long-term lithium therapy develop some degree of kidney resistance to vasopressin. Sodium levels as high as 196 mmol/L have been documented in lithium users.
Other medications that can push sodium up include:
- Loop diuretics, which force the kidneys to excrete more water
- Amphotericin B, an antifungal that can damage the kidney’s water-reabsorbing cells
- Corticosteroids, which increase the body’s production of urea, driving osmotic water loss
- Lactulose and sorbitol, osmotic laxatives that pull water into the gut
- Mannitol, used in hospital settings to reduce brain swelling, which causes significant water loss through the kidneys
- Foscarnet, an antiviral, and demeclocycline, an antibiotic, both of which can cause the kidneys to stop responding to vasopressin
Too Much Salt Intake
Less commonly, high sodium comes not from water loss but from taking in too much sodium directly. This is rarely a dietary issue from everyday eating. Instead, it tends to happen in specific scenarios: accidental ingestion of large amounts of salt (especially in children), drinking seawater, overuse of sodium bicarbonate (baking soda) as a home remedy, or receiving concentrated saline solutions in a hospital. Hyperaldosteronism, a condition where the adrenal glands produce too much of a hormone that causes sodium retention, can also contribute.
Why Older Adults Are Especially Vulnerable
Aging changes several systems that protect against high sodium. The thirst drive weakens significantly. In studies where older and younger adults were both deprived of water for 24 hours, the older participants felt less thirsty and didn’t drink enough afterward to bring their sodium back to normal levels, even though their bodies needed the fluid just as much.
Total body water also decreases with age. In younger adults, water makes up roughly 60% to 65% of body weight. In older adults, that drops to around 50%, and it can be even lower in women. With less water in the body to begin with, even modest fluid losses can concentrate sodium quickly. The kidneys also lose some of their ability to concentrate urine with age, meaning they waste more water even under normal conditions.
People with dementia or delirium face a compounded risk because they may not recognize thirst or be unable to ask for water. Nursing home residents who depend on caregivers for hydration are particularly at risk. This is one reason hypernatremia is sometimes considered a marker of inadequate care in institutional settings.
Risks for Infants
Babies can develop dangerously high sodium from causes that wouldn’t affect adults. Improperly mixed formula is a well-documented trigger. Adding too little water, whether intentionally (some parents concentrate formula hoping to relieve constipation) or accidentally (confusion over different scoop sizes between formula brands), creates a solution with more sodium than an infant’s immature kidneys can handle.
Breastfeeding difficulties can also lead to hypernatremic dehydration if a newborn isn’t getting enough milk but the problem goes unrecognized. Because infants can’t communicate thirst and depend entirely on caregivers for fluid, the condition can progress quickly before anyone notices.
How High Sodium Affects the Body
The symptoms of high sodium are mostly neurological because the brain is especially sensitive to changes in water balance. As sodium rises in the blood, water gets pulled out of brain cells, causing them to shrink. In mild cases, this produces thirst, restlessness, and irritability. As levels climb higher, symptoms progress to lethargy, confusion, and muscle twitching. Severe hypernatremia above 160 mmol/L can cause seizures, coma, and permanent brain damage. Levels above 180 mmol/L carry high mortality, particularly in older adults.
Interestingly, when sodium rises slowly over days or weeks (chronic hypernatremia), the brain partially adapts by generating new particles inside its cells to draw water back in. This adaptation means chronic cases may have surprisingly mild symptoms relative to the sodium number. But it also creates a treatment challenge: if sodium is corrected too quickly, water rushes back into brain cells that have adapted, causing dangerous swelling. Guidelines recommend lowering sodium by no more than 12 mmol/L per day, or about 0.5 mmol/L per hour, to avoid triggering cerebral edema, seizures, or coma during treatment.
The Thirst Mechanism as a Safety Net
Under normal circumstances, the body has a powerful defense against high sodium: thirst. When sodium starts to rise, the brain detects the increased concentration and triggers an intense urge to drink. This mechanism is so effective that sustained hypernatremia almost never develops in a person who has a normal thirst drive and access to water. The condition becomes dangerous specifically when one of those two conditions fails: either the person can’t feel thirst (due to age, brain injury, or certain genetic conditions called hypodipsia or adipsia), or they can’t act on it (infants, people with physical disabilities, patients who are sedated or restrained, or anyone without access to fluids).