Low Sodium (Hyponatremia): Causes, Symptoms and Tests

The blood sodium concentration does not tell you how much sodium is 'missing' from the body; it tells you the ratio of sodium to water in the extracellular fluid. Sodium is the main determinant of plasma osmolality, and the body guards osmolality very precisely: a change of just 1–2% is enough for the hypothalamic-pituitary system to trigger thirst or the release of vasopressin (antidiuretic hormone, ADH). Vasopressin acts on V2 receptors in the renal collecting ducts and causes water channels (aquaporin-2) to be inserted so that water returns to the circulation instead of being excreted. When this system works properly, excess water is quickly excreted in urine and sodium stays within a narrow range of 135–145 mmol/l.

Hyponatremia appears when the kidneys cannot keep up with water excretion. There are three main scenarios. First: vasopressin is released despite low plasma osmolality (because of drugs, pain, nausea, lung or central nervous system disease, cancers), so the kidney retains water the body does not currently need. Second: vasopressin is released 'appropriately' because the body senses a fall in effective circulating volume, as in heart failure, cirrhosis, fluid loss or diuretic use. Third: vasopressin is switched off, but the kidney has too little solute to make a large volume of dilute urine, because the diet is low in salt and protein (the so-called 'tea and toast' diet, beer potomania) or because someone drinks more water than even healthy kidneys can excrete.

That is why saying someone 'has too little salt' is misleading in most cases. If dilution results from excess water, adding salt to meals usually changes little, and may make things worse, because some patients also have heart failure or hypertension, where excess dietary sodium is undesirable. A proper diagnosis starts with the question of why the body is holding on to water.

Two measurement pitfalls are worth knowing. First, there is 'hypertonic' or translocational hyponatremia: with very high glucose, water moves out of cells into the blood and dilutes sodium, so its value is low even though plasma osmolality is high; once glucose is lowered, sodium returns to normal. Second, with very high lipid or protein concentrations (for example in monoclonal gammopathy), some indirect measurement methods give a falsely low result (pseudohyponatremia). That is why the first step for a doctor is to check osmolality and glucose rather than take the number at face value.

The European guideline developed jointly by three scientific societies (intensive care, endocrinology and nephrology) and the JAMA review propose sorting hyponatremia by volume status, i.e. the volume of extracellular fluid. This is the most clinically useful division because treatment depends on it; for hypovolemic and hypervolemic forms it is in fact opposite.

Behind this scheme stands a simple set of tests: plasma osmolality (confirms hypotonicity), urine osmolality (whether vasopressin is 'working'; a value below 100 mOsm/kg points more toward excess water drinking or very low solute intake) and urine sodium concentration (a threshold of 30 mmol/l helps distinguish renal sodium loss or a diuretic effect from extrarenal loss and from SIAD). Added to this is the clinical assessment of volume status, and in euvolemic hyponatremia TSH and a morning cortisol are mandatory, because hypothyroidism and adrenal insufficiency are common, reversible causes that must be excluded before SIAD is diagnosed.

Why does the distinction matter so much? Because a person who is dehydrated after vomiting needs fluids and salt, while a person with SIAD or heart failure needs the opposite, a fluid restriction. Using the wrong strategy is not neutral: a saline infusion in a patient with SIAD can paradoxically lower sodium even further, and restricting water in a dehydrated person will deepen the problem. This is the main reason why 'treating' hyponatremia at home on your own makes no sense.

Drugs are one of the most common reversible causes of hyponatremia, especially in older people taking several medications at once. The best-documented groups are thiazide and thiazide-like diuretics (hydrochlorothiazide, indapamide, chlortalidone), antidepressants (SSRIs, SNRIs, tricyclics), antiepileptic drugs (carbamazepine, oxcarbazepine), antipsychotics, desmopressin used for night-time urination, some cytotoxic drugs (cyclophosphamide, vincristine) and psychoactive substances such as MDMA. The mechanisms differ, from increased vasopressin release to enhanced vasopressin action in the kidney, but the end result is shared: the kidney retains water.

A 2022 review of drug mechanisms (J Clin Med) notes that in many cases, including thiazides and some antidepressants, hyponatremia results not from excess vasopressin but from direct activation of the renal water pathway (increased aquaporin-2 expression), classified as nephrogenic syndrome of inappropriate antidiuresis. The practical conclusion for the patient is simple: low sodium after starting a new drug, especially in the first weeks of therapy, should be reported to your doctor rather than assumed to be chance.

A note on interpretation: the percentages come from studies with different definitions of hyponatremia (different sodium cut-offs, different populations), so they should not be read as a guaranteed risk for any individual. Most patients treated with SSRIs do not develop clinically significant hyponatremia; the risk is higher in older people, women, lean individuals, and when a diuretic is taken at the same time. Never stop an antidepressant or a diuretic on your own because of low sodium; abrupt discontinuation can do more harm than the lab value itself.

This matters because many people assume that hyponatremia 'without symptoms' is harmless. The observational data cited in the review suggest otherwise: chronically lowered sodium, even mildly, is linked to subtle disturbances of balance and attention that in practice translate into falls and, in older people, into fractures. At the same time it must be stressed that observational studies show an association; they do not prove that low sodium itself causes fractures, because people with hyponatremia also tend to have more comorbidities and take more medications.

The severity of symptoms depends not only on the sodium value itself but above all on how fast it fell. The brain has a limited ability to adapt: when sodium drops within hours, brain cells take up water and swell, which causes neurological symptoms even at relatively moderate values. When it falls slowly, over weeks, cells release some of their osmolytes and adapt, so a value of 125 mmol/l may be tolerated with mild complaints. This adaptation is the reason chronic hyponatremia must be corrected carefully.

Because these complaints are nonspecific, hyponatremia is very often found by chance on a routine electrolyte panel. That is why, in people taking the drugs listed above and in older patients with new falls or 'odd' behavior, checking sodium is one of the cheapest and most worthwhile tests. We describe interpretation of the electrolyte panel itself in the entry in our knowledge base on sodium, potassium and chloride.

The first step is to repeat the measurement (if the value is mildly low and there are no symptoms) and to exclude measurement errors and non-hypotonic hyponatremia. A doctor then usually orders a set of tests that lets the hyponatremia be assigned to one of the three types and the cause to be found. The list below shows what you can expect.

SIAD is a diagnosis of exclusion: it requires hypotonic hyponatremia, inappropriately high urine osmolality (above 100 mOsm/kg), raised urine sodium with normal salt intake, normal thyroid, adrenal and kidney function, and no recent diuretic use. A 2023 review in Endocrine Reviews points out that SIAD is the most common cause of hypotonic hyponatremia, that its etiology is often multifactorial (tumors, lung disease, central nervous system disorders, drugs), and that first-line treatment is fluid restriction, which fails in roughly half of patients, explaining the interest in urea, tolvaptan and SGLT2 inhibitors.

A brain that has adapted to low sodium over days or weeks is vulnerable to an overly rapid rise. Correcting chronic hyponatremia too fast can lead to osmotic demyelination syndrome, a rare but serious neurological complication with parkinsonism, quadriparesis or even death. That is why the 2014 European guideline and the JAMA review recommend not exceeding a rise of 10 mmol/l in the first 24 hours (in people with risk factors such as alcoholism, malnutrition, hypokalemia or advanced liver disease, more cautious limits are used). Severe symptomatic cases are treated in hospital with hypertonic saline given in controlled boluses.

It is fair to add that this question is not completely settled. A 2025 meta-analysis (JAMA Internal Medicine) covering 16 cohort studies and over 11,000 adults with severe hyponatremia suggests that slower correction was associated with higher in-hospital mortality than faster correction, and that rapid correction was not statistically significantly associated with a higher risk of demyelination. These are, however, observational studies, prone to distortion (the sickest patients are corrected differently), and the authors themselves do not encourage breaking safety rules. For the reader the conclusion is one: the pace of correction is a decision made in hospital under repeated sodium measurements, not something to do on your own with salt, isotonic drinks or tablets.

A second common myth concerns drinking water: 'the more the healthier'. Healthy kidneys excrete water very effectively under typical conditions, but their capacity has limits; it depends on the supply of solutes (sodium, protein), that is, on diet. With a diet very low in protein and salt, combined with heavy beer or tea consumption, and in people with psychiatric disorders and compulsive drinking (psychogenic polydipsia), excess fluid can cause hyponatremia. In athletes a similar mechanism applies to overdrinking during long events, which we describe in a separate article on exercise-related hyponatremia and sweating.

Hyponatremia is a rare case of a result in which 'one number' combines many different stories: from a harmless drug side effect, through unrecognized hypothyroidism, to a first sign of heart disease or lung cancer. The most valuable approach is therefore to treat it as a diagnostic question. Pay attention to three things: your current list of drugs and supplements, the amount and kind of fluids you drink, and any chronic diseases. With that knowledge, a conversation with your primary care doctor becomes far more specific.

At the same time, there is no need to panic over a single result of 133 or 134 mmol/l without symptoms; biological and analytical variability is real, and a repeat test often comes back normal. What matters is not to ignore values that persist or keep falling, and to plan an electrolyte check in the first weeks after starting drugs that affect water balance. It is a simple practice that can prevent not only uncomfortable symptoms but also falls.