Sodium, serum

Sodium, serum
S -Na KL 2382 

Sodium serves as the primary extracellular cation in the body, and its concentration is meticulously regulated within specific limits to maintain proper metabolic function. Approximately 60% of sodium is present in body fluids, with 97% of this amount located in the extracellular fluid space, and the remaining 40% found in bones. The regulation of sodium content is primarily managed by the kidneys and is influenced by the body’s water intake.

Various enzymes and hormones, such as the RAA system (renin-angiotensin-aldosterone), play crucial roles in the intricate control of sodium levels. The RAA system is involved in blood pressure regulation and operates on the kidney-adrenal axis. Additionally, heart-derived natriuretic peptides and the pituitary antidiuretic hormone (ADH) are instrumental in regulating water secretion and absorption, which indirectly affects sodium content. 


Monitoring the balance of fluid and electrolyte.


1 mL of serum, minimum 0.5 mL. Separated plasma can be stored refrigerated for three days. Freeze the sample for longer storage.

Storage and delivery 

The sample can be refrigerated for three days, but for longer storage, it should be kept frozen. Delivery at room temperature, if it arrives within 24 hours. 


Ion selective electrode (ISE). Accreditated method.

Turnaround time

1 – 2 weekdays

Reference ranges

137 – 145 mmol/L 

Interpretation of results

Hypernatremia, which is an increased serum sodium concentration, is typically linked to insufficient water intake or excessive water loss. Inadequate drinking, especially among the elderly due to reduced thirst and minimal fluid intake, is the most common cause of this condition. Hypernatremia can also result from disturbances in the thirst center caused by factors like cerebral blood flow disorders, brain tumors, or head injuries. Diabetes insipidus, a rare dehydration disorder characterized by a lack of ADH, leads to excessive urine production (more than 10 liters/day) and subsequently increased sodium concentration. Additionally, primary hyperaldosteronism, Cushing’s disease, and excessive administration of sodium-containing IV solutions can contribute to hypernatremia.

Severe hypernatremia, with serum sodium concentration above 155 mmol/L, can lead to symptoms like muscle twitching, convulsions, confusion, and even unconsciousness.

On the other hand, hyponatremia, characterized by low sodium concentration, can be caused by either sodium loss or excessive fluid accumulation in the body. Conditions such as prolonged vomiting and diarrhea can lead to sodium loss. However, the more common cause of hyponatremia is either sodium loss due to profuse sweating (during hot weather or marathon running) or excessive water accumulation in the body. Excessive secretion of the hormone ADH by the pituitary gland, which reduces water excretion through the kidneys, can be responsible for the excessive water accumulation.

Certain medications like antiepileptic drugs (carbamazepine, valproate, lamotrigine), antidepressants, and cytotoxic drugs (e.g., cyclophosphamide and vincristine) can increase ADH secretion or enhance its effect, leading to hyponatremia. Overuse of the diuretic thiazide can also cause this condition. Other causes of hyponatremia may include adrenal insufficiency (Addison’s disease), heart failure, nephrotic syndrome, kidney failure, and cirrhosis of the liver.

Hyponatremia is considered mild when the serum sodium concentration ranges from 130–135 mmol/L, and severe when it falls below 125 mmol/L. Severe hyponatremia can result in symptoms such as fatigue, weakness, headache, nausea, and muscle cramps. In severe cases, it may lead to nervous system symptoms, convulsions, and confusion.


Last update 8.8.2023