Key Benefits

'- Spot low sodium (hyponatremia) by measuring your blood’s sodium level.

• Clarify symptoms like headache, nausea, confusion, cramps, or seizures from low sodium.
• Explain whether dehydration, water overload, or hormone-driven retention is causing low sodium.
• Guide fluid, salt, and medication adjustments to correct sodium safely and steadily.
• Protect medication safety by flagging diuretics, some antidepressants, carbamazepine, or desmopressin as triggers.
• Support pregnancy by monitoring sodium during severe nausea, labor fluids, or postpartum changes.
• Track trends in heart failure, cirrhosis, kidney disease, or water-retaining conditions.
• Best interpreted with serum osmolality, urine sodium, glucose, and your symptoms.

What are Hyponatremia

Hyponatremia biomarkers are the indicators that show how your body is handling water and salt and why blood sodium is low. The core marker is the sodium level in blood (serum sodium), which confirms the problem. Together with the concentration of dissolved particles in blood (serum osmolality) and in urine (urine osmolality), they reveal whether excess water is diluting sodium and how the kidneys are responding to water‑regulating signals. The amount of sodium in urine (urine sodium) shows if the kidneys are holding onto salt or losing it. Hormone markers such as the brain’s water‑retaining signal (vasopressin, often tracked via copeptin), the kidney–adrenal regulators of salt balance (renin and aldosterone), and heart stretch signals (natriuretic peptides like BNP) point to the body system driving the imbalance. Additional checks for thyroid and adrenal function (TSH, cortisol) and for purine handling (uric acid) help identify endocrine or dilutional causes. Together, these biomarkers localize the source—water load, hormone effect, kidney handling, or circulation—and guide safe, targeted correction.

Why are Hyponatremia biomarkers important?

Hyponatremia biomarkers—chiefly serum sodium, supported by serum/urine osmolality and urine sodium—reveal how the body governs water–salt balance, the force that sets plasma tonicity and cell volume. Because neurons are highly volume‑sensitive, even small sodium shifts can affect brain, muscle, heart, and bone function.

Typical sodium is about 135–145, with health strongest in the middle and stable over time. When values fall, there is too much water relative to sodium—often from excess vasopressin or reduced renal water clearance in heart failure, cirrhosis, diuretic use, or adrenal/thyroid disease—so water moves into cells and the brain swells. Nausea, headache, fatigue, confusion, and gait unsteadiness can progress to seizures and coma if the drop is rapid or deep. Premenopausal women and children are more vulnerable to dangerous cerebral edema; older adults often show attention lapses, falls, and fractures. Chronic mild hyponatremia is linked to lower bone density and cognitive slowing.

When sodium runs high, it usually signals water loss or impaired thirst—dehydration or diabetes insipidus—shrinking cells. Thirst, irritability, lethargy, and neurologic symptoms are common, especially in frail elders and infants.

Big picture: sodium integrates the brain–kidney–hormone axis (vasopressin), adrenal and thyroid function, and the circulation of heart and liver. Persistent dysnatremia flags stress across these systems and associates with longer hospital stays, fractures, osteoporosis, and mortality. Keeping mid‑range supports stable cell volume and resilient brain function.

What Insights Will I Get?

Hyponatremia biomarker testing matters because sodium concentration in the blood drives water balance, cell volume, and electrical signaling across the body. Shifts here affect brain function, muscle performance, blood pressure regulation, and hormone and kidney coordination. At Superpower, we test these specific biomarkers: Sodium.

Sodium is the primary extracellular cation that sets plasma osmolality—the pull that determines where water moves. Hyponatremia means the sodium concentration is low, most often reflecting too much water relative to sodium rather than a pure sodium deficit. It commonly arises from increased antidiuretic hormone (ADH/vasopressin) activity, impaired kidney water excretion, or endocrine and medication effects. Many labs define normal serum sodium roughly in the mid‑130s to mid‑140s.

Sodium levels indicate the stability of osmotic and volume regulation. When sodium is in range, osmoregulation, renal handling, and neurohormonal systems (ADH, renin‑angiotensin‑aldosterone) are generally coordinated, supporting steady blood pressure, cognition, and neuromuscular function. Low sodium signals water excess relative to solute, increasing brain water content (cerebral edema risk) and impairing attention, gait, and reaction time; deeper reductions can cause headache, nausea, cramps, and—if severe—seizures. Whether the fall is acute or chronic changes physiologic impact.

Notes: Interpretation depends on volume status, acuity, and tonicity. Age, pregnancy, strenuous exercise, and acute illness can alter ADH activity. Medications (e.g., thiazide diuretics, SSRIs, anticonvulsants, antipsychotics, desmopressin) are common contributors. Hyperglycemia can lower measured sodium via water shifts; severe hyperlipidemia or paraproteinemia can artifactually lower results on some assays.