Hyponatremia (<135 mEq/L) is a common electrolyte abnormality caused by an excess of total body water in comparison to that of the total body sodium content. Measuring the serum osmolality, urine sodium concentration and urine osmolality helps to differentiate among the possible causes. The severity of this electrolyte abnormality ranges from asymptomatic to seizures, coma and death as a consequence of cerebral swelling.
Pseudohyponatremia is due to hypertriglyceridemia or multiple myeloma. In regular subjects, the plasma water is 93% of the plasma volume. Plasma water part falls lower than 80% in cases with noticeable hyperlipidemia (triglycerides >1500 mg/dL) or hyperproteinemia (protein >10 mg/dL). Rise in blood urea causes the hyponatremia in renal failure.
True hyponatremia is having a fall in serum osmolality and is divided into hypervolemic, hypovolemic, and euvolemic based on volume status.
Osmoreceptors in the hypothalamus detect the plasma osmolality. If Posm >285 mOsm/kg, osmoreceptors stimulate the release of anti-diuretic hormone (ADH) from the posterior pituitary into the circulation, as well as stimulate thirst. ADH release is also stimulated in states of low effective circulating volume. Circulating ADH binds to receptors on the principal cells of the collecting duct in the kidneys and activates a cellular pathway which ultimately results in water reabsorption. This results in a decrease in the serum osmolality and an increase in the urine osmolality (Uosm). In certain states, ADH can be released inappropriately or ectopically, meaning that ADH is released without an osmotic or hemodynamic stimulus. When ADH is suppressed, water is renally excreted.
Another important physiological pathway is the renin-angiotensin-aldosterone system (RAAS). This pathway is activated in states of low effective circulating volume and/or when there is reduced sodium in the renal tubules. These conditions stimulate the release of renin from the juxtaglomerular cells, which are part of the afferent arterioles. The activation of RAAS ultimately results in increased sodium reabsorption, arteriolar vasoconstriction and release of ADH from the posterior pituitary. Measured urine sodium concentration (UNa) is a reflection of intravascular volume; UNa is elevated with volume expansion and reduced with volume depletion.
