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Pathophysiology of Hyponatremia in SIADH

Water retention secondary to increased vasopressin and sodium excretion

The syndrome of inappropriate antidiuretic hormone (SIADH) is the most common cause of euvolemic hyponatremia. SIADH accounts for 60% of all types of chronic hyponatremia and is the most common etiology of hyponatremia in hospitalized patients.1

Hyponatremia in SIADH is marked by water retention secondary to an increase in serum vasopressin and urinary sodium excretion.2

Different patterns of vasopressin release with type A vs type B SIADH

In type A SIADH, found in approximately 40% of SIADH cases, the excessive and erratic vasopressin release is unrelated to serum osmolality. Ectopic production of vasopressin by tumor tissue may account for this type of SIADH.3

In type B SIADH (also designated reset osmostat), the response of vasopressin to changes in serum osmolality is preserved and urine-diluting capacity is intact, but the osmotic threshold for vasopressin release is lowered.3

Pattern of vasopressin release in SIADH

In type A SIADH, vasopressin release has no linear relationship to plasma osmolality. In type B SIADH, vasopressin release has a linear relationship to plasma osmolality, but the threshold is lower than normal. Adapted from Raftopolous, Support Care Cancer, 2007.3

Changes in sodium in SIADH can be attributed to an increase in vasopressin. The diagnosis of SIADH is made in the context of hyponatremia with plasma hypotonicity; urine osmolality exceeding plasma osmolality; elevated urinary sodium excretion despite normal salt and water intake; absence of edema or volume depletion; and normal renal, adrenal and thyroid function.1

Several factors explain the changes in sodium excretion seen in SIADH2:

  • Decreased aldosterone secretion secondary to increased extracellular fluid volume
  • Increased filtered sodium as a result of increased glomerular filtration rate (GFR)
  • Suppressed sodium resorption in the proximal tubules