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About Hyponatremia
Pathophysiology of
Euvolemic Hyponatremia
Pathophysiology of
Hypervolemic Hyponatremia
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Pathophysiology of Hypervolemic Hyponatremia

Hypervolemic hyponatremia occurs when extracellular sodium is normal or even slightly elevated, but extracellular fluid is greatly elevated. These patients have signs of clinical hypervolemia, such as pitting edema or ascites. Two of the major etiologies of hypervolemic hyponatremia are heart failure (HF) and cirrhosis.1

Pathophysiology of hyponatremia in heart failure2*

Hyponatremia in HF involves a complex interaction of processes. The excessive water and sodium retention characteristic of HF leads to a reduction in glomerular filtration and increased reabsorption into the body. The activation of the renin-angiotensin system (RAS) also enhances water and sodium reabsorption, as well as stimulating the thirst center of the brain, promoting the ingestion of excessive amounts of fluid.

In addition, high levels of the hormone arginine vasopressin (AVP) are found in patients with HF. AVP binds to V2 receptors in the collecting ducts of the kidneys, resulting in free water reabsorption rather than excretion in the urine. The AVP activity combines with other dilutional pathophysiologies to result in hyponatremia.

Pathophysiology of hyponatremia in cirrhosis3

Multiple factors lead to the development of hyponatremia in cirrhotic patients. Portal hypertension in cirrhosis leads to decreased systemic vascular resistance, which initiates a cascade of events leading to non-osmotic release of AVP. AVP activity leads to excessive water retention and hyponatremia, accompanied by volume overload. Decreased glomerular filtration rate and cardiac function also contribute to hyponatremia in cirrhosis.

Pathophysiology of hyponatremia in renal disease

Hyponatremia commonly occurs in both acute and chronic renal failure, because the kidneys cannot maximally excrete excess ingested or infused water. Hyponatremia is not very common in nephrotic syndrome unless associated with a substantial decrease in glomerular filtration rate (GFR); however, with severe hypoalbuminemia of <2 g/dL, intravascular hypovolemia may occur and lead to the non-osmotic release of AVP and subsequent retention of fluids, resulting in hyponatremia.1

Read a case study of a patient with hyponatremia secondary to decompensated heart failure.

*Vaprisol has not been shown to be effective for the treatment of the signs and symptoms of heart failure and is not approved for this indication. Safety data on use of Vaprisol in these patients is limited. Consider other treatment options.



REFERENCES: 1. Verbalis JG, Goldsmith SR, Greenberg A, Schrier RW, Sterns RH. Hyponatremia treatment guidelines 2007: expert panel recommendations. Am J Med. 2007;120:S1-S21. 2. Greenberg B. Managing hyponatremia in patients with heart failure. J Hosp Med. 2010;5(suppl3):S33-S39. 3. Ross E, Sigal SH. Managing hyponatremia in cirrhosis. J Hosp Med. 2010;5(suppl3):S8-S17.