Hyponatremia and Mortality
A plasma sodium concentration even slightly outside the normal range is associated with increased mortality; however, deaths from neurological complications of hyponatremia, cerebral edema, and osmotic demyelination are rare.[10,26–29] Taurine and myoinositol, organic osmolytes that many cells lose in response to hyponatremia, are normally protective against oxidative injury. In addition, a low plasma sodium concentration, independent of osmolality, decreases the activity of the vitamin C transporter – an important finding, because ascorbic acid is an essential defense against oxidative stress.[2,17] Prolonged chronic hyponatremia in an animal model results in hypogonadism, increased body fat, decreased muscle mass, and cardiomyopathy. It is unclear whether the increased mortality associated with hyponatremia is an effect of hyponatremia itself, or whether it reflects the underlying disorders that cause hyponatremia. If hyponatremia itself were responsible, a dose-response relationship, with lower serum sodium associated with higher mortality, would be expected. Although this may be true between 135 and 125 mEq/l (levels often associated with severe underlying illness) it does not hold true for lower serum sodium concentrations, which are often drug induced. A large Danish study confirmed that although in-hospital, 30-day, and 1-year mortality rises as the serum sodium falls to 132 mEq/l, there was no further increase in mortality as the serum sodium concentration fell progressively below 132 mEq/l.
Curr Opin Nephrol Hypertens. 2016;25(2):114-119. © 2016 Lippincott Williams & Wilkins