How Disease States Affect the Function of Sodium in the Body

High sodium intake is associated with various disease conditions such as hypertension, cardiovascular disease (Erdem et al., 2010; Strazzullo, Campanozzi, & Avallone, 2012), and kidney disease (Wright & Cavanaugh, 2010). In kidney disease, high sodium intake is associated with renal injury, the potential mechanisms of such injury being proposed to arise either via direct or indirect sodium activity (Wright & Cavanaugh, 2010). In the indirect pathway, the high plasma sodium levels are associated with hypertension and proteinuria, which are proposed to mediate vascular and renal injury (Erdem et al., 2010; Wright & Cavanaugh, 2010). A direct impact of high sodium intake, independent of the hypertension pathway, is proposed to be via increased oxidative stress in the kidney due to sodium-mediated increase in reactive oxygen species (ROS; TGFb1 and nitric oxide) (Wright & Cavanaugh, 2010).

Another example of indirect, sodium-mediated renal injury is proposed to result from the inhibition of Na/K-pump by ouabain within the kidney’s epithelial cells. Such inhibition is proposed to reduce the threshold needed to activate transcription factor NF-Kβ, which has a regulatory role on the expression of genes that function in apoptosis (cell death) and inflammation, by increasing frequency of calcium oscillations (Wright & Cavanaugh, 2010). Similarly, impairment in renal excretion of sodium due to altered activity of Na/K-pump in the kidney epithelial cells is suggested to mediate hypertension and CVD, independently of the NF-Kβ-mediated model (Cook et al., 2009).  To manage such kidney diseases, a nutritional approach would be to lower sodium intake and, in addition, recommend diuretics in severe cases (Ritz & Mehls, 2009).

Food Sources of Sodium and Toxicity

Sodium is found in many foods as sodium chloride (Nacl), common salt (Gropper, Smith, & Groff, 2009, p. 452), but also as sodium bicarbonate (baking soda; leavening agent) and sodium glutamate (flavor enhancer) in processed foods. The USDA national nutrient database for standard reference (2012) provides a wide spectrum of sodium-containing foods including alcoholic beverages, fruits (e.g. apples, bananas, apricot, and avocado), cereals, meat, vegetables (e.g. broccoli and cabbage) and a wide range of processed foods.  Comparing such standards with manufacturer/ restaurant- provided data, Champagne and Lastor (2009) report wide variations in sodium-composition thus recommending the need to monitor sodium content regularly for one to adhere to the recommended daily consumption amount.

Sodium toxicity, hypernatremia, could occur when its concentration in the serum exceeds 145 mmol/L (Lindner & Funk, 2013). In description, the sodium serum concentration, [Na+], as envisaged by Edelman equation (cited by Lindner & Funk, 2013, p. 216.e11), is the ratio of the total exchangeable sodium and potassium in the body, to total body water. As such, hypernatremia could result from increased intake of sodium, excessive loss of water from the body, or occurrence of both conditions. In health individuals, the decline in water leads to the activation of a physiological defense mechanism, thirst, to spur individuals into taking corrective action (Lindner & Funk, 2013). In the critically ill, who may not have the strength to drink water on their own, hypernatremia threat becomes more likely (Lindner & Funk, 2013).

Sodium plays critical roles in the body in the regulation of body fluid, nerve impulse conduction and muscle contraction which are ensured through the absorption mechanisms in the small intestines and sodium that involve both passive and active mechanisms. However, at high doses, sodium becomes a potential source of hypertension, CVD and kidney disease. When present in the body at very high concentrations (145 mmol/L), sodium toxicity could result, whose outcome could be fatal.

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