January 10th, 2018
Nutritional Overview of Sodium and Effect of Kidney Disease State
Continued high consumption of sodium has been a cause of concern due to the adverse outcomes attributed to such high intake. In the U.S, the National Health and Nutrition Examination Survey (NHANES) in its 2005-2006 and 2009-2010 versions indicated that the average sodium consumption in America remains above the recommended daily amounts of 2.3 grams (Wright & Cavanaugh, 2010, p. 415; U.S. Department of Agriculture, Agriculture Research Service [USDA], 2012). Such high intake of sodium is associated with various adverse outcomes, despite sodium being an important mineral in the regulation of body fluid volume.
Composition and chemical structure
Sodium (Na) is an alkali metal, which was discovered in 1807 by an English chemist named Humphry Darvy (Halka, 2010). Since Na has only one electron in its outermost energy level, with the electron configuration of [Ne]3S1 (Halka, 2010, p. 17), it readily donates the lone electron to an electron acceptor such as chlorine to form a stable compound. The active form of sodium nutrient is the cation (Na+), which functions in enzymes such as Na+/K+– ATPase (the sodium-potassium pump; Salyer et al., 2013; Weigand, Swarts, Fedosova, Russel, & Koenderink, 2012).
Digestion, Absorption and Metabolism
Sodium is ingested as part of human diet in various forms with at least 95 per cent being absorbed and the remaining percent being excreted principally via urine (Gropper, Smith, & Groff, 2009, p. 452). Absorption-mechanisms involve active and passive means. The first means of absorption, Na+/glucose co-transport system, is advanced to take place throughout the small intestines (Gropper et al., 2009, p. 452) and involves the binding of sodium on the extracellular surface of the transporter protein (SGLT) to expose the sugar-binding site (Wright, Loo, & Hirayama, 2011, p. 737). Once bound, the sugar and Na+ are co-transported into the cytoplasm, where they are released and the SGLT re-conforms to expose the Na+ binding site (Wright et al., 2011, p. 737). The Na released into the cytoplasm is transported back to the extracellular surface via the action of the Na/K- pump in an energy-consuming process (Gropper et al., 2009, p. 452).
A second mode of Na absorption is a Na+ and Cl– co-transport system advanced to operate in the small intestines and the proximal colon sites (Gropper et al., 2009, p. 452). The neutral absorption of Nacl is proposed to proceed through a coupled exchange of Na+ for H+ and Cl‑ for HCO3– (Manoharan et al., 2013; Gropper et al. 2009, p. 452). Once into the cell, the Na+ is extruded via the activity of Na/K- pump, with Cl‑ transfer across the basolateral membrane occurring thereafter through diffusion (Gropper et al. 2009, p. 452). The H+ and HCO3– used in this process arise from intracellular carbonic anhydrase activity (Gropper et al. 2009, p. 452). The presence of short-chain fatty acids (except for acetate) in the colon, has been shown to stimulate this type of absorption without the metabolism of the short-chain fatty acids (to provide energy for the epithelial cells) or carbonic anhydrase activity (to provide intracellular H+ and HCO3–) (Zaharia et al., 2001).
A third pathway is proposed to function in the colon due to an electron gradient that allows Na transport via amiloride-sensitive Na+ channels (Horisberger, 2000). Lower concentrations of Na+ in the intracellular space that facilitate a favorable gradient for absorption of sodium result from Na/K- pump activity. To avert the back-leak of the Na+ through the Na channels, the epithelia cells are linked via tight junctions characterized by low ionic permeability (Horisberger, 2000). As such, the transport of Na+ back has to involve the active mechanism provided by Na, K-pump.
Sodium occurs in widespread sites in the body but the main reservoir is in blood. Sodium plasma levels are sustained through the actions of hormones such as vasopressin, aldosterone, atrial natriuretic hormone, renin, and angiotensin II (Gropper et al. 2009, p.453). The renin-angiotensin mechanism plays a core role in maintaining blood pressure by producing of angiotensin II, which induces the secretion of aldosterone, facilitates vascular constriction, and regulates expression of genes that code for proteins involved in the reabsorption process in the kidney tubules (Quiroz-Leite, Peruzzetto, Neri, & Reboucas, 2011).
The tests for sodium levels in the body involve analysis of electrolytes in blood and urine samples using ion selective electrodes (ISE), either in direct or indirect ISE technology (Dimeski & Barnett, 2005). Direct ISE is the measurement of electrolytes in undiluted samples such as plasma blood component and serum, usually used with analyzers at the point-of-care testing (Dimeski & Barnett, 2005). Indirect ISE assesses analytes in samples diluted with a solvent of a specified ionic strength (Dimeski & Barnett, 2005). In a case presentation, Dhatt, Talor and Kazory (2012) report that use of indirect ISE could lead to underreporting of serum sodium levels in patients with a reduced plasma water phase due to increased solid component. In the case, measurement with direct ISE corrected for such underestimates (Dhatt, Talor, & Kazory, 2012). Accordingly, the authors of the case advice the use of direct ISE to assess plasma sodium where an evaluation of serum osmolality in patients indicated with low serum sodium concentrations indicate presence of an osmolal gap (difference between measured and calculated serum osmolarity). Further analysis of sodium concentrations in urine can provide diagnostic information such as elucidating the different causes of low urine output (Phillips et al., 2007). In such assays, sodium concentration can be assessed in undiluted urine samples via ISE following the removal of lipophilic interfering compounds via “solvent-solvent extraction, membrane-immobilized solvent extraction and solid phase extraction” (Phillips et al., 2007, p. 258).
Sodium functions in the body to maintain the balance between water and electrolytes. This occurs through various mechanisms including the absorption processes in the small intestines and the colon (Salyer et al., 2013; Weigand et al., 2012), and the re-absorption in the kidney tubules through the rennin-angiotensin-mediated process (Quiroz-Leite et al., 2011; Salyer et al., 2013). The maintenance of sodium levels also affects muscle contractions and nerve transmission/ impulse conduction through the energy potential generated via the Na/K – pump located in the muscle and nerve cells (Gropper et al. 2009, p.453). Although sodium deficiency rarely occurs due to its presence in many foods, deficiency is associated with nausea, shock, muscle cramps and comma (Gropper et al. 2009, p.453).