What Causes Low Sodium And Potassium Levels In The Elderly – Salt (sodium chloride) is essential for life. Total body sodium in an average 70-kg person is about 4,200 mmol (~100 g), of which 40% is found in bone and 60% in the fluid inside and outside cells (1 ). Total body chloride averages 2, 310 mmol (~ 82 g), of which 70% is distributed in the extracellular fluid and the rest is found in connective tissue collagen (1). Multiple mechanisms work together to tightly regulate the body’s sodium and chloride concentrations. Although this review emphasizes the function and requirements of sodium, sodium and chloride ions work together to control extracellular volume and blood pressure (1).

) are the main ions in the extracellular compartment, which includes blood plasma, interstitial fluid (fluid between cells), and transitional fluid (eg, cerebrospinal fluid, joint fluids). Therefore, they play a vital role in various life-sustaining processes.

What Causes Low Sodium And Potassium Levels In The Elderly

Sodium and chloride are electrolytes that contribute to the maintenance of concentration and charge differences across cell membranes. potassium (K

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) is the main positively charged ion (cation) inside cells, while sodium is the main cation in the extracellular fluid. Potassium concentrations are about 30 times higher inside than outside cells, and sodium concentrations are more than 10 times lower inside than outside cells. The concentration differences between potassium and sodium across cell membranes create an electrochemical gradient called membrane potential. The cell membrane potential is maintained by ion pumps in the cell membrane, especially the Na

ATPase pumps. These pumps use ATP (energy) to pump sodium out of the cell in exchange for potassium (Figure 1). Their activity is estimated to account for 20%-40% of the resting energy expenditure in a typical adult. The large proportion of energy devoted to maintaining sodium/potassium gradients emphasizes the importance of this function in sustaining life. Tight control of cell membrane potential is essential for nerve impulse transmission, muscle contraction, and cardiac function (2-4).

Sodium absorption in the small intestine plays an important role in the absorption of chloride, amino acids, glucose, and water. Similar mechanisms are involved in reabsorbing these nutrients after they have been filtered from the blood by the kidneys. Chloride, in the form of hydrochloric acid (HCl), is also an important component of gastric juice, which aids in digestion and absorption of many nutrients (5).

Because sodium is the primary determinant of extracellular fluid volume, including blood volume, several physiological mechanisms that regulate blood volume and blood pressure work by altering sodium content. of the group. In the circulatory system, pressure receptors (baroreceptors) sense changes in blood pressure and send excitatory or inhibitory signals to the nervous system and/or endocrine glands to influence sodium regulation by the kidneys. In general, sodium retention leads to water retention, and sodium loss means water loss (6). Below are descriptions of three mechanisms that contribute to a larger multifactorial homeostatic control system that regulates blood volume and blood pressure through the regulation of sodium balance. These regulatory mechanisms are particularly important for controlling sodium transport in various parts of the nephron (the basic structural unit of the kidney), including the proximal and distal convoluted tubules, the thick limb of the loop of Henle, and the collection duct.

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In response to a significant decrease in blood volume or pressure (eg, severe blood loss or dehydration), the kidneys release renin into the circulation. Renin is an enzyme that cleaves a small peptide (angiotensin I) from a larger protein (angiotensinogen) produced by the liver. Angiotensin I is split into a smaller peptide (angiotensin II) by angiotensin-converting enzyme (ACE), an enzyme present on the inner surface of blood vessels and in the lungs, liver and kidneys. Angiotensin II stimulates the narrowing of small arteries, resulting in increased blood pressure. Angiotensin II is also a strong stimulator of aldosterone synthesis by the adrenal glands. Aldosterone is a steroid hormone that acts on the kidneys to increase sodium reabsorption and potassium excretion. Sodium retention by the kidneys increases water retention, resulting in more blood and blood pressure (7).

Secretion of anti-diuretic hormone (ADH; also known as arginine vasopressin [AVP]) by the posterior pituitary gland is stimulated by a significant reduction in blood volume or pressure. In conjunction with the renin-angiotensin-aldosterone system, ADH stimulates epithelial sodium channels (ENaC) in the apical cell membrane along distal nephron renal tubules to increase sodium and water reabsorption (8) .

Dopamine is produced from L-DOPA in the renal proximal tubules and acts on dopamine receptors distributed throughout the proximal tubules and thick limb of the loop of Henle to regulate sodium transport. Dopamine stimulates sodium excretion (natriuresis) by inhibiting the Na

ATPase is enhanced by the natriuretic hormone, atrial natriuretic peptide (ANP), which is secreted by cardiac muscle cells into the circulation (9).

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]) <136 mmol/liter (mM), may be due to increased sodium retention (impaired hyponatremia) or increased sodium loss. Inadequate sodium intake rarely causes hyponatremia, even in those on a very low-salt diet, because the kidneys increase water excretion to maintain serum osmolality (ie, electrolyte balance- water). The results of the 1999-2004 US National Health and Nutrition Examination Survey (NHANES) indicated an overall prevalence of hyponatremia of 1.9% in a representative US population sample of 14,697 participants aged 18 and older (10). Hyponatremia was found to be more common in older people (3.1% in those aged 65 to 84 years) and in those suffering from hypertension (2.9%), diabetes mellitus (3.3%), coronary heart disease (CHD; 2.6%), stroke (3.6%), chronic obstructive pulmonary disease (COPD; 3.9%), cancer (3.4%), and psychiatric disorders (2.9% ) (10). Hyponatremia is also common in hospitalized patients, with approximately 15%-30% having mild hyponatremia (serum [Na

Dilutional hyponatremia may result from inappropriate secretion of anti-diuretic hormone (ADH), which is associated with disorders affecting the central nervous system, and by ‘ the use of certain drugs (see Drug Interactions). In some cases, excessive water intake can lead to mild hyponatremia (see also exercise-related hyponatremia). Conditions that increase sodium and chloride loss include severe or prolonged vomiting or diarrhea, chronic excessive sweating, use of certain diuretics, and certain types of kidney disease. Excessive restriction of dietary sodium intake in renal patients with hypertension and congestive heart failure may also cause chronic body depletion of sodium (1).

Exercise-associated hyponatremia (EAH) is a mild hyponatremia that occurs in individuals who compete in endurance (up to 6 h in duration) and ultra-endurance exercise events (> 6 h) in length), such as marathons, Ironman triathlons, mountain bike races, walkers. trails, and open water cross-distance swimming events. Of note, symptomatic EAH has been increasingly reported in shorter events, such as half marathons and sprint triathlons. The development of hyponatremia during or up to 24 h after intense and/or sustained physical activity has been linked to fluid overload due to excessive water intake, urinary water deficit due to continuous ADH secretion, and very low ambient temperature or very high (12). ). Risk factors include preexercise hyperhydration, use of nonsteroidal anti-inflammatory drugs (NSAIDs), and prolonged exercise (>4 h) (reviewed in 12).

Symptoms of hyponatremia include headache, nausea, vomiting, muscle cramps, fatigue, indigestion, and fainting. Complications of severe and rapidly developing hyponatremia can include cerebral edema (swelling of the brain), seizures, coma, and brain damage. Acute or severe hyponatremia can be fatal without prompt and appropriate medical treatment (13).

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Chronic mild hyponatremia has been associated with deficits in movement and attention, falls, and bone loss and fractures, especially in women and the elderly (14, 15). A recent 11-year cohort study in more than 3,000 men free of cardiovascular disease (CVD) also reported significantly higher risks of stroke, coronary heart disease, total CVD events, CVD-related mortality, and all-cause mortality in participants with moderate to severe hyponatremia (serum [Na

] between 139 mM and 144 mM (16). Furthermore, in a meta-analysis of 81 observational studies in patients with diverse medical conditions (including cardiovascular disease, lung disease, and cirrhosis), the mortality risk was found to be nearly threefold. times greater in hyponatremic compared to normonatremic subjects (17). ). Development or normalization of serum [Na

] in hyponatremic subjects associated with a reduced mortality rate in patients with various clinical conditions (18).

In 2019, the Food and Nutrition Board (FNB) of the National Academy of Medicine revised the dietary reference intakes (DRIs) for sodium (20). The FNB did not find sufficient evidence to determine an Estimated Average Requirement (EAR) and receive a Recommended Redemption Allowance (RDA). Instead, they established an acceptable intake (AI) for sodium (Table 2; 20). Considerations reported by the FNB for establishing an AI for sodium included that the available evidence was insufficient to identify adverse health effects associated with low dietary sodium intake and that there is substantial evidence that suggests long-term health benefits may be associated with reducing sodium intake below normal. 2, 300 mg/day (see Reducing the Risk of Chronic Disease for sodium). The AI ​​could not be derived from the average dietary intake of people in the US because average intake levels are well above 2,300 mg/day (see Sources).

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Most of the sodium and chloride in the

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