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Last updated: 11/24/2009
Sodium is the principal extracellular cation and potassium the principal intracellular cation. A cation is an ion with a positive charge. An anion is an ion with a negative charge. Sodium levels are directly related to the osmotic pressure of the plasma....
In fact, since an anion is always associated with sodium (usually chloride or bicarbonate), the plasma osmolality (total dissolved solute concentration) can be estimated. Since water will often follow sodium by diffusion, loss of sodium leads to dehydration and retention of sodium leads to edema. Conditions that promote increased sodium, called hypernatremia, do so without promoting an equivalent gain in water. Such conditions include diabetes insipidus (water loss by the kidneys), Cushing's disease, and hyperaldosteronism (increased sodium reabsorption). Many other conditions, such as congestive heart failure, cirrhosis of the liver, and renal disease result in renal retention of sodium, but an equivalent amount of water is retained as well. This results in a condition called total body sodium excess, which causes hypertension and edema, but not an elevated serum sodium concentration. Low serum sodium, called hyponatremia, may result from Addison's disease, excessive diuretic therapy, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), burns, diarrhea, vomiting, and cystic fibrosis. In fact, the diagnosis of cystic fibrosis is made by demonstrating an elevated chloride concentration (greater than 60 mmol/l) in sweat.
Potassium is the electrolyte used as a hallmark sign of renal failure. Like sodium, potassium is freely filtered by the kidney. However, in the distal tubule sodium is reabsorbed and potassium is secreted. In renal failure, the combination of decreased filtration and decreased secretion combine to cause increased plasma potassium. Hyperkalemia is the most significant and life-threatening complication of renal failure. Hyperkalemia is also commonly caused by hemolytic anemia (release from hemolysed red blood cells), diabetes insipidus, Addison's disease, and digitalis toxicity. Frequent causes of low serum potassium include alkalosis, diarrhea and vomiting, excessive use of thiazide diuretics, Cushing's disease, intravenous fluid administration, and SIADH.
Calcium and phosphorus are measured together because they are both likely to be abnormal in bone and parathyroid disease states. Parathyroid hormone causes resorption of these minerals from bone. However, it promotes intestinal absorption and renal reabsorption of calcium and renal excretion of phosphorus. In hyperparathyroidism, serum calcium will be increased and phosphorus will be decreased. In hypoparathyroidism and renal disease, serum calcium will be low but phosphorus will be high. In vitamin D dependent rickets (VDDR), both calcium and phosphorus will be low; however, calcium is normal while phosphorus is low in vitamin D resistant rickets (VDRR). Differential diagnosis of an abnormal serum calcium is aided by the measurement of ionized calcium (i.e., calcium not bound by protein). Approximately 45% of the calcium in blood is bound to protein, 45% is ionized, and 10% is complexed to anions in the form of undissociated salts. Only the ionized calcium is physiologically active, and the level of ionized calcium is regulated by parathyroid hormone (PTH) via negative feedback (high ionized calcium inhibits secretion of PTH). While hypoparathyroidism, VDDR, renal failure, hypoalbuminemia, hypovitaminosis D, and other conditions may cause low total calcium, only hypoparathyroidism (and alkalosis) will result in low ionized calcium. Conversely, while hyperparathyroidism, malignancies (those that secrete parathyroid hormone-related protein), multiple myeloma, antacids, hyperproteinemia, dehydration, and hypervitaminosis D cause an elevated total calcium, only hyperparathyroidism, malignancy, and acidosis cause an elevated ionized calcium.
Serum magnesium levels may be increased by hemolytic anemia, renal failure, Addison's disease, hyperparathyroidism, and magnesium-based antacids. Chronic alcoholism is the most common cause of a low serum magnesium owing to poor nutrition. Serum magnesium is also decreased in diarrhea, hypoparathyroidism, pancreatitis, Cushing's disease, and with excessive diuretic use. Low magnesium can be caused by a number of antibiotics and other drugs and by administration of intravenous solutions. Magnesium is needed for secretion of parathyroid hormone, and therefore, a low serum magnesium can induce hypocalcemia. Magnesium deficiency is very common in regions where the water supply does not contain sufficient magnesium salts. Magnesium acts as a calcium channel blocker, and when cellular magnesium is low, high intracellular calcium results. This leads to hypertension, tachycardia, and tetany. Unfortunately serum total magnesium levels do not correlate well with intracellular magnesium levels, and serum measurement is not very sensitive for detecting chronic deficiency because of compensatory contributions from bone. Ionized magnesium levels are better correlated with intracellular levels because the ionized form can move freely between the cells and extracellular fluids.
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Tests that measure the concentration of electrolytes are useful in the emergency room and to obtain clues for the diagnosis of specific diseases. Electrolyte tests are used for diagnosing dietary deficiencies, excess loss of nutrients due to urination, vomiting, and diarrhea, or abnormal shifts in the location of an electrolyte within the body. When an abnormal electrolyte value is detected, the physician may either act to immediately correct the imbalance directly (in the case of an emergency) or run further tests to determine the underlying cause of the abnormal electrolyte value. Electrolyte disturbances can occur with malfunctioning of the kidney (renal failure), infections that produce severe and continual diarrhea or vomiting, drugs that cause loss of electrolytes in the urine (diuretics), poisoning due to accidental consumption of electrolytes, or diseases involving hormones that regulate electrolyte concentrations.
Electrolyte tests are typically conducted on blood plasma or serum, urine, and diarrheal fluids. Electrolytes can be classified in at least five different ways. One way is that some electrolytes tend to exist mostly inside cells, or are intracellular, while others tend to be outside cells, or are extracellular. Potassium, phosphate, and magnesium occur at much greater levels inside the cell than outside, while sodium and chloride occur at much greater levels extracellularly. A second classification distinguishes those electrolytes that participate directly in the transmission of nerve impulses and those that do not. Sodium, potassium, and calcium are the important electrolytes involved in nerve impulses, and disorders affecting them are most closely associated with neurological disorders. A third classification focuses on electrolytes that are able to form a tight union, or complex, with one another. Calcium and phosphate have the greatest tendency to form complexes with each other. Disorders that cause an increase in either plasma calcium or phosphate can result in the deposit of calcium-phosphate crystals in the soft tissues of the body. A fourth classification concerns those electrolytes that influence the acidity or alkalinity of the bloodstream, also known as the pH. The pH of the bloodstream is normally in the range of 7.35-7.45. A decrease below this range is called acidosis, while a pH above this range is called alkalosis. The electrolytes most closely associated with the pH of the bloodstream are bicarbonate, chloride, and phosphate.
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In 2000, the estimated number of hospital admissions among adults aged 18 or older with urinary incontinence listed as a diagnosis was of 47,802 hospital stays (1,332 men; 46,470 women).
From: NKUDIC
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