Disorders Involving Calcium, Phosphorus, and Magnesium
The protein-bound form of calcium accounts for approximately 40% of total serum calcium, of which 80% is bound to albumin and the remaining. As you can see from the above discussion, calcium and phosphorus have an inverse relationship: when calcium levels increase, phosphorus levels decrease, . the following 4 key components: serum calcium, serum phosphate, A prospective cohort study by Vaidya indicated that a connection exists.
A buildup of these deposits causes calcification in the tissue, which can disrupt normal organ function. People with chronic kidney disease should work closely with their dietitian and doctor to control phosphorus, calcium and parathyroid levels. Bone Health About 85 percent of the body's phosphorus and 99 percent of calcium are found in the bones. People with impaired kidney function are at greater risk for bone disease because they are more likely to have high phosphorus and PTH levels, which can lead to progressive bone loss.
According to the Linus Pauling Institute, there is increasing concern for the effect of a high intake of phosphorus even in healthy individuals due to its possible impact on bone health.
There was a problem providing the content you requested
Excessive consumption of foods with phosphorus additives and a low calcium intake seem to be especially harmful. Calcium and Phosphorus in Food Calcium and phosphorus levels are controlled in part through dietary intake. The Food and Nutrition Board set the recommended dietary allowance of phosphorus at milligrams daily.
General Principals of Current Testing Methods Although spectrophotometry is the typical method of choice for measuring serum magnesium levels, numerous techniques have been implemented over the years, such as fluorometry, atomic absorption spectrometry, and flame emission spectroscopy. The dyes and indicators used to measure magnesium are metallochromic, selectively binding magnesium; several are used routinely in laboratories.
Calmagite, magon, methylthymol blue and xylidyl blue complex with magnesium are used in alkaline conditions and are measured at nm for calmagite and nm for each of the others.
Ethylene glycol tetraacetic acid EGTA is commonly used in conjunction with these indicators to chelate calcium; this effectively reduces interference, which can lead to overestimation. Enzymes using magnesium—adenosine triphosphate ATPsuch as hexokinase, have also been used to measure serum magnesium levels. The rate of the reaction directly depends on the concentration of magnesium, and the formation of nicotinamide adenine dinucleotide phosphate NADPH is measured at nm when the reaction is coupled with glucosephosphate dehydrogenase.
Alternatively, a less complex enzymatic reaction that uses isocitrate has also been developed, which produces NADPH directly on activation by magnesium.
As discussed previously herein, hypomagnesemia, or magnesium deficiency, is prevalent in hospitalized patients; also, magnesium is administered in a variety of different diseased states. Thus, monitoring the free, or ionized, magnesium level of a patient is important in preventing life-threatening complications that can occur due to low or high levels of magnesium; free magnesium levels can be measured using ISEs.
The electrodes are neutral carriers, binding calcium and magnesium nonselectively. Thus, to accurately quantify magnesium concentration, one should also quantitate calcium and correctly adjust its interference to reflect an accurately measured magnesium value. Also, the binding of magnesium to the ionophore is pH dependent; hence, pH should be measured simultaneously. Reference intervals for free magnesium are instrument dependent. Serum and heparinized plasma are acceptable specimens for measuring magnesium levels.
Newer formulations of heparins for determining free calcium concentrations should be avoided because they falsely elevate the free-magnesium concentration. Also, anticoagulants that chelate calcium, such as EDTA, citrate, and oxalate, form complexes with magnesium; thus, they are also unacceptable for use in this context.
Hemolysis greatly affects magnesium levels in serum and plasma, whereas lipemic or icteric specimens may or may not affect measured magnesium levels, depending on the assay used. Collected urine specimens are to be held for 24 hours, in 20 to 30 mL of 6 M HCl, to prevent the precipitation of magnesium.
Before analysis, the container must be warmed and its contents acidified and mixed well before an aliquot is removed for measurement of magnesium levels. Plasma concentrations of magnesium do not correlate well with total body magnesium; thus, serum is the preferred specimen type to detect magnesium deficiency. Also, normal serum-magnesium values do not consistently reflect intracellular levels; thus, intracellular magnesium levels also can be measured, to determine whether true deficiency exists.
Clinical symptoms of true magnesium deficiency, such as hypocalcemia or kalemia, neuromuscular hyperactivity, and cardiac arrhythmias, should be assessed in conjunction with the results of these tests in making a final diagnosis. When comparing free- and total-magnesium measurements, it is important to note the health of the patient.
Conflicting results between free and total magnesium levels have been observed in patients with cardiovascular disease, diabetes mellitus, alcoholism, and other conditions, as well as in pregnancy.
The assay is also prone to interference with substances such as thiocyanates in tobacco smokers. Therefore, it is important to review patient history before acting on an abnormal magnesium result, to rule out preanalytical variables.
Phosphate Overview of Analyte Phosphate plays an important role in structural support and soft tissue. It is the major component of hydroxyapatite in bone, whereas the phosphate found in soft tissue is cellular in nature. Although phosphate can be found in organic and inorganic forms, only levels of the inorganic form can be measured in the clinical laboratory.
Phosphate plays important roles in the body; organic phosphate is one of the building blocks of DNA, phospholipids, and high-energy compounds such as ATP. Phosphate is regulated by fibroblast growth factor—23 and is secreted by osteoclasts and osteoblasts in the bone in response to levels of serum phosphate and 1,dihydroxyvitamin D.
Clinical Significance Hypophosphatemia is defined as a serum- or plasma-measured phosphate level below the reference interval, usually 2. Decreased intestinal absorption is usually caused by ingestion of antacids that contain aluminum or magnesium. These analytes bind phosphate that has been ingested and secreted; as a result, the analytes form insoluble salts that the body cannot resorb.
Inadequate intake can also cause hypophosphatemia but is rarely the reason for decreased phosphate levels. Chronic diarrhea and renal phosphate wasting can also cause hypophosphatemia.
Calcium, Magnesium, and Phosphate | Laboratory Medicine | Oxford Academic
In the latter case, phosphate wasting is observed as a result of an increase in PTH levels, such as in primary or secondary hyperparathyroidism. The movement of phosphate into intracellular spaces is the most common cause of hypophosphatemia and can be motivated by multiple different situations.
Insulin stimulation causes glucose and phosphate to shift into the cells. This phenomenon is most severe in patients with underlying hypophosphatemia and in malnourished individuals. Acute respiratory alkalosis can also shift phosphate into cells by inducing glycolysis.
There are 3 main circumstances in which this occurs: The most common cause is decreased renal phosphate excretion, which can occur due to renal failure, hypoparathyroidism, or PTH resistance. In renal failure, the decrease is typically observed due to a decrease in the glomerular filtration rate.
The Balance of Calcium & Phosphorus
Hyperphosphatemia due to hypoparathyroidism or PTH resistance results in increased phosphate reabsorption, as PTH modulates phosphate tubular reabsorption. Also, acromegaly, bisphosphonates, and vitamin D toxicity can also cause increased tubular reabsorption and hyperphosphatemia. An increase in the phosphate load can also cause hyperphosphatemia, whether from an exogenous source, such as phosphate administration, or an endogenous source, as observed in rhabdomyolysis or tumor lysis syndrome.
Preventing hypercalcemia and hypocalcemia is largely the result of robust endocrine control systems. Body Distribution of Calcium and Phosphate There are three major pools of calcium in the body: A large majority of calcium within cells is sequestered in mitochondria and endoplasmic reticulum.
Intracellular free calcium concentrations fluctuate greatly, from roughly nM to greater than 1 uM, due to release from cellular stores or influx from extracellular fluid. These fluctuations are integral to calcium's role in intracellular signaling, enzyme activation and muscle contractions. Calcium in blood and extracellular fluid: Roughly half of the calcium in blood is bound to proteins. The concentration of ionized calcium in this compartment is normally almost invariant at approximately 1 mM, or 10, times the basal concentration of free calcium within cells.
Also, the concentration of phosphorus in blood is essentially identical to that of calcium. A vast majority of body calcium is in bone.
The remainder of body phosphate is present in a variety of inorganic and organic compounds distributed within both intracellular and extracellular compartments. Normal blood concentrations of phosphate are very similar to calcium. Fluxes of Calcium and Phosphate Maintaining constant concentrations of calcium in blood requires frequent adjustments, which can be described as fluxes of calcium between blood and other body compartments.
Three organs participate in supplying calcium to blood and removing it from blood when necessary: The small intestine is the site where dietary calcium is absorbed.