Magnesium and phosphate relationship

Disorders Involving Calcium, Phosphorus, and Magnesium

magnesium and phosphate relationship

UpToDate, electronic clinical resource tool for physicians and patients that provides information on Adult Primary Care and Internal Medicine, Allergy and. In our presentation we will attempt to explore the relationship between the. Serum Magnesium Tubular Reabsorption Serum Phosphorus Phosphate Depletion. The increase in dialysate magnesium resulted in a decrease in serum PTH, calcium, and phosphate concentration, while a decreased dialysate magnesium .

When body stores of these ions decline significantly, gastrointestinal absorption, bone resorption, and renal tubular reabsorption increase to normalize their levels. Under physiologic conditions, the whole body balance of calcium, phosphate, and magnesium is maintained by fine adjustments of urinary excretion to equal the net intake. This review discusses how calcium, phosphate, and magnesium are handled by the kidneys.

The kidney plays a critical role in regulating serum levels of these ions.

Effect of magnesium on phosphorus and calcium metabolism.

Regulation of calcium, phosphate, and magnesium occurs in different parts of the nephron and involves a number of different channels, transporters, and pathways. Below we describe the mechanisms governing renal control of these ions. Calcium The total amount of calcium in the human body ranges from to g. Serum calcium concentration is held in a very narrow range in both spaces. Calcium serves a vital role in nerve impulse transmission, muscular contraction, blood coagulation, hormone secretion, and intercellular adhesion 12.

Gastrointestinal Absorption of Calcium Calcium balance is tightly regulated by the concerted action of calcium absorption in the intestine, reabsorption in the kidney, and exchange from bone, which are all under the control of the calciotropic hormones that are released upon a demand for calcium Figure 1A.

Likewise, increases in calcium concentration lead to inhibition of PTH synthesis and release. PTH acts on bone and kidney tissue; it stimulates bone turnover, which results in release of calcium into the extracellular fluid. In the renal tubules, PTH stimulates reabsorption of calcium and loss of phosphate ions. PTH actually promotes the final activation step of vitamin D the 1-hydoxylation step in the renal tubular cells.

Calcitonin, released from the parafollicular cells of the thyroid gland in response to high levels of ionized calcium, will decrease calcium resorption from bone.

However, calcitonin does not appear to be physiologically important in humans. Abnormalities in Calcium Concentration Hypercalcemia Link with Hyperparathyroidism This condition is most commonly associated with asymptomatic elevation of total and ionized calcium levels.

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Most cases result from a single parathyroid adenoma. Nephrolithiasis is the most common clinical problem, whereas overt bone disease is uncommon.

PTH concentrations are inappropriately elevated in hyperparathyroidism. In this condition, serum inorganic phosphate levels may be low, and there may be a non—anion gap metabolic acidosis.

Calcium, Magnesium, and Phosphate | Laboratory Medicine | Oxford Academic

Hyperparathyroidism may occur as an isolated disorder; however, it can also herald the presence of multiple endocrine neoplasia MEN syndrome, in the form of variant MEN1 or MEN2.

There are different isoforms of this protein, which is widely expressed in many tissues. HHM is frequently associated with severe hypercalcemia at levels of greater than 13 mg per dL 3. Hypercalcemia due to local malignant lytic effects.

This condition is classically observed in multiple myeloma but may also occur in other hematologic malignant neoplasms. This entity is, therefore, a local osteolytic hypercalcemia. This has been particularly noted in sarcoidosis. It arises as a consequence of a mutation in the calcium-sensing receptor found on parathyroid and renal tubule cells. The condition involves excessive renal reabsorption of calcium, whereas the PTH level may be slightly elevated.

FHH may be mistaken for hyperparathyroidism. Hypocalcemia The most common cause of hypocalcemia is renal failure. Hypocalcemia and hyperphosphatemia are hallmarks of end-stage renal disease, as is an elevated PTH level. The latter represents secondary hyperparathyroidism—the PTH responds to the low amount of calcium in an attempt to elevate the serum concentration. Less common causes of hypocalcemia include the following: Hypoparathyroidism—Acquired hypoparathyroidism may follow surgical removal of or damage to the parathyroid glands during thyroid surgery.

Radiation, infiltrative disorders, or autoimmune disease may also damage the parathyroid glands. Vitamin D deficiency—Classic nutritional rickets follows depletion of vitamin D resulting from nutritional deprivation and poor exposure to sunlight. In the absence of adequate vitamin D, calcium uptake from the gastrointestinal tract is impaired.

PTH concentrations will be high in an attempt to compensate for the inadequate calcium absorption.

magnesium and phosphate relationship

Malabsorption can impair intake of calcium and vitamin D, resulting in a deficiency of both. Acute pancreatitis—The mechanism of this condition is thought to be fat saponification. Hydrolysis of triglycerides by pancreatic enzymes releases fatty acids that form salts with calcium; these salts precipitate in the tissues. Total Calcium General Principals of Current Testing Methods The field method for total serum or plasma calcium depends on reaction with a chelating compound that results in color development that can be measured optically.

For example, calcium reacts with o-cresolphthalein complexone o-CPC under alkaline conditions to form a violet-colored complex that is monitored at nm. The addition of 8-hydroxyquinoline to the reaction prevents interference by magnesium. The latter binds magnesium but not calcium. The reference method for determining total calcium concentration is atomic absorption spectrophotometry. In this technique, the sample is vaporized in an air-acetylene flame. Calcium atoms in the flame specifically absorb light of a particular wavelength from a hollow cathode lamp.

The free-calcium concentration is proportional to the potential difference between the indicator electrode and the reference electrode.

The indicator electrode usually contains a liquid membrane with a calcium-binding agent or calcium ionophore. The calcium ISE has the advantage of producing an accurate result in serum, plasma, or whole blood; it is now a standard component of modern blood-gas analyzers. Free-calcium determinations are critically dependent on pH; therefore, it is extremely important to maintain the original pH of the specimen.

Preanalytical Factors A number of factors change the serum albumin level, leading to an apparent alteration of the total serum calcium concentration. Chief amongst these is hemoconcentration, which produces hyperalbuminemia and an elevation in the level of total calcium.

Hemoconcentration may occur when a tourniquet is placed too tightly for an extended period during phlebotomy. In contrast to what many might expect, blood drawn into sodium citrate tubes 3. Ionized calcium in blood collected in sodium citrate is very low or undetectable. Ionized calcium is pH dependent; in theory, a delay in specimen testing of whole blood or plasma or serum may produce an inaccurate result for several reasons.

In practice, specimens are more stable than one might predict, particularly if they are kept sealed from room air. This can be achieved in a filled syringe or a sealed blood-draw tube. The latter can also be spun to remove the red cells with a plasma separator or serum separator tube.

Centrifuged serum specimens remain highly stable for several hours.

magnesium and phosphate relationship

This can be prevented by not using excessive amounts of heparin or by using calcium-titrated heparin. Magnesium Overview of the Analyte Of all the cations in the body, magnesium is the fourth most prevalent and the second most abundant intracellularly. Physiologically, magnesium acts as a cofactor for more than enzymes, not only complexing with ATP to form enzyme substrates but also acting as an allosteric activator. It plays a role in numerous important regulatory systems, such as oxidative phosphorylation, replication, protein synthesis, and glycolysis.

Magnesium is required for guanosine triphosphate GTP —coupled receptor signaling and is also important in controlling neuronal conduction. It acts as a competitive inhibitor to calcium, preventing calcium entry into the presynaptic nerve and thus inhibiting the release of neurotransmitters. Thus, it is apparent that a deficiency in magnesium can lead to numerous metabolic and nervous-system pathologic manifestations. Clinical Significance Disorders involving magnesium are categorized into 2 groups, namely, hypomagnesemia and hypermagnesemia.

Although magnesium loss can occur through vomiting or nasogastric suction, its occurrence is usually due to magnesium wasting in the gastrointestinal GI tract from diarrhea or in the kidneys from various renal pathologic manifestations.

Thus, diseases of the lower GI tract are commonly complicated by hypomagnesemia. Renal etiologies for magnesium loss include hypercalcemia; alcohol; drugs such as aminoglycosides, diuretics, and cyclosporine; metabolic acidosis; and renal diseases such as nephritis and renal tubular acidosis. Due to the numerous ways that magnesium deficiency can occur, it can be difficult to detect when a patient develops this deficiency because the primary disease may mask or be complicated by the deficiency itself.

An example of this phenomenon is the effect of magnesium on PTH secretion.

  • Disorders Involving Calcium, Phosphorus, and Magnesium
  • Renal Control of Calcium, Phosphate, and Magnesium Homeostasis

When a deficiency in magnesium occurs, it impedes PTH secretion and also causes the bones and kidneys to become resistant to signaling effects from PTH. Thus, the cause of osteoporosis in patients who have magnesium deficiency could be misdiagnosed if the treating physician and other health care staff fail to notice this condition.

Another example of the effects of magnesium deficiency causing serious complications in patient care is cardiac arrhythmia. Intracellular losses of potassium and hypokalemia as an effect of renal wasting due to magnesium deficiency may be culpable for atrial and ventricular tachycardia and fibrillation.