Why phosphate is important

These 12 foods high in phosphorous can help ensure you're getting…. Multiple tests can analyze metabolism. Most need blood drawn, but some can be ordered online and done at home.

Here are 2. This simple, at-home test can introduce you to your metabolic hormones. Health Conditions Discover Plan Connect. How Your Body Uses Phosphorus.

Medically reviewed by Graham Rogers, M. Phosphates Phosphorus in the body Insufficient phosphorus Excess phosphorus Getting phosphorus High-phosphorus foods Low-phosphorus foods Effects on kidneys Supplements and medications Takeaway Share on Pinterest. What is phosphorus? What are phosphates? How phosphorus works in the body. Symptoms of too little phosphorus. Symptoms of too much phosphorus. How to get the right amount of phosphorus.

Foods with high levels of phosphorus. Foods that are low in phosphorus. How phosphorus affects the kidneys. Livshits: Bone mineralization and regulation of phosphate homeostasis. Phosphate is ubiquitous and present in all natural foods. All foods composed of animal or plant cells are rich in phosphate, with the major sources being protein-rich foods and cereal grains.

Milk and its products are the richest sources of phosphate in the diet. Other good sources of phosphate are meat, fish, poultry eggs, and peanuts. Phosphate interacts with several dietary minerals, such as calcium, sodium, and magnesium. For example, an increase in dietary magnesium results in a decrease in phosphate absorption, whereas an adequate luminal concentration of sodium is essential to ensure phosphate absorption. Intestinal phosphorus absorption occurs through both cellular and paracellular pathways.

Phosphate ingested through the diet is absorbed by the epithelium of the small intestine duodenum and jejunum via both a passive diffusional, load-dependent process and an active sodium-dependent process [ 8 ]. While the former depends on the amount of phosphorus in the gut, the latter is increased by 1,25 OH 2 D 3. NaPiIIa and NaPiIIc are primarily expressed in the apical brush border membrane of the renal proximal tubule and are central to the process of renal phosphate reabsorption see below.

NaPiIIb has a low affinity for phosphate, and humans with NaPiIIb-inactivating mutations do not have reduced serum phosphate levels [ 22 ].

Indeed, studies in NaPiIIb null mice have demonstrated that while the transporter has a central role in active intestinal phosphate absorption, its deletion results in a reciprocal increase in the expression of NaPiIIa in the renal proximal tubule and, consequently, the serum phosphate concentration remains normal.

Changes in intestinal phosphate absorption may, therefore, affect renal phosphate handling, perhaps indirectly through alterations in serum phosphate concentration, or possibly through the production of intestinally derived circulating peptides or by FGF or other phosphatonins see below [ 2 ].

Phosphate transport in the intestine. The sodium-dependent phosphate transporters of the NaPi-IIb type are present at the luminal surface of the enterocyte brush border membrane. NaPi-IIb transporters are electrogenic and have high affinity for inorganic phosphate Pi. The phosphate incorporated into the enterocytes by this mechanism is transferred to the circulation by poorly understood mechanisms.

Phosphate absorption also occurs via a sodium-independent process es , such as diffusional movement across the intercellular spaces in the intestine. Adapted from T. Reprinted from www. However, the finding that upregulation of NaPiIIb in response to a low phosphate diet occurs in vitamin D receptor null mice, as well as in 1-OHase-deficient mice suggests that diet-related alterations in intestinal phosphate absorption can occur independently of changes in 1,25 OH 2 D 3 [ 23 , 24 ].

As discussed below, this phenomenon may be explained, at least in part, by changes in circulating levels of FGF, which also affect phosphate transporters in the gut. Crucial to the activity of osteoblasts and osteocytes in the process of matrix mineralization is the maintenance of adequate inorganic phosphorus levels. Inorganic phosphorus is one of the two main ionic components required for hydroxyapatite formation during the mineralization of the extracellular matrix [ 25 ].

The enzymatic activity of alkaline phosphatase is required to generate enough of the free mineral. This enzyme is located at the plasma membrane with its catalytic unit oriented outside. The enzyme cleaves phosphorus from beta-glycerol phosphate, and the free mineral enters the cell via a sodium-dependent phosphate transporter and is maintained intracellularly within a narrow range. In cases of hypophosphatemia, alkaline phosphatase activity rises in order to try to provide more phosphate to the bone cells.

Monitoring the activity of bone-specific alkaline phosphatase may therefore provide more precise information about bone metabolism than can be obtained by measuring total alkaline phosphatase activity.

A function of FGF is to protect the cells from too high levels of phosphorus, which negatively impact osteoblasts and practically result in cell death.

Although numerous observations have shown the association between increased dietary phosphate load and concomitant high serum phosphate, due to either increased intake or decreased clearance as in renal failure and increased production of FGF, the precise mechanism of this association is yet unknown [ 2 , 4 , 7 , 26 ].

The kidney is the major organ involved in the regulation of minute-to-minute phosphate homeostasis. Renal handling of phosphate is regulated by a variety of hormonal and non-hormonal factors along the proximal convoluted and straight tubule of the kidney, including serum PTH, calcium, 1,25 OH 2 D 3 and bicarbonate concentrations, sodium reabsorption, hypercapnia or hypocapnia, dopamine, and serotonin [ 12 ].

There is little phosphate reabsorption in the proximal straight tubule in the presence of PTH. Changes in the urinary excretion of phosphate are almost invariably mirrored by changes in the apical expression of NaPiIIa and NaPiIIc in the proximal tubules [ 2 , 12 ]. Phosphate transport across the renal proximal tubular cell is largely unidirectional and involves uptake across the brush border membrane, translocation across the cell, and efflux at the basolateral membrane.

NaPiIIa has been shown to be localized throughout the proximal tubule S1—S3 segments , with the highest protein levels found in the S1 segment Fig. Border brush membrane expression of NaPiIIa is reduced within minutes in response to PTH [ 27 ] and within 2 h in response to altered dietary phosphate load [ 28 ].

This adaptation occurs through activation of molecular motifs within the protein that are responsible for its endocytosis or exocytosis, together with alterations in protein—protein interactions that stabilize the protein at the brush border membrane [ 29 ]. Phosphate transcellular transport in the proximal tubule.

Phosphate movement from the renal tubule fluid to the peritubular capillary blood indicates that phosphate reabsorption is principally a unidirectional process that proceeds by a transcellular mechanism.

Phosphate enters the tubular cell across the luminal membrane via a saturable, active, and sodium-dependent transport system. Figure is adapted from Naderi and Reilly [ 11 ] and reprinted with permission from Macmillan Publishers.

NaPiIIc protein is highly expressed in rodents during weaning, with levels diminishing with age, and this protein is only present in the S1 segment of the proximal tubule [ 30 ]. Changes in NaPiIIc protein levels in response to dietary phosphate occur over a longer time course than those in NaPiIIa [ 28 ], and the cellular mechanisms of internalization of the transporter are different [ 32 ].

In humans, NaPiIIc might have a larger role in renal phosphate reabsorption, as inactivating mutations in the gene encoding NaPiIIc lead to hypophosphatemic syndromes see below [ 34 ]. Even in the absence of type II transporters, there is still residual renal phosphate reabsorption [ 33 ]. Thus, other phosphate transporters are able to maintain some phosphate reabsorption. PiT2 protein, a member of the SLC20 family and a type III transporter, has been localized in the kidney at the brush border membrane, and its abundance is regulated by dietary phosphate [ 28 ].

Under normal phosphate conditions the protein is restricted to the S1 segment, whereas dietary phosphate restriction induces expression of PiT2 protein in all segments of the proximal tubule.

This type III transporter adapts to dietary phosphate composition more slowly than the type IIa transporters [ 28 ], and the involvement of PiT2 in phosphate uptake can vary with pH, making a modest contribution to renal phosphate reabsorption [ 35 ]. Insulin enhances proximal tubule phosphate reabsorption by stimulating brush—border membrane Na—Pi cotransport and prevents the phosphaturic action of PTH.

Growth hormone stimulates proximal tubule Na—Pi cotransport, an effect that is partially mediated by insulin-like growth factor 1 IGF1. Epidermal growth factor stimulates phosphate reabsorption in perfused proximal tubules, but inhibits phosphate transport in opossum kidney cells. Thyroid hormone increases proximal tubule phosphate reabsorption by specifically enhancing brush—border membrane Na—Pi cotransport. Calcitonin and glucocorticoids inhibit proximal tubule brush—border reabsorption [ 11 , 12 ].

Reduced or increased phosphate intake results in the increased or decreased expression of NaPiIIa, respectively. During periods of rapid growth and development, as in infancy and puberty, a positive phosphate balance is established. At least part of this phenomenon can be attributed to the effect of growth hormone on phosphate reabsorption.

The primary function of PTH is to tightly regulate serum calcium concentration. In this regard, hypocalcemia stimulates the parathyroid glands to produce and release the hormone. PTH also enhances calcium reabsorption in the distal convoluted tubule [ 12 ].

In the bone, PTH stimulates the release of calcium into the extracellular fluid by increasing osteoclastic bone resorption. In addition to its effects on calcium, PTH is one of the best characterized hormonal regulators of plasma phosphate concentration. This effect results from the relatively rapid internalization and subsequent degradation of NaPiIIa and NaPiIIc proteins, a process that in the short term occurs independently of the regulation of the expression of the co-transporters at the transcriptional level.

The end result of the presence of long-standing high PTH concentration in the setting of normal kidney function is a decrease in serum phosphate, which in certain disease conditions may lead to rickets and osteomalacia. Serum Pi level is maintained within a narrow range through a complex interplay between intestinal absorption, exchange with intracellular and bone storage pools, and renal tubular reabsorption.

Pi is abundant in the diet, and intestinal absorption of Pi is efficient and minimally regulated. The kidney is a major regulator of Pi homeostasis and can increase or decrease its Pi reabsorptive capacity to accommodate Pi need. Phosphorus is a mineral found in your bones. Along with calcium, phosphorus is needed to build strong healthy bones, as well as, keeping other parts of your body healthy. Normal working kidneys can remove extra phosphorus in your blood.

When you have chronic kidney disease CKD , your kidneys cannot remove phosphorus very well. High phosphorus levels can cause damage to your body. Extra phosphorus causes body changes that pull calcium out of your bones, making them weak.

High phosphorus and calcium levels also lead to dangerous calcium deposits in blood vessels, lungs, eyes, and heart. Over time this can lead to increased risk of heart attack, stroke or death. Phosphorus and calcium control are very important for your overall health.

A normal phosphorus level is 2. Ask your kidney doctor or dietitian what your last phosphorus level was and write it down to help keep track of it.