Why phosphate

These studies raised the question as to whether normalization of serum calcium, phosphate, or both is required to prevent the rachitic phenotype [ 48 , 49 ]. The apoptosis of epiphyseal chondrocytes is multifactorial and both provides a mechanism for the removal of terminally differentiated cells from cartilage columns and promotes invasion of the vascular elements of bone marrow, for the generation of new bone [ 9 ].

This apoptosis process is defective in rickets, and the availability of phosphorus is essential for proper apoptosis of the terminal hypertrophic cell. The observation that inhibition of phosphate transport prevents phosphate-mediated apoptosis in hypertrophic chondrocytes [ 25 ] further reinforces the notion that circulating phosphate, rather than the presence of local mineralized matrix, is a key determinant of hypertrophic chondrocyte apoptosis [ 50 ].

The prevention of rickets in patients with VDR mutations and in VDR knock-out mice administered high amounts of dietary calcium demonstrates that neither vitamin D nor the VDR is required for normal growth plate maturation and that rickets develops due to impaired mineral ion homeostasis [ 9 ].

Furthermore, apoptosis in VDR null mice was rescued by restoring phosphorus serum levels without any correction of serum calcium levels [ 9 ]. Prior to treatment, hypophosphatemia was associated with a decrease in the number of apoptotic hypertrophic chondrocytes and expansion of the growth plate, indicating that the histological findings observed are not unique to VDR null mice, but rather a general phenomenon coincident with hypophosphatemia [ 47 ].

It is important to remember that in addition to the growth plate, the rest of the skeleton is also affected by hypophosphatemia, resulting in osteomalacia, i. In the child, both rickets and osteomalacia will be manifested, whereas the adult will have only osteomalacia. Thus, craniotabes in the infant, bowed legs in the older child, and bone pain and fractures in the adult are all clinical manifestations of osteomalacia.

Whereas for many generations physicians were taught to think of rickets as a calcium disorder, evidence in recent years points to phosphate as the main culprit. The presence of phosphate is crucial for bone growth and mineralization and in its absence in sufficient amounts, rickets and osteomalacia will develop. The maintenance of optimal phosphate balance is managed by complex interactions between the gut, kidney, and bone, involving multiple regulators.

Future studies will hopefully provide additional insight into phosphate homeostasis. National Center for Biotechnology Information , U. Pediatric Nephrology Berlin, Germany. Pediatr Nephrol. Published online May 3. Maria Goretti M. Penido 1 and Uri S. Alon 2. Uri S. Author information Article notes Copyright and License information Disclaimer. Corresponding author. This article has been corrected. See Pediatr Nephrol. This article has been cited by other articles in PMC. Abstract Phosphate is one of the most abundant minerals in the body, and its serum levels are regulated by a complex set of processes occurring in the intestine, skeleton, and kidneys.

Introduction Maintaining physiological phosphate balance is of crucial biological importance for bone health. Phosphate homeostasis Phosphorus is an essential element and plays an important role in multiple biological processes [ 10 ].

Open in a separate window. The gastrointestinal—bone—renal axis Intestinal phosphate absorption Phosphate is ubiquitous and present in all natural foods. Bone Crucial to the activity of osteoblasts and osteocytes in the process of matrix mineralization is the maintenance of adequate inorganic phosphorus levels. Renal phosphate reabsorption The kidney is the major organ involved in the regulation of minute-to-minute phosphate homeostasis. Hormones involved in phosphate homeostasis Parathyroid hormone The primary function of PTH is to tightly regulate serum calcium concentration.

Fibroblast growth factor The phosphatonins are a group of proteins that have emerged as novel candidates in the regulation of phosphate homeostasis. Role of phosphate in the growth plate: physiology and pathophysiology The epiphyseal growth plate has a crucial role in bone growth. Conclusions Whereas for many generations physicians were taught to think of rickets as a calcium disorder, evidence in recent years points to phosphate as the main culprit.

References 1. Phosphate homeostasis and the renal-gastrointestinal axis. Am J Physiol Renal Physiol. Evidence for a signaling axis by which intestinal phosphate rapidly modulates renal phosphate reabsorption. Regulation of phosphate homeostasis by the phosphatonins and other novel mediators.

Regulation of the rat intestinal Na-dependent phosphate transporters by dietary phosphate. Fibroblast growth factor 23 and its role in phosphate homeostasis. Eur J Endocrinol. Gattineni J, Baum M. Regulation of phosphate transport by fibroblast growth factor 23 FGF : implications for disorders of phosphate metabolism.

Amanzadeh J, Reilly RF. Nat Clin Pract Nephrol. Tiosano D, Hochberg Z. Hypophosphatemia: the common denominator of all rickets.

J Bone Miner Metab. Hereditary disorders of renal phosphate wasting. Nat Rev Nephrol. Recent advances in renal phosphate handling. Bergwitz C, Huppner H. Annu Rev Med. Alon US. Clinical practice: Fibroblast growth factor FGF a new hormone. Eur J Pediatr. Age-dependent regulation of rat intestinal type IIb sodium-phosphate cotransporter by 1, OH 2 vitamin D3. Am J Physiol Cell Physiol. Tenenhouse HS. Annu Rev Nutr. Wesseling-Perry K. FGF in bone biology. Regulation of the human sodium-phosphate cotransporter NaPi-IIb gene promoter by epidermal growth factor.

Glucocorticoid regulation and glycosylation of mouse intestinal type IIb Na-Pi cotransporter during ontogeny. Regulation of intestinal NaPi-IIb cotransporter gene expression by estrogen. Regulation of intestinal phosphate transport. The sodium phosphate cotransporter family SLC Intestinal Na-P i cotransporter adaptation to dietary P i content in vitamin D receptor null mice. Phosphate is a specific signal for ATDC5 chondrocyte maturation and apoptosis-associated mineralization: possible implication of apoptosis in the regulation of endochondral ossification.

J Bone Miner Res. Dietary phosphorus regulates serum fibroblast growth factor concentrations in healthy men. J Clin Endocrinol Metab. Kidney Int. Regulation of phosphate transport in proximal tubules.

J Biol Chem. Latest findings in phosphate homeostasis. Internalization of renal type IIc Na-Pi cotransporter in response to a high-phosphate diet. Type IIc sodium-dependent phosphate transporter regulates calcium metabolism. J Am Soc Nephrol. SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis.

Am J Hum Genet. Villa-Bellosta R, Sorribas V. Silver J, Naveh-Many T. FGF and the parathyroid glands. The rest of it is stored in tissues throughout the body. The kidneys help control the amount of phosphate in the blood. Extra phosphate is filtered by the kidneys and passes out of the body in the urine.

A high level of phosphate in the blood is usually caused by a kidney problem. The amount of phosphate in the blood affects the level of calcium in the blood. Calcium and phosphate in the body react in opposite ways: as blood calcium levels rise, phosphate levels fall.

A hormone called parathyroid hormone PTH regulates the levels of calcium and phosphorus in your blood. When the phosphorus level is measured, a vitamin D level, and sometimes a PTH level, is measured at the same time. Vitamin D is needed for your body to take in phosphate. The relation between calcium and phosphate may be disrupted by some diseases or infections.

For this reason, phosphate and calcium levels are usually measured at the same time. This test may be done to check phosphate levels if you have kidney disease or bone disease. It helps find problems with certain glands, such as the parathyroid glands. The test is also used to find a cause for abnormal vitamin D levels. Tell your doctor ALL the medicines, vitamins, supplements, and herbal remedies you take. Some may affect the test results. Your doctor will tell you if you should stop taking any of them before the test and how soon to do it.

A heel stick is used to get a blood sample from a baby. The baby's heel is poked, and several drops of blood are collected. A baby may have a tiny bruise where the heel was poked. When a blood sample is taken, you may feel nothing at all from the needle. Or you might feel a quick sting or pinch. A brief pain, like a sting or a pinch, is usually felt when the lancet punctures the skin.

A baby may feel a little discomfort with the skin puncture. There is very little chance of having a problem from this test. Your kidney dietitian and doctor will help you with this. Below is a list of foods high in phosphorous and lower phosphorus alternatives to enjoy:. Lower phosphorus alternatives to enjoy: water, coffee, tea, rice milk unenriched , apple juice, cranberry juice, grape juice, lemonade, ginger ale, lemon lime soda, orange soda, root beer.

Lower phosphorus alternatives to enjoy: rice milk, almond milk, cottage cheese, vegan cheese, sherbet, popsicles. Lower phosphorus alternatives to enjoy: apples, berries, grapes, carrot sticks, cucumber, rice cakes, unsalted pretzels, unsalted popcorn, unsalted crackers, pound cake, sugar cookies. Your kidney doctor may order a medicine called a phosphate binder for you to take with meals and snacks.

This medicine will help control the amount of phosphorus your body absorbs from the foods you eat. There are many different kinds of phosphate binders.

Pills, chewable tablets, powders, and liquids are available. Some types also contain calcium, while others do not. You should only take the phosphate binder that is ordered by your doctor or dietitian. Skip to main content. Phosphorus and Your Diet. What is phosphorus? Why is phosphorus important to you?