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Hyperphosphatemia is a condition characterized by elevated levels of phosphate in the blood. Under normal conditions phosphate is used to construct bones and cell membranes, as well as a coenzyme that regulates intracellular enzymes. Phosphate levels in the blood are carefully regulated by vitamin D and parathyroid hormone.


Signs and symptoms associated with acute hyperphosphatemia are caused by hypocalcemia and include:

However, some symptoms are considered to be exclusively caused by elevated levels of phosphate ions. Cataracts can be attributed to hyperphosphatemia. Additionally, cardiovascular and nervous system dysfunction results in hypotension, prolonged QT syndrome, delirium, and possibly coma.

Developmental Delay
  • Children with developmental delay often display bowel dysfunction and chronic constipation and are therefore high-risk patients. The accepted opinion-that these enemas are not absorbed and therefore systemically inactive-is not true.[ncbi.nlm.nih.gov]
  • Usually a plethora of tests are performed to assist in diagnosing the underlying condition. Treatment Treating elevated levels of phosphate in the blood and the underlying condition should be accomplished in tandem.[symptoma.com]
  • Findings associated with hyperphosphatemia include lethargy, dizziness, stiffness, tachypnea, tachycardia and severe dehydration in almost all cases, and tetany, carpopedal spasm, and prolonged QT interval in a subset.[ncbi.nlm.nih.gov]
Calcinosis Cutis
  • In the two subjects with systemic inflammation, interleukin-1 (IL-1) antagonists significantly decreased CRP levels with resolution of calcinosis cutis and perilesional inflammation in one subject and improvement of overall well-being in both subjects[ncbi.nlm.nih.gov]


Laboratory Studies
Hyperphosphatemia is diagnosed by a simple blood test to measure phosphate. However, other testing is necessary to evaluate other electrolytes, kidney function, and parathyroid function. The recommended blood tests include:

  • BUN
  • Calcium
  • Creatinine
  • Magnesium
  • Parathyroid hormone (PTH)
  • Phosphate [8]
  • Vitamin D

Testing the urine has no role in evaluating hyperphosphatemia.

Imaging Studies
Most imaging studies are not warranted; however, metastatic calcifications can be evaluated and monitored by radiography. These calcifications can be found in the basal ganglia and periarticular joint spaces.

Secondary hyperparathyroidism due to renal failure requires long-bone studies to assess for hyperparathyroid bone disease. Densitometry is recommended in cases where excess bone loss is suspected. Coronary artery calcifications and calcifications of the peripheral vasculature can be assessed by electron beam CT. Studies suggest patients with renal failure and patients on dialysis with valvular and coronary artery calcifications have a poor outcome.

Imaging, especially bone studies and coronary calcification, can provide useful information regarding chronicity and are useful in determining the patient’s prognosis. A chronic process may show kidney shrinkage, a sign of kidney failure, and coronary calcifications.

Bone biopsy findings may be helpful to differentiate osteomalacia (bone softening due to low levels of Vitamin D, seen in adults) from parathyroid bone disease.

Calcium Decreased
  • decreases, and vice versa) Aid for gastric motility Foods containing phosphorus If you consume too much phosphorus, the kidneys normally will excrete the excess.[consultant360.com]


Diagnosing and treating the underlying cause of hyperphosphatemia should be completed in parallel with restoring phosphate levels to normal. Dietary modification is a very effective method in controlling phosphate levels. Medications may also be necessary. There are two classes of drugs to control phosphate levels: phosphate binders and loop diuretics.
Phosphate binders are taken orally and neutralize phosphate ions and phosphorous in the GI tract, allowing it to bypass absorption and be excreted with the stool. These include:

Calcium Phosphate Binders

Non Calcium Phosphate Binders

  • Aluminum hydroxide
  • Magnesium hydroxide
  • Lanthanum carbonate
  • Sevelamer hydrochloride [10]

In patient with end-stage renal disease there is an increased risk for aluminum-related osteomalacia. Aluminum hydroxide should not be used as a phosphate binder in this population. A physician should use calcium carbonate or calcium acetate instead. Patients on dialysis have an increased risk of vascular calcification when taking phosphate binders that contain calcium. Sevelamer is a phosphate binding resin that does not contain calcium and should be used with this population.

Loop diuretics improve phosphate excretion from the kidneys. However, side effects include other electrolyte imbalance including hyponatremia and hypokalemia. These include:

In patients with limited or no kidney function, phosphate can be removed during dialysis treatment. This may be the most effective method to remove phosphate from the body.


Acute hyperphosphatemia is usually an asymptomatic condition. Even a large increase in phosphate concentration in the blood rarely results in immediate clinical manifestation. Acutely, complications of hyperphosphatemia include hypocalcemia and tetany. Additionally, excessive phosphate will precipitate with calcium ions in joints and other soft tissues. The main concern regarding hyperphosphatemia is the underlying condition that caused the increased concentration. For instance, ingestion of large amounts of phosphosoda can result in acute hyperphosphatemia but also acute renal failure and, often, chronic kidney disease (CKD) [5] [6]. The prognosis of a short term elevation in phosphate is good; however, in chronic hyperphosphatemia the prognosis is often mixed. Excess of phosphate for a long period of time can damage most organ systems. The cardiovascular system, bones, joints, and skin are most susceptible to damage by chronic hyperphosphatemia. In CKD, prolonged hyperphosphatemia is an independent risk factor for cardiovascular disease. This population has an 18-39% higher mortality rate if their phosphate levels exceed 6.5 mg/dL compared to patients with CKD and normal or even slightly elevated phosphate levels.

Renal disease and Hyperphosphatemia
Mortality rates are higher in patients with hyperphosphatemia and kidney transplant, chronic kidney disease and end-stage renal disease [7]. Preventing this condition early in the course of kidney failure can prevent or postpone the development of chronic hyperphosphatemia complications. In this population the key is to prevent ingestion and absorption with dietary changes and using oral phosphate binders that neutralize phosphate in the gastrointestinal system, allowing it to pass with the stool instead of being absorbed by the small intestine. If elevated phosphate levels are not addressed, then pathologic changes will occur in joints, bones, vascular tissue and other soft tissues. These changes are usually permanent.


Phosphate levels in the blood rise when any of the following conditions are present [3]:

Excessive intake

Phosphate and phosphorous are absorbed through the upper half of the small intestine. Any excess phosphate absorbed by the gastrointestinal system is excreted by the kidneys under normal circumstances. If the kidneys are injured or hypoperfused, then even a minor dietary phosphate increase may lead to hyperphosphatemia. Phosphate absorption in the gut and excretion by the kidneys is regulated by vitamin D. Excess vitamin D can also lead to hyperphosphatemia by increasing absorption rates.
Hyperphosphatemia may result from excessive phosphate intake via any of these mechanisms:

  • Phosphorus poisoning
  • Liberal use of saline phosphate enemas
  • Excess vitamin D intake [4]
  • Phosphate injections (IV or IM)
  • Milk-alkali syndrome

Decreased Excretion
Kidney injury may result in a reduction of phosphate excretion. Patients with poor kidney function have to carefully regulate their dietary phosphate levels. Vitamin D regulates phosphate absorption in the gastrointestinal system and reabsorption in healthy kidneys. Increased levels of Vitamin D result in the reabsorption of more phosphate by the tubules of the kidneys and less excretion. Reabsorbed phosphate re-enters the blood and increases plasma concentration. This process is balanced by parathyroid hormone (PTH), which is secreted by the parathyroid gland. PTH stimulates the kidneys to excrete phosphate. When PTH levels are low, more phosphate is reabsorbed by the kidneys. Therefore, hypoparathyroidism can lead to hyperphosphatemia.
Hyperphosphatemia may result from reduced phosphate excretion via any of these mechanisms:

Phosphate shift from the intracellular space to the extracellular space
A majority of the phosphate in the body is stored in the bones. A much smaller portion is used by cells and an even smaller portion is found circulating in the blood. Under certain circumstances the intracellular phosphate is released into the blood. This can contribute to hyperphosphatemia. Circumstances under which phosphate can be released into the circulation include:


Hyperphosphatemia is a rare condition. It is more common in patients with advanced chronic kidney disease and acute kidney disease. In this population the prevalence approaches 70%. Dialysis-dependent kidney failure also poses a major risk for developing hyperphosphatemia. These trends are similar in the developed and developing worlds.

Sex distribution
Age distribution


Phosphate ion concentration is not measured directly in the blood. However, calcium is carefully measured. Vitamin D and parathyroid hormone are secreted in response to calcium levels. Plasma phosphorous levels change as calcium levels are adjusted. Bones and cells absorb and release calcium and phosphate in response to these signals. The gastrointestinal system and kidneys absorb and excrete phosphate and calcium in response to these hormone signals as well. Hyperphosphatemia is the result of an excessive phosphate load and three mechanisms can induce this imbalance [3]:

  • Increased phosphate intake by the GI system.
  • Decreased phosphate excretion by the kidneys.
  • Intracellular shift of phosphate ions to the extracellular space.

The signs and symptoms of hyperphosphatemia are the same irrespective of the cause. A healthy patient can ingest large quantities of phosphate without developing hyperphosphatemia due to tissue absorption and kidney excretion.


Reducing and eliminating phosphate and phosphorous from the diet is necessary and effective in any treatment protocol. This step alone may normalize phosphate levels in the blood, but it is unlikely to treat the underlying condition. Phosphorous is found in many foods. These include the following:

Dark green vegetables and grain:

  • Artichoke
  • Asparagus
  • Broccoli
  • Corn
  • Mushrooms
  • Whole grains including whole grain food products

Other foods:

  • Chocolate
  • Cola drinks (Coke, Pepsi, etc.)
  • Fish (pollock, sardines, walleye, etc.)
  • Organ meat
  • Legumes (beans, lentils, peas, etc.)
  • Milk and dairy


Hyperphosphatemia is a result of an imbalance in the absorption and excretion of phosphate. When phosphorus is oxidized it transforms into phosphate ions (PO43-), the most common form of phosphorous in the body. Both the ion and elemental forms are absorbed by the gastrointestinal system and are excreted by the kidneys. It is also excreted through the loss of gastrointestinal cells that are replaced at a rapid pace. Vitamin D and other hormones regulate the absorption, storage, and excretion of phosphate [1]. Phosphate ions are biologically important. Only a very small number of phosphate ions are found in the blood, yet they have many roles throughout the body. They are an integral part of the mineral matrix that forms the skeleton [2]. The bones store a majority of the body’s total phosphate concentration and this phosphate is in constant flux with calcium and magnesium. In cells, phosphate forms adenosine triphosphate (ATP), a major source for chemical energy in the cell and a coenzyme that regulates many intracellular enzymes. Phosphate is also a significant part of DNA and RNA, and a component of cell membranes.

Patient Information

Hyperphosphatemia describes the condition of elevated phosphate ions in the blood. Hyperphosphatemia may be described as high levels of phosphate ions in the blood. Normal range for phosphorous is 2.5-4.5 mg/dL; however, normal values vary slightly from laboratory to laboratory. Phosphate is used with calcium to form bones, and it is found in all types of cells in the body. Just as vitamin D is an important regulator of calcium in the body, it also regulates the absorption and excretion of phosphate.


Elevated phosphate levels in the blood (hyperphosphatemia) is often caused by the kidney's inability to excrete sufficient amounts to maintain balance. This condition is seen with: 

Sign and symptoms

Patients with hyperphosphatemia are usually symptom-free. There is usually an underlying condition (for example, kidney failure) causing this electrolyte disorder and there may be symptoms associated with that underlying condition.


A blood test is used to diagnose hyperphosphatemia. Usually a plethora of tests are performed to assist in diagnosing the underlying condition.


Treating elevated levels of phosphate in the blood and the underlying condition should be accomplished in tandem. The most effective way to reduce phosphate levels is to limit phosphate intake and absorption through the intestinal lining. Phosphate binders are oral medications that bind to and neutralize phosphorous and phosphate in the gut, allowing it to pass without absorption into the blood. Other medication includes diuretics that help to excrete phosphate with the urine. Dialysis is effective in cases of chronic kidney disease.



  1. Shaikh A, Berndt T, Kumar R. Regulation of phospahte homeostasis by the phosphatonins and other novel mediators. Pediatr Nephrol. 2008; 23:1203-1210.
  2. Virkki LV, Biber J, Murer H, Forster IC. Phosphate transporters: a tale of two solute carrier families. Am J Physiol Renal Physiol. 2007; 293:F643-F654.
  3. Malberti F. Hyperphosphataemia: treatment options. Drugs. 2013 May; 73(7):673-88.
  4. Tessitore, N, Venturi, A, Admai, et al. Relationship between serum vitamin D metabolites and dietary intake of phosphate in patients with early renal failure. Miner Electrolyte Metab. 1987; 13:38–44.
  5. Beloosesky Y, Grinblat J, Weiss A, et al. Electrolyte disorders following oral sodium phosphate administration for bowel cleansing in elderly patients. Arch Intern Med. 2003 Apr 14; 163(7):803-8.
  6. Gumurdulu Y, Serin E, Ozer B, Gokcel A, Boyacioglu S. Age as a predictor of hyperphosphatemia after oral phosphosoda administration for colon preparation. J Gastroenterol Hepatol. 2004. 19:68-72.
  7. Hruska KA, Mathew S, Lund R, Qiu P, Pratt R. Hyperphosphatemia of chronic kidney disease open link. Kidney International. 2008. 74:148-157.
  8. Hawley C. Serum phosphate. Nephrology. 2006 Apr; 11(S1):S201-5.
  9. Ketteler M. Phosphate Metabolism in CKD Stages 3-5: Dietary and Pharmacological Control. Int J Nephrol. 2011; 970245.
  10. Spaia S. Phosphate binders: Sevelamer in the prevention and treatment of hyperphosphataemia in chronic renal failure. Hippokratia. 2011 Jan; 15:22-6.

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Last updated: 2019-07-11 21:32