Hyperphosphatemia: Description, Causes and Risk Factors:
Abnormally high concentration of phosphates in the circulating blood.
Phosphate is often the forgotten electrolyte. Many intensivists brush off low serum phosphates as unimportant, usually due to a lack of coherent understanding of the importance of this blood test. Phosphate is a predominantly intracellular anion, and at this level it is involved in virtually every cellular reaction. In the serum it's role is limited. Does a low serum phosphate mean a low intracellular level? This is hard to say, however we meticulously treat low serum potassium, and this is predominantly an intracellular cation. The objective of this tutorial is to discuss what is known of phosphate in physiology, and to discuss pathological levels of this agent in the blood.
One hundredth of the body's mass is made up of phosphate. Most of this is stored as hydroxyapetite crystals in the bone matrix. Only 15 % is metabolically active, and 1% is present in the blood. Phosphorous is the most abundant intracellular anion, it's concentration is approximately 100mmol/L. The intracellular concentration of phosphorous is 100 times greater than the plasma concentration. This figure is somewhat misleading, nonetheless, as the multiple functions of the anion ensure that only a small amount of it is in the free (inorganic) form. The average diet provides 800-1400 mg of phosphorous daily. Of this, 70% is absorbed through the gut, mainly by passive transport, but there is also some active transport, stimulated by vitamin D metabolites. Normal plasma range is between 2.8 and 4.5 mg/dL. The main organ of regulation of phosphate is the kidney. Phosphorous is filtered by the nephron, and mostly reabsorbed in the proximal tubule in a cotransport with sodium. This cotransport is regulated by phosphorous intake (i.e. serum phosphorous levels) and parathyroid hormone (PTH). PTH inhibits the co-transport mechanism, and increases urinary excretion of phosphorous.
Causes and Risk Factors:
Cell Lysis: Cells contain large amounts of phosphate. When a large number of cells die suddenly and are broken down, this releases the phosphate into the bloodstream. Some conditions that can cause this massive release of phosphate are rhabdomyolysis (where muscle cells are suddenly broken down) and tumor lysis syndrome (a result of killing tumors with radiation and chemotherapy). This can also lead to hyperphosphatemia.
- Kidney Failure: One of the main roles that the kidneys have is processing and excreting waste through the production of urine. When the kidneys fail, the compounds that the kidneys normally excrete, such as phosphate, begin to build up in the bloodstream. This condition can eventually lead to hyperphosphatemia.
- A rare cause of hyperphosphatemia, excessive intake of phosphate can cause hyperphosphatemia. Foods that are high in phosphate are soda, chocolate, biscuits (from the supermarket), ketchup, frozen pizza and hot dogs. Massive intake of these foods can result in hyperphosphatemia, especially if kidney function is not ideal.
- One function of vitamin D is to help absorption of phosphate by the gastrointestinal system and then secretion by the kidneys. As a result, large amounts of vitamin D could cause hyperphosphatemia if phosphate builds up in the gastrointestinal system. In general, these levels of vitamin D intake can only occur by taking too many vitamin supplements, as there are no foods with enough vitamin D to easily cause vitamin D intoxication.
- Hypoparathyroidism: The parathyroid is a gland that is located very near the thyroid gland, and it is responsible for secreting the parathyroid hormone. If the parathyroid becomes damaged via trauma or an autoimmune disease, decreased parathyroid hormone will result. One of the functions of parathyroid hormone is to make the kidney secrete phosphate, so hypoparathyroidism can lead to hyperphosphatemia.
The prevalence of hyperphosphatemia in the general population and in persons with renal failure is similar throughout the world.
Hyperphosphatemia is a well recognized risk factor for cardiovascular mortality in dialysis patients. Despite advanced technology and regular and ef?cient dialysis treatment the prevalence of hyperphosphatemia is still high. The goal of normalization of serum phosphorus (iP) levels can only be reached by optimization of dialysis prescription in combination with individualized dietary and medical strategies. Due to the unique characteristics of intradialytic iP kinetics, dialysis treatment time and frequency are the most effective factors governing intradialytic iP removal. Although the combination of diffusive and convective removal by hemodia?ltration allows a further increase in iP mass removal, a neutral phosphorus balance without dietary restrictions and the use of phosphate binders has only be achieved by daily nocturnal hemodialysis. Strict dietary phosphate restriction bears the risk of inadequate protein intake and the development of protein/calorie malnutrition. Although phosphate binders (PB) can effectively lower serum iP levels into the normal range, this is rarely achieved in clinical practice probably due to inadequate relation of PB dose to dietary phosphorus intake. Developing methods to enable patients to self-adjust phosphate binder dose to individual meal phosphate content, similar to adjusting insulin dose to carbohydrate intake, may lead to further improvements in phosphate management.
Individuals suffering from disorders causing this condition are at high risk of suffering from Hyperphosphatemia. They should be regularly screened with the aid of blood tests and a complete electrolyte panel. This can allow care providers to detect problems quickly, before non-treatment results in complications. This disease may also be diagnosed while a routine blood panel is being carried out for identifying other conditions.
Typically, most patients with hyperphosphatemia are asymptomatic. However, patients occasionally report hypocalcemic symptoms such as muscle cramps, tetany, and perioral numbness or tingling. Other symptoms include bone and joint pain, pruritus, or rash. More commonly, patients report symptoms related to the underlying cause of the hyperphosphatemia, generally uremic symptoms such as fatigue, shortness of breath, anorexia
, nausea, vomiting
, and sleep disturbances.
Therefore, important information to obtain is related to causes of hyperphosphatemia, such as a history of diabetes mellitus or hypertension (causes of renal failure), a history of neck surgery or irradiation (causes of hypoparathyroidism), or a history of excessive vitamin D or milk ingestion.
The following measurements are indicated in patients with hyperphosphatemia:
Serum phosphate level
- Reference range in adults - 2.5-4.5 mg/dL.
- Reference range in children - 3-6 mg/dL.
Serum calcium level.
- BUN and creatinine levels.
- Serum magnesium level (may be low).
- Hemolysis or hyperlipidemia of the serum sample may lead to falsely elevated phosphorus levels.
Imaging Studies: Radiography is not necessary for the workup but may reveal evidence of metastatic calcifications (eg, bilateral, symmetric calcifications of the basal ganglia; periarticular calcifications around large joints; soft-tissue calcifications at pressure point areas).
The ECG may show QT interval prolongation.
The first step in curing hyperphosphatemia is to determine the condition causing it. Once the cause is diagnosed, cure or management can begin while caregivers work on bringing stability in the electrolyte levels of the patient. This can be done by encourage elimination of waste products through the kidneys by using a diuretic and supplemental water. Patients having this condition as a result of kidney injury can be cured by reducing the absorption of phosphate from gastrointestinal tract as well as lowering its intake. Sufferers must avoid food items that are rich in phosphate content. Antacids comprising of calcium must be taken along with meals to make the calcium bind to the intestinal phosphates and not get absorbed. Prolonged stimulation of parathyroid glands can lead to hyperparathyroidism, making surgical removal of glands necessary.
Treatment for acute hyperphosphatemia involves administering phosphate binding salts such as aluminum, magnesium and calcium. However aluminum is not administered in patients with renal failure. This is because there can be a deposition of Aluminum. It is preferable to use calcium in such cases.
Reduced dietary intake of phosphate and phosphate binders can help avoid increase of this salt in the bloodstream. Moderate exercise and drinking lots of fluids can help one get rid of imbalance in the bloodstream by utilizing excess phosphates. If these methods are found inadequate in improving the situation, doctors may use binding agents.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.