Hyperphosphatemia
Overview
In hyperphosphatemia, the patient has a too high concentration of phosphorus in the blood. This can be caused by either too efficient uptake of phosphorus through the intestine, or too inefficient excretion of the mineral by the kidneys.
A too high phosphorus concentration in the blood leads to calcium-phosphate salt deposits in soft tissues and blood vessels, causing harm to all organs. It also leads to a depletion of calcium in the body (hypocalcemia), leading to weakened bones and corresponding symptoms.
Hyperphosphatemia is treated by reducing phosphate or binding surplus phosphate in the blood by medication.
Symptoms
Patients with hyperphosphatemia can show some of the following symptoms:
- Tetany and seizures through low calcium levels (hypocalcemia)
- Calcium-phosphate salt depositions in soft tissues
- Calcification of blood vessels, heart and other organs
- Bone related symptoms (Bone weakness / pain / fractures)
Source:
West J Med 1987 Nov; 147:569-576
Causes
Phosphorus is for each living being an essential mineral, since it is a major component of the genetic material and of the bones, and it is also involved in various important metabolic reactions in the body. Phosphorus is ingested with the normal diet in sufficient amounts and is absorbed via the intestine. It is stored in the cells of the body and the skeleton, surplus phosphorus is secreted via the kidneys. It is also a major compound of the genetic information in the body (nucleic acids RNA and DNA) and its major energy source (ATP). Furthermore, phosphorus is an important pH buffer in the blood and phosphorus in combination with calcium is necessary for the stability of the bones in our skeleton.
Phosphorus is ingested via the diet, absorbed through the intestine and stored in an exchangeable phosphorous pool intracellularly (70%), in the skeleton (29%) and the serum (1%). Phosphorus absorption in the intestine is regulated by vitamin D. Surplus phosphorus is secreted in healthy persons through the kidneys, which is regulated by the parathyroid hormone.
A disturbance of the balance between phosphate uptake and phosphate excretion can lead to a state of too high concentrations of phosphorus in the blood (Hyperphosphatemia).
The uptake of too much phosphate via the intestine can be caused by a vitamin D intoxication, the ingestion of phosphate-containing laxatives or enemas as well as the direct administration of phosphate.
On the other hand, an inefficient secretion of phosphate can be caused by kidney injury / kidney diseases, acromegaly, hyperthyroidism, hypoparathyroidism and tumoral calcinosis.
A third possibility is that too much phosphorus stored intracellularly is secreted by the cells of the body. This extracellular phosphate load shift can be caused by lactic or respiratory acidosis, untreated diabetic ketoacidosis or different tumors leading to cell lysis (leukemia, lymphoma).
Excess phosphorus forms complexes with calcium which deposit in blood vessels and other soft tissues, leading to atherosclerotic cardiovascular disease. Furthermore, elevated phosphorus levels can cause bone loss, decreased bone density, fibrosis and bone fractures.
Sources:
Kindey Int. 2008 July; 74(2):148-157
J Ren Nutr. 2008 May; 18(3): 256-261
West J Med 1987 Nov; 147:569-576
Diagnosis
To diagnose hyperphosphatemia, the blood serum of the patient can be analyzed for the concentration of the following components:
- Phosphate and calcium
- Creatinine (indicates renal failure)
- Parathyroid hormone (indicates hypoparathyroidism as a cause)
- Vitamin D
Source:
Medscape.com
Prognosis
Hyperphosphatemia is largely an asymptomatic condition. Morbidity is more commonly associated with the underlying condition than with the actual hyperphosphatemia. On the other hand, long-term complications of chronic hyperphosphatemia can be devastating and can affect any organ system, including bones, skin, joints and heart.
Source:
Medscape.com
Treatment
The treatment principle of hyperphosphatemia is reducing the phosphorus intake and increasing its excretion through the kidneys. The patient can be treated with
- Vitamin D analogs (limits phosphorus absorption)
- Increased phosphate binder prescription
- Limited dietary phosphorus intake
- Calcium supplementation if necessary
Sources:
J Ren Nutr. 2008 May; 18(3): 256-261
West J Med 1987 Nov; 147:569-576
Resources
West J Med 1987 Nov; 147:569-576
J Ren Nutr. 2008 May; 18(3): 256-261
Kindey Int. 2008 July; 74(2):148-157
Medscape.com