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Phosphorus (P), Urine 24h

Urine phosphorus measurement is used to evaluate hyper- and hypophosphatemia as well as to monitor patients with nephrolithiasis.

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Most of the phosphorus (P, PO4, inorganic phosphate) in the body is bound together with calcium in the bones. About 15% of the phosphorus is present in the blood, making it the major anion of the intracellular environment. It has various functions, including its role in glucose and lipid metabolism, the storage and transfer of energy within the body, the creation of bone tissue, and the maintenance of acid-base balance. Phosphorus is absorbed into the small intestine with the help of vitamin D. Like calcium, phosphorus is controlled by parathyroid hormone (PTH). It has an inverse relationship with calcium: an increase in the serum of one causes the kidneys to excrete the other. Parathyroid hormone increases the release of calcium and phosphorus from the bones and reduces calcium excretion and increases the excretion of phosphorus in the urine.

About 80% of the phosphorus that is filtered into the urine is reabsorbed by the proximal renal tubules. The regulation of phosphorus excretion in the urine depends mainly on the regulation of phosphorus uptake by the proximal renal tubules. Factors that increase phosphorus excretion in the urine include, phosphorus-rich diet, parathyroid hormone, increased extracellular volume, low potassium uptake and damage to the proximal renal tubules (eg Fanconi syndrome). Factors that reduce urinary excretion of phosphorus include low dietary phosphorus intake, insulin, high dietary potassium intake, and reduced intestinal phosphorus uptake (eg phosphate-binding antacids, vitamin D deficiency), situations of malabsorption).

An increase in serum phosphorus concentration is known as hypophosphatemia while a decrease in its concentration is known as hypophosphatemia. Hyperphosphatemia is associated with low calcium levels and has symptoms such as tetanus, arrhythmias and seizures. Hypophosphatemia is associated with muscle weakness, encephalopathy, poor platelet function, decreased cardiac contractility and paresthesias.

Phosphorus-rich foods include beans, chicken, eggs, fish, milk, and dairy products.

Possible Interpretations of Pathological Values
  • Increase: Bone fractures (transient), Fanconi syndrome (renal tubular damage), familial hypophosphatemia, hyperparathyroidism, non-renal acidosis (because phosphorylation is a regulatory mechanism), paraplegia, vitamin D-resistant rickets, vitamin D toxicity. Medications: Acetazolamide, Asparagine, Bicarbonates, Bismuth salts, Calcitonin, Corticosteroids, Diuretics, Hydrochlorothiazide, Metolazone, Phosphates (increased intake), Parathyroid hormone, Valine, and Vitamin D. products containing aristolochic acid
  • Decrease: Hypothyroidism or parathyroidectomy, pseudopropathyroidism. Medications: Antioxidants Containing Aluminum (Aluminum), Alanine, Renagel (Phosphorus Binding)




Important Note

Laboratory test results are the most important parameter for the diagnosis and monitoring of all pathological conditions. 70%-80% of diagnostic decisions are based on laboratory tests. Correct interpretation of laboratory results allows a doctor to distinguish "healthy" from "diseased".

Laboratory test results should not be interpreted from the numerical result of a single analysis. Test results should be interpreted in relation to each individual case and family history, clinical findings and the results of other laboratory tests and information. Your personal physician should explain the importance of your test results.

At Diagnostiki Athinon we answer any questions you may have about the test you perform in our laboratory and we contact your doctor to get the best possible medical care.

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