Urine phosphorus measurement evaluates hyper- and hypophosphatemia and monitors patients with nephrolithiasis.
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Most of the body's phosphorus (P, PO4, inorganic phosphate) is bound 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, storing and transferring energy within the body, creating bone tissue, and maintaining 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, reduces calcium excretion, and increases the excretion of phosphorus in the urine.
About 80% of the phosphorus filtered into the urine is reabsorbed by the proximal renal tubules. The regulation of phosphorus excretion in the urine depends mainly on phosphorus uptake by the proximal renal tubules. Factors that increase phosphorus excretion in the urine include a phosphorus-rich diet, parathyroid hormone, increased extracellular volume, low potassium uptake, and damage to the proximal renal tubules (e.g., Fanconi syndrome). Factors that reduce urinary excretion of phosphorus include low dietary phosphorus intake, insulin, high dietary potassium intake, and decreased intestinal phosphorus uptake (e.g., phosphate-binding antacids, vitamin D deficiency), situations of malabsorption).
An increase in serum phosphorus concentration is known as hyperphosphatemia, 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 phosphate excretion 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, vitamin D. Herbal or natural remedies including products containing aristolochic acids
- Decrease: Hypoparathyroidism or parathyroidectomy, pseudohypoparathyroidism. Medications: Antacids containing aluminum (aluminum), alanine, Renagel (phosphorus binder)
Important Note
Laboratory test results are the most critical parameter for diagnosing and monitoring all pathological conditions. Between 70 to 80% of diagnostic decisions are based on laboratory tests. Correctly interpreting 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 analyzed based on each case and family history, clinical findings, and the results of other laboratory tests and information. Your 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 contact your doctor to ensure you receive the best possible medical care.
