Phosphorus in urine (daily urine)

Why this test?

For differential diagnosis of diseases accompanied by hyperphosphatemia (chronic renal failure, hypoparathyroidism, tumor lysis syndrome) and hypophosphatemia (hyperparathyroidism, Fanconi syndrome and others).

For the prevention of excess vitamin D in the treatment of rickets.

For the diagnosis of nephrolithiasis.

In what cases is it prescribed?

When examining a patient with diseases of the kidneys (chronic renal failure), skeleton (rickets) and parathyroid glands (primary hyper- and hypoparathyroidism).

With symptoms of nephrolithiasis: intense pain in the lower back or flank, with irradiation in the inguinal and femoral region, accompanied by gross hematuria, nausea and vomiting, as well as the passage of visible stones with urine.

Test information

Phosphorus is one of the main trace elements of the body, which is part of high-energy molecules (ATP, creatine phosphate), cell membrane proteins (phospholipids, specific receptors), nucleic acids (DNA, RNA), calcium hydroxyapatite of bone tissue and other organic and inorganic compounds. In addition, phosphoric acid compounds are involved in maintaining the acid-alkaline state of the body.

Phosphorus level regulation is a complex system of interactions between PTH and vitamin D, which ensure its absorption in the intestine, mobilization from bone tissue and reabsorption in the kidneys. Diseases of the parathyroid glands, bone tissue, and kidneys are accompanied by a violation of phosphorus metabolism, so their diagnosis includes a study of its metabolism. The degree of loss of this element by the body is assessed using daily urine analysis.

Daily portion of urine is studied. This is due to the fact that the concentration of phosphorus normally varies during the day within wide limits (up to 50%). In addition, it depends on nutrition: a high carbohydrate content leads to redistribution of phosphorus inside cells and a decrease in its concentration in plasma and urine.

Analysis of phosphorus in urine is performed in the differential diagnosis of hypophosphatemia. At the same time, increased excretion of phosphorus indicates renal causes of the disease and excludes nutritional deficiency of this trace element and redistribution of phosphorus in tissues. Normally, proximal renal tubules ensure almost complete reabsorption of phosphorus. Loss of phosphorus in the urine (phosphaturia) develops when the kidneys stop performing this function. The most common cause of this is the effect on the renal tubules of an excessive amount of parathyroid hormone produced by an adenoma of the parathyroid glands (primary hyperparathyroidism) or parathyroid hormone-related protein secreted by some malignant tumors (for example, squamous cell lung cancer). Patients suffering from long-term diabetes and alcoholism are also prone to phosphaturia. More rare causes of phosphaturia include diseases caused by genetic defects of phosphorus transporter proteins in the proximal renal tubules (Fanconi syndrome, X-linked hypophosphatemic rickets, and others). The consequences of phosphorus loss in the body vary and depend on its degree. As a rule, chronic phosphaturia that developed in adulthood is not accompanied by bright clinical symptoms and includes complaints of pain and weakness in proximal muscle groups. On the other hand, chronic phosphaturia in childhood can lead to rickets. Therefore, such signs as growth retardation and bone deformation are a reason to examine the child for phosphaturia.

Phosphorus absorption in the small intestine is significantly enhanced under the influence of vitamin D. Therefore, the analysis of phosphorus in urine is used in pediatrics to monitor the effectiveness of rickets treatment. A significant increase in phosphaturia indicates an excess of vitamin D and allows timely adjustment of the dose. At the same time, the urine test appears to be a more convenient and comfortable method for the child, in contrast to the blood test.

In addition, the level of phosphorus in urine is determined in the differential diagnosis of hyperphosphatemia. At the same time, a decrease in the concentration of phosphorus in the urine indicates a violation of the normal excretion of phosphorus by the kidneys and excludes extrarenal causes of hyperphosphatemia (rhabdomyolysis, hyperthermia, metabolic and respiratory acidosis). Most often, excretion of phosphorus is disturbed due to chronic renal failure, primary hypoparathyroidism and heparin therapy. An excess of phosphorus in the plasma leads to the deposition of calcium phosphate salts in soft tissues (in the heart, lungs, and kidneys). Therefore, when examining a patient with signs of nephrocalcinosis, the laboratory minimum must include a test for phosphorus in the urine.

Phosphorus metabolism depends on the influence of some other trace elements (primarily, calcium and magnesium), as well as a number of hormones (growth hormone, triiodothyronine, and others), so the assessment of phosphorus level disorders requires a comprehensive approach and should include several laboratory tests.