Phosphorus deficiency

phosphorus deficiencyHypophosphatemia (phosphorus deficiency) is a condition of the insufficient amount of phosphorus or its inadequate utilization in the body.


Hypophosphatemia is defined as a serum phosphate level less than 2.5 mg/dL or 0.8 mmol/L.

Intracellular phosphate is involved in various cellular processes. It is a component of the nucleic acids that comprise the major molecules of all the living – DNA and RNA. Phosphorus deficiency is an essential component of ATP and ADP – the molecules that provide energy supply for the cells and tissues. The addition and deletion of phosphate groups to enzymes and proteins are the spread mechanisms for the regulation of their activity.

It was estimated that about 300 mg of phosphate per day enters and exits bone tissue. Phosphate is considered to be one of the most valuable mineral for the skeleton. If the skeleton loses phosphate and is not getting enough phosphate back occurs osteomalacia. Bone metabolism of phosphate is influenced by a variety of factors that determine bone formation and destruction (parathyroid hormone, vitamin D, sex hormones, acid-base balance, generalized inflammation etc.).

Causes and risk factors

Hypophosphatemia is usually not a solely disorder or a disease itself, but a condition that occurs in association with other disorders such as:

  • Bone fractures;
  • Malabsorption;
  • Alcohol abuse;
  • Refeeding syndrome – metabolic disturbances that occur as a result of reinstitution of nutrition to a person who is starved or malnourished);
  • Exposure to heavy metals and antacids;
  • Bone marrow transplant;
  • Diabetic ketoacidosis;
  • Poor nutrition, starvation, and parental (intravenous) nutrition;
  • Treatment in intensive care unit;
  • Intake of glucocorticoids, cisplatin, or pamidronate;
  • Intake of growth factors;
  • HIV infection treatment;

See also: Fluoride deficiency

Some genetic disorders cause excessive wasting of phosphate and lead to skeletal abnormalities – short stature and bone deformities. These may be the following diseases:

  • X-linked hypophosphatemic rickets;
  • Autosomal dominant hypophosphatemic rickets;
  • Hereditary hypophosphatemic rickets with hypercalciuria (excessive level of Calcium in the urine);
  • Vitamin D–resistant rickets;
  • Mutations in the type 2a sodium-phosphate cotransporter;
  • Fibrous dysplasia/McCune-Albright syndrome (includes polyostotic fibrous dysplasia, skin pigmentation and autonomous endocrine hyperfunction);

Hypophosphatemia (Phosphorus deficiency) is a common complication of the kidney transplantation.

Some acquired conditions may also cause renal phosphate wasting:

  • Vitamin D deficiency;
  • Primary hyperparathyroidism (hyperfunction of parathyroid glands);
  • Heavy metal intoxication and paraproteinemias (Fanconi syndrome);
  • Oncogenic osteomalacia – the resorbtion of the bone due to the presense of the tumor (usually those neoplasms that arise from  mesenchyma);
  • Administration of loop diuretics (furosemide, torsemide etc), acetazolamide and bisphosphonates;
  • Chemotherapy (cisplatinum, bevacizumab, sorafenib, ifosfamide and many others);


Recommended daily intake and the sources

Recommended daily intake of phosphorus depends on the age of the person:

  • 0 to 6 months: 100 mg/day;
  • 7 to 12 months: 275 mg/day;
  • 1 to 3 years: 460 mg/day;
  • 4 to 8 years: 500 mg/day;
  • 9 to 18 years: 1,250 mg/day;
  • Adults: 700 mg/day;
  • Pregnant or lactating women: younger than 18: 1,250 mg/day; older than 18: 700 mg/day.

The main dietary sources of phosphorus deficiency include milk products, eggs (especially yolk), legumes, nuts, and whole grains.


Chronic hypophosphatemia (usually due to genetic disorders) in children causes the short stature and symptoms of rickets, with bowing of the legs. In adults, chronic hypophosphatemia leads to pain upon palpation.

If hypophosphatemia develops acutely it has a severe course and causes:

  • Muscle pain, dysfunction and weakness, especially in major muscles. It also may manifest as: diplopia (double vision), low cardiac output (cardiac insufficiency), dysphagia (difficulties by the swallowing), and respiratory depression due to the weakness of respiratory muscles;
  • Mental status changes – from irritability to gross confusion, disorientation, delirium, and coma;
  • Seizures and focal neurologic disorders (paralysis, paresis, paresthesia etc.);
  • White blood cell dysfunction that leads to immunity impairment and  worsening of infections;
  • Low levels of ATP disturb the stability of cell membrane, this results in rhabdomyolysis (rapid muscle breakdown) and also hemolytic anemia (low red blood cells count due to cell destruction);
  • Large pulp chambers in the teeth.


To verify the diagnosis the measurement of serum phosphate is performed. Serum phosphate concentration < 2.5 mg/dL (< 0.81 mmol/L) is an indicator of hypophosphatemia. The levels of calcium, magnesium, serum albumin, parathyroid and vitamin D may also be helpful to determine the underlying disorder. Phosphorus deficiency.
Urine may be collected during 24 hours to indicate renal wasting of phosphates.


Usually the treatment depends on the cause of hypophosphatemia. Phosphates may be administered by mouth (in tablets containing sodium phosphate or potassium phosphate) or intravenously (when serum phosphate is < 1 mg/dL or symptoms are severe).  Oral phosphate supplements are especially effective in case of genetic disorders of renal phosphate wasting.
Primary hyperparathyroidism treatment requires parathyroidectomy.

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