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Causes of decreased phosphorus in the blood (hypophosphatemia)
Last reviewed: 06.07.2025
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Hypophosphatemia may occur due to impaired intestinal absorption of phosphate, increased renal excretion, or intracellular absorption. Severe hypophosphatemia (less than 1 mg% or less than 0.32 mmol/L) usually indicates a decrease in the total amount of phosphorus in the body and occurs with alcohol abuse, respiratory alkalosis, intestinal absorption disorders, severe burns, treatment of diabetic ketoacidosis, and use of phosphate binders.
Moderate hypophosphatemia (1–2.5 mg% or 0.32–0.80 mmol/L) is not always due to depletion of total phosphate stores. In addition to the causes listed above, it may be caused by glucose infusion; vitamin D deficiency in the diet or decreased intestinal absorption; increased renal phosphate losses, which occurs in hyperparathyroidism, during the diuretic phase of acute tubular necrosis, after kidney transplantation, in hereditary X-linked hypophosphatemia, in Fanconi syndrome, paraneoplastic osteomalacia, and in cases of increased extracellular fluid volume.
In clinical practice of intensive care units, intravenous glucose infusions are the main cause of hypophosphatemia, with a decrease in the concentration of inorganic phosphorus occurring after several days. The hypophosphatemic effect of glucose is due to insulin, which facilitates the transport of glucose and phosphate across cell membranes in the liver and skeletal muscles.
Respiratory alkalosis, as a cause of hypophosphatemia, may be important in patients on mechanical ventilation. The mechanism of hypophosphatemia is due to an increase in intracellular pH, which stimulates glycolysis, and increased glucose phosphorylation promotes transmembrane transfer of phosphate anions.
In patients with sepsis, the concentration of inorganic phosphate in the blood serum decreases quite early, so an unexplained decrease in the phosphate content in the blood should always cause some concern in clinicians aimed at searching for infection.
Glucosuria increases the excretion of phosphates in the urine, so patients with diabetic ketoacidosis have a deficiency, despite normal or even elevated levels of inorganic phosphorus in the blood serum.
Clinical manifestations of hypophosphatemia occur only when the total body phosphate reserve is depleted and the serum phosphate concentration falls to less than 1 mg% (less than 0.32 mmol/L). Muscular abnormalities include weakness, rhabdomyolysis, decreased diaphragmatic function, respiratory failure, and congestive heart failure. Neurological abnormalities include paresthesia, dysarthria, confusion, stupor, seizures, and coma. Rarely, hemolysis, thrombocytopathy, and metabolic acidosis are observed. Acute phosphate deficiency reduces cardiac contractility, while chronic phosphate deficiency results in cardiomyopathy. Chronic hypophosphatemia causes rickets in children and osteomalacia in adults.