Hypophosphatemia is defined as a serum
phosphate level of less than 2.5 mg/dL (0.8 mmol/L).
Hypophosphatemia is caused by inadequate intake, decreased intestinal absorption, excessive urinary excretion, or a shift of
phosphate from the extracellular to the intracellular compartments. Renal
phosphate wasting can result from genetic or acquired renal disorders. Acquired renal
phosphate wasting syndromes can result from
vitamin D deficiency hyperparathyroidism, oncogenic osteomalecia, and
Fanconi syndrome.
Genetic disorders of renal hypophosphatemic disorders generally manifest in infancy and are usually transmitted as an
X-linked hypophosphatemic rickets. Symptoms of
hypophosphatemia are nonspecific and most patients are asymptomatic. Severe
hypophosphatemia may cause skeletal muscle weakness, myocardial dysfunction,
rhabdomyolysis, and altered mental status. The diagnostic approach to
hypophosphatemia should begin with the measurement of fractional
phosphate excretion; if greater than 15% in the presence of
hypophosphatemia, the diagnosis of renal
phosphate wasting is confirmed. Renal
phosphate wasting can be divided into 3 types based upon serum
calcium levels:
primary hyperparathyroidism (high serum
calcium level),
secondary hyperparathyroidism (low serum
calcium level), and primary renal
phosphate wasting (normal serum
calcium level).
Phosphate supplementations are indicated in patients who are symptomatic or who have a renal tubular defect leading to chronic
phosphate wasting. Oral
phosphate supplements in combination with
calcitriol are the mainstay of treatment. Parenteral
phosphate supplementation is generally reserved for patient with life-threatening
hypophosphatemia (serum
phosphate < 2.0 mg/dL). Intravenous
phosphate (0.16 mmol/kg) is administered at a rate of 1 mmol/h to 3 mmol/h until a level of 2 mg/dL is reached.