New data demonstrate that serum phosphate, similar to serum calcium, is a signaling molecule. The mechanisms for sensing serum phosphate signal transduction concentration are not understood. This chapter considers serum phosphorus in a context greater than mineral and metabolic homeostasis. The bulk of total body phosphate (85%) is in the bone as part of the mineralized extracellular matrix. This phosphate pool is accessible, albeit in a limited fashion through bone resorption. Phosphate is a predominantly intracellular anion with an estimated concentration of approximately 100 mmol/L, most of which is either complexed or bound to proteins or lipids. Serum phosphorus concentration varies with age, time of day, fasting state, and season. It is higher in children than adults. Phosphorus levels exhibit a diurnal variation with the lowest phosphate level occurring near noon. Serum phosphorus concentration is regulated by diet, hormones, and physical factors such as pH. Importantly, because phosphate moves in and out of cells under several influences, the serum concentration of phosphorus may not reflect phosphate stores.
- Serum inorganic phosphorus (Pi) concentration greater than 2.5–4.5 mg/dL or 0.75–1.45 mM in adults or 6 or 7 mg/dL in children.
- Consequence of increased intake of Pi, decreased renal excretion of Pi, or translocation of Pi from tissue breakdown into extracellular fluid.
- Short-term consequences are hypocalcemia and tetany.
- Long-term consequences are soft tissue calcification and secondary hyperparathyroidism.
Serum inorganic phosphorus (Pi) concentrations are generally maintained at 2.5–4.5 mg/dL or 0.75–1.45 mM in adults, whereas hyperphosphatemia is not present in children unless serum Pi levels are greater than 6 or 7 mg/dL. Hyperphosphatemia may be the consequence of an increased intake of Pi, a decreased excretion of Pi, or translocation of Pi from tissue breakdown into the extracellular fluid (Table 7–1). Because the kidneys are able to excrete phosphate very efficiently over a wide range of dietary intake, hyperphosphatemia most frequently results from renal insufficiency and the attendant inability to excrete Pi. However, in metabolic bone disorders such as osteoporosis and renal osteodystrophy, the skeleton is a poorly recognized contributor to serum phosphorus.
Table 7–1. Causes of Hyperphosphatemia. |Favorite Table|Download (.pdf)
Table 7–1. Causes of Hyperphosphatemia.
Intravenous—sodium or potassium phosphate
Rectal—Fleets phosphosoda enemas
Decreased renal excretion
Renal insufficiency/failure—acute or chronic
Excess bone resorption
Transcellular shift from intracellular to extracellular spaces
Rhabdomyolysis—crush injuries or nontraumatic
Cytotoxic therapy—tumor lysis
Acidosis—metabolic or respiratory
Hyperphosphatemia can be the consequence of an increased intake or administration of Pi. Intravenous administration of Pi during parenteral nutrition, the treatment of Pi depletion, or hypercalcemia can cause hyperphosphatemia, especially in patients with underlying renal insufficiency. Hyperphosphatemia may also result from overzealous use of oral phosphates or ...