Phosphate is an inorganic molecule consisting of a central phosphorus atom and four oxygen atoms. In the steady state, the serum phosphate concentration is primarily determined by the ability of the kidneys to excrete dietary phosphate. The diagnostic approach to hyperphosphatemia involves elucidating why phosphate entry into the extracellular fluid exceeds the degree to which it can be excreted in order to maintain normal plasma levels.
A broad overview of the causes and treatment of hyperphosphatemia is presented in this topic. Detailed discussions of renal osteodystrophy and the treatment of hyperphosphatemia in patients with chronic kidney disease (CKD) are found elsewhere. (See "Overview of chronic kidney disease-mineral bone disease (CKD-MBD)" and "Treatment of hyperphosphatemia in chronic kidney disease" and "Management of secondary hyperparathyroidism and mineral metabolism abnormalities in dialysis patients".)
OVERVIEW OF THE CAUSES OF HYPERPHOSPHATEMIA
Renal excretion is so efficient in normal subjects that balance can be maintained with only a minimal rise in serum phosphate concentration even if phosphate intake is increased to as much as 4000 mg/day (130 mmol/day). Phosphate intake above 4000 mg/day (130 mmol/day) causes only small elevations in serum phosphate concentrations as long as the intake is distributed over the course of the day. If, however, an acute phosphate load is given over several hours, transient hyperphosphatemia will ensue.
The diagnostic approach to hyperphosphatemia involves elucidating why phosphate entry into the extracellular fluid exceeds the degree to which it can be excreted or why the renal threshold for phosphate excretion is increased above normal. There are four general circumstances in which this occurs (table 1):
●Acute phosphate load