For further information, see CMDT Part 21-11: Hyperphosphatemia
The two most common etiologies of hyperphosphatemia are decreased kidney clearance from CKD and transcellular shift
Increased dietary intake of phosphates in the setting of advanced CKD can cause hyperphosphatemia
Phosphate containing laxatives taken as preparation for a gastrointestinal procedure routinely cause transient hyperphosphatemia, unless the patient has impaired kidney function
Rapid cell breakdown from tumor lysis syndrome, rhabdomyolysis and massive hemolysis, releases intracellular phosphate
Hyperphosphatemia from insulin deficiency can occur in diabetic ketoacidosis
These patients, however, are typically phosphate depleted and are at risk for developing hypophosphatemia with insulin therapy
The clinical manifestations are those of the underlying disorder or associated condition
Acute hyperphosphatemia is generally asymptomatic and symptoms are generally associated with concurrent hypocalcemia
Patients with acute severe hyperphosphatemia require hospitalization for emergent therapy, possibly including dialysis
Concomitant illnesses, such as acute kidney injury or cell lysis, may necessitate admission
et al. Tumor lysis syndrome: review of pathogenesis, risk factors and management of a medical emergency. Expert Rev Hematol. 2016;9:197.
et al. Treating hyperphosphatemia—current and advancing drugs. Expert Opin Pharmacother. 2016;17:1873.
et al. Phosphate-binding agents in adults with CKD: a network meta-analysis of randomized trials. Am J Kidney Dis. 2016;68:691.