21-11: Hyperphosphatemia

GENERAL CONSIDERATIONS

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 GI 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 (DKA). These patients, however, are typically phosphate depleted and are at risk for developing hypophosphatemia with insulin therapy. Other causes are listed in Table 21–9.

CLINICAL FINDINGS

A. Symptoms and Signs

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.

B. Laboratory Findings

In addition to elevated phosphate, blood chemistry abnormalities are those of the underlying disease.

TREATMENT

Treatment is directed at the underlying cause. Acute hyperphosphatemia with symptomatic hypocalcemia and ECG changes (QTc prolongation) can be life-threatening. Intravenous calcium can be given in this situation, though it should be avoided in asymptomatic patients due to the risk of vascular calcification. Hemodialysis may be necessary in patients with impaired kidney function. In chronic hyperphosphatemia, dietary phosphate intake should be decreased and absorption reduced with oral phosphate binders, such as calcium acetate, calcium carbonate, sevelamer, or ferric citrate.

WHEN TO ADMIT

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.