Hyperphosphatemia

Causes
 Decreased excretion: hypoparathyroidism, acute or chronic renal failure, volume depletion.
 Increased intake: vitamin D excess with increased GI absorption, fertilizer poisoning, excess
administration of phosphorus supplements, excess use of Phosphorus containing laxatives or
enemas
 Extracellular shifts: respiratory acidosis and metabolic acidosis, diabetic ketoacidosis, infection
 Movement of phosphorus out of cells: Neoplastic disease (leukemia, lymphoma), increased
tissue catabolism (trauma, crush injury), tumor lysis syndrome, chemotherapy, rhabdomyolysis
(breakdown of striated muscle)

Signs & Symptoms

tetany, muscle weakness, nausea, vomiting, anorexia, tachycardia, hyperreflexia

Most symptoms associated with hyperphosphatemia are actually associated with the accompanying
hypocalcemia that often occurs. Other symptoms may occur in metastatic disease due to soft tissue
calcification: corneal haziness, conjunctivitis, oliguria, irregular HR, and papular eruptions.

Lab Tests
 Blood urea nitrogen (BUN): assess renal status
 Creatinine: assess renal status
 Imaging: assess bone density: osteodystrophy
 Parathyroid hormone: decreased – identify hyperparathyroidism
 Serum calcium: help identify primary cause
 Serum phosphorus: increased

Treatment: Medications
Treat underlying cause: correct volume depletion, treat secondary hyperparathyroidism in chronic
renal failure: in chronic renal failure excess PTH can lead to elevated phosphorus and bone disease.
Vitamin D can help reduce PTH levels.

Limit Phosphorus intake: avoid high phosphorus foods.

Phosphate binders: (Renvela) Phosphate binders bind to Phosphorus in the GI tract to decrease
absorption.

Antacids to bind phosphorus (Aluminum, Calcium, or Magnesium antacids): These medications will
bind to phosphorus and decrease absorption. In renal failure Calcium is preferred to Magnesium or
Aluminum.

Dialysis: Dialysis may be necessary in severe acute hyperphosphatemia, with symptomatic

hypocalcemia.