• Acute increase serum phosphate
    • Rhabdomyolysis
    • Tumor lysis syndrome
    • Exogenous phosphate (fleets enema, fosphenytoin)
    • Extracellular shift from lactic acidosis, DKA, severe Hyperglycemia
    • Tissue necrosis
    • Hyperparathyroidism
    • Vitamin D excess
    • Hemolysis
    • Transfusion of blood products
    • Malignant hyperthermia
  • Impaired exertion
    • Renal failure
    • Hypoparathyroidism
    • Elevated growth hormones, insulin-like growth factor (acromegaly)
    • Tumoral calcinosis
    • Medications: bisphosphonates, Vitamin D


  • Most are asymptomatic
  • Symptoms related to hypocalcemia and hypomagnesium
  • Muscle cramps, tetany, perioral sensations, pruritus, fatigue

Physical Exam/Signs

  • General appearance, vitals
    • Variable, fever
    • Post surgical scar (thyroidectomy)
  • Cardiovascular
    • Prolong QTc (hypocalcemia)
  • Abd/GI/GU
    • Muscle cramps, decreased urinary output
    • Abdominal pain
  • Musculoskeletal/Nervous System
    • Altered Mental Status, Delirium
    • Seizures, Cramps
    • Chvostek and Trousseau signs
    • Paresthesia, trauma
  • Skin/Extremities
    • Pruritus, burns, trauma


  • Labs/Tests
    • CMP, CBC +Diff
    • CPK, LFTs
    • Lactate
    • PTH
    • Serum Calcium, Magnesium
    • Serum phosphate (normal 2.4-4.1 mg/dL)
  • Imaging
    • Generally not indicated (evaluate for metastatic disease, renal ultrasound, bone density)

Differential Diagnosis

  • Psuedohypoparathyroidism
  • Phosphate poisoning
  • Hemolysis
  • Dehydration
  • Rhabdomyolysis
  • Tumor Lysis syndrome
DISORDERS Serum Ca Vit D PO4 ALP PTH Comments
Osteoporosis -- -- -- -- -- bone mass
Osteopetrosis - / -- -- -- -- Dense, brittle bones. Ca in severe, malignant disease
Paget disease -- -- -- -- Abnormal “mosaic” bone architecture
Osteomalacia/rickets   Soft bones
Hypervitaminosis D -- Caused by over-supplementation or granulomatous disease (e.g., sarcoidosis)
Osteitis fibrosa cystica           “Brown tumors” due to fibrous replacement of bone, subperiosteal thinning
Primary Hyperparathyroidism - /↓ Idiopathic or parathyroid hyperplasia, adenoma, carcinoma
Secondary Hyperparathyroidism Often as compensation for ESRD (PO4 excretion and production of activated vitamin D)
Tertiary Hyperparathyroidism       ↑↑ Squamous Cell Carcinoma (lung) = PTH-Like (PTHrP) = Hypercalcemia = Renal Calculi


  1. Initial/Prep/Goals
    • ABCs, IV access if necessary
    • Monitors if necessary
    • If symptomatic, admit for dialysis
  2. Asymptomatic
    • Phosphate restriction
    • Phosphate Binders
      • Aluminum hydroxide: 300-600 mg PO TID
      • Calcium Phosphate: 1334 PO TID with meals
      • Sevelamer: 800-1600 mg PO TID
      • Lanthanum carbonate: 1500-3000mg/day
      • Calcium Acetate (Eliphos, PhosLo, Phoslyra) 3-4 capsules (2001-2868 mg) PO with each meal
      • Renvela (Sevelamer)
        • Initial dose
          • Serum PO4 >9 mg/dL [2.91 mmol/L]: 1600 mg PO q8hr with meals
          • Serum PO4 7.5-9 mg/dL [2.42-2.91 mmol/L]: 1200-1600 mg PO q8hr with meals
          • Serum PO4 5.5-7.5 mg/dL [1.78-2.42 mmol/L]: 800 mg PO q8hr with meals
        • Maintenance dose
          • Serum PO4 >5.5 mg/dL [>1.78 mmol/L]: Increase dose by 400-800 mg per meal
          • Serum PO4 3.5-5.5 mg/dL [1.13-1.78 mmol/L]: Maintain current dose
          • Serum PO4 <3.5 mg/dL [1.13 mmol/L] decrease by 400-800 mg per meal
      • Fosrenol (Lanthanum)
        • Initial: 750-1500 mg/day PO in divided doses
        • Titrate q2-3Weeks until acceptable serum phosphate level attained
      • Amphojel (Aluminum Hydroxide)
      • Velphoro (Sucroferric oxyhydroxide)
        • Initial: 500 mg PO TID with each meal
    • No Mg-containing antacids in renal insufficiency
  3. Diuretics:
    • Lasix 40mg IV x1
      • Furosemide inhibits the resorption of sodium and chloride in the loop of Henle and the proximal and distal tubules of the kidney. Its onset of action is rapid after an intravenous dose.
      • This agent increases the excretion of phosphate
    • Acetazolamide
  4. Surgical/Procedural
    • Acute symptomatic
      • Hemodialysis with concurrent Mg2+ & Ca2+ IV (wait until hemodialysis has begun)
      • Admit to hospital

  5. Management of secondary Hyperparathyroidism:
    • Just as better control of hyperphosphatemia in patients with renal failure helps to prevent the nearly universal development of secondary hyperparathyroidism, better control of hyperphosphatemia is achieved through control of secondary hyperparathyroidism. The agents commonly used to control secondary hyperparathyroidism are vitamin D metabolites and the calcium-sensing receptor agonists
  6. Management of secondary Hypoparathyroidism:
    • For the rare cases of hypoparathyroidism, calcium and vitamin D are prescribed, predominantly for treatment of the hypocalcemia. Given with meals, the oral calcium can ameliorate the hyperphosphatemia of hypoparathyroidism, although this effect has to be carefully balanced against the phosphate absorption–promoting effects of the vitamin D. Over the long term, this therapy may result in nephrocalcinosis. Recombinant PTH injections can be considered but are not commonly used in clinical practice, because of the efficacy of calcium and vitamin D, as well as the cost and inconvenience of injected PTH


  1. Admit if symptomatic
  2. Consult appropriate specialty for underlying illness/disorder
  3. Discharge with close follow-up