Treatment Guideline Chart

Hypophosphatemia is an electrolyte imbalance where there is a decrease in the serum phosphate level that is less than the normal range.

It is recognized most often in critically ill patients, decompensated diabetics, alcoholics or other malnourished persons, and acute infectious or pulmonary disorders.

It may be transient and reflect intracellular shift with minimal clinical consequences.

Hyperphosphatemia is an electrolyte disturbance in which an increase in the serum phosphate level of more than the normal range is present.

Most symptoms of acute hyperphosphatemia are due to secondary hypocalcemia.

Hypophosphatemia%20-and-%20hyperphosphatemia Treatment

Principles of Therapy


Decision to Correct Hypophosphatemia
  • Presence of signs and symptoms suggestive of phosphate deficiency
    • Most important consideration 
  • Estimated severity of cellular phosphate deficit
  • Overall clinical status of the patient
  • Renal insufficiency, simultaneous administration of intravenous (IV) glucose or hyperalimentation solutions
  • Risk of aggravating coexistent hypocalcemia


  • In an asymptomatic patient with normal renal function, hyperphosphatemia usually resolves spontaneously as the excess phosphate is excreted
  • In symptomatic patients with impaired renal function, management includes:
    • Dietary phosphate intake restriction
    • Use of phosphate-lowering therapy (eg calcium-based and non-calcium based)
    • In patients with CKD grade 5, intensified dialysis schedule should be done
  • Phosphate-lowering therapies should be given in patients with CKD when there is progressive or persistent hyperphosphatemia and are not to be used as prophylaxis
Initial Management
  • Correction of hypocalcemia and its complications
    • Calcium has potential to accelerate metastatic calcification
Goals of Therapy
  • Resolve underlying cause
  • Resolution of symptoms
  • Maintain serum calcium level within the normal reference range




Intravenous (IV) 

  • In patients without severe renal insufficiency or hypocalcemia, IV phosphate at a rate of 2-8 mmol/hr of elemental phosphorous over 4-8 hours often corrects hypophosphatemia without inducing hyperphosphatemia or hypocalcemia
  • Monitor serum calcium and phosphate every 6-12 hours during and after phosphate therapy
  • Recurrent hypophosphatemia within 24-48 hours of apparently successful replacement may require additional infusions


  • In patients with less acute or severe hypophosphatemia, oral (or enteral) phosphate supplements are generally given as a total of 1-2 g/day in 3-4 divided doses
  • It may cause gastrointestinal symptoms eg nausea or diarrhea
  • Monitor serum phosphate 2-12 hours after the last dose of phosphate therapy


Oral Phosphate Binders

  • Most commonly used are calcium binders (eg Calcium acetate, Calcium carbonate, Calcium citrate), anion exchange resins (eg Sevelamer carbonate, Sevelamer hydrochloride), Lanthanum carbonate, Aluminum hydroxide
  • Administered to decrease gastrointestinal (GI) absorption of phosphorous in patients with chronic hyperphosphatemia
  • Patients who have CKD stage 4 or 5 who are not on dialysis: Treatment options include calcium-based phosphate binders and non-calcium based binders eg Sevelamer, Lanthanum
  • Patients with CKD stage 5 currently undergoing dialysis: Treatment options include calcium-based phosphate binders and non-calcium based binders eg Sevelamer, Lanthanum
  • Calcium-containing phosphate binders may increase calcium-phosphate product and induce vascular calcium deposition
    • Dose of calcium-based phosphate binders in patients with CKD grades 3-5 is suggested to be restricted
  • Resin binders (eg Sevelamer) promote excretion of phosphorous without affecting calcium
  • Avoid aluminum-containing phosphate binders in patients with renal failure
  • Further studies are needed to prove the efficacy and safety of magnesium salts for patients with hyperphosphatemia
    • Several studies reported hypercalcemia and magnesium accumulation with magnesium salt treatment


  • Those that act on the proximal tubules (eg Acetazolamide) may be considered to promote renal phosphate excretion

Non-Pharmacological Therapy


  • In most asymptomatic patients, serum phosphate level spontaneously normalizes within several days when factors that trigger hypophosphatemia are corrected
  • Dairy products (eg skim milk) supply absorbable calcium that help avoid hypocalcemia that may result from more aggressive replacement therapies



  • Foods that are high in phosphorus (eg meat, poultry, fish, eggs, dairy products, nuts, legumes) should be avoided
  • According to National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF/KDOQI) guidelines, 800-1000 mg/day should be the restriction for dietary phosphorus
  • It is suggested that dietary phosphate intake be limited in patients with CKD grades 3-5 in the treatment of hyperphosphatemia only or in combination with other treatments
    • In making dietary recommendations, phosphate sources (eg animal, vegetable, additives) should be assessed substantially and patient education be given
    • Adequate protein intake should not be compromised in the restriction of dietary phosphate


  • Hemodialysis or peritoneal dialysis is indicated for severe refractory cases and for patients with renal failure
  • Continuous venovenous hemodiafiltration is considerably effective than intermittent hemodialysis to address the slow rate of phosphate mobilization from intracellular stores
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