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.

The significant level of hyperphosphatemia in adults is >6 mg/dL.

Principles of Therapy


Decision to Correct Hypophosphatemia
  • Presence of signs & 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 w/ normal renal function, hyperphosphatemia usually resolves spontaneously as the excess phosphate is excreted
  • In symptomatic patients w/ impaired renal function, management includes:
    • Dietary phosphate intake restriction
    • Use of phosphate-lowering therapy (eg calcium-based & non-calcium based)
    • In patients w/ CKD grade 5, intensified dialysis schedule should be done
  • Phosphate-lowering therapies should be given in patients w/ CKD when there is progressive or persistent hyperphosphatemia & not to be used as prohphylaxis
Initial Management
  • Correction of hypocalcemia & its complications
    • Ca has potential to accelerate metastatic calcification
Goals of Therapy
  • Resolve underlying cause
  • Resolution of symptoms
  • Maintain serum Ca level within the low 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 Ca & phosphate every 6-12 hours during & after phosphate therapy
  • Recurrent hypophosphatemia within 24-48 hours of apparently successful replacement may require additional infusions
  • In patients w/ 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


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 w/ chronic hyperphosphatemia
  • Patients who have CKD stage 4 or 5 who are not on dialysis, treatment options include calcium-based phosphate binders & non-calcium based binders eg Sevelamer, Lanthanum
  • Patients w/ CKD stage 5 currently undergoing dialysis, treatment options include calcium-based phosphate binders & non-calcium based binders eg Sevelamer, Lanthanum
  • Ca-containing phosphate binders may increase Ca-phosphate product & induce vascular calcium deposition
    • Dose of calcium-based phosphate binders in patients w/ CKD grades 3-5 is suggested to be restricted
  • Resin binders (eg Sevelamer) promote excretion of phosphorous without affecting Ca
  • Avoid aluminum-containing phosphate binders in patients w/ renal failure
  • Further studies are needed to prove the efficacy & safety of Magnesium salts for patients w/ hyperphosphatemia
    • Several studies reported hypercalcemia & Mg accumulation w/ 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 Ca 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 w/ CKD grade 3-5 in the treatment of hyperphosphatemia only or in combination w/ other treatments
    • In making dietary recommendations, phosphate sources (eg animal, vegetable, additives) should be assessed substantially & 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 & for patients w/ renal failure
  • Continuous venovenous hemodiafiltration is considerably effective than intermittent hemodialysis to address the slow rate of phosphate mobilization from intracellular stores
Digital Edition
Asia's trusted medical magazine for healthcare professionals. Get your MIMS Endocrinology - Malaysia digital copy today!
Sign In To Download
Editor's Recommendations
Most Read Articles
5 days ago
Podcast: Dr Shamir Mehta briefly discusses the clinical impact of findings from the COMPLETE trial
6 days ago
In type 2 diabetes patients taking sulfonylureas, hypoglycaemia duration is longer at night and is inversely correlated with the level of glycated haemoglobin (HbA1c), a new study reports.
5 days ago
Podcast: Prof Derek Chew explains the importance of a 1-hour troponin T protocol in suspected ACS as discussed in the RAPID-TnT trial
5 days ago
Sodium-glucose transport protein 2 (SGLT2) inhibitors exert a putative epigenetic regulation of the protecting cardiovascular effect, reports a study, adding that dapagliflozin may protect the kidneys by preserving renal vasodilating capacity.