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Hypophosphatemia: Evaluation and treatment

Hypophosphatemia: Evaluation and treatment
Authors:
Alan S L Yu, MB, BChir
Jason R Stubbs, MD
Section Editor:
Stanley Goldfarb, MD
Deputy Editor:
Albert Q Lam, MD
Literature review current through: May 2022. | This topic last updated: Apr 27, 2022.

INTRODUCTION — True hypophosphatemia can be induced by decreased net intestinal absorption, increased urinary phosphate excretion, or acute movement of extracellular phosphate into the cells. Spurious hypophosphatemia can be caused by interference of paraproteins or medications with the phosphate assay [1,2]. (See "Hypophosphatemia: Causes of hypophosphatemia".)

The normal renal response to phosphate depletion is to increase phosphate reabsorption, leading to the virtual abolition of phosphate excretion in the urine. Most of the filtered phosphate is reabsorbed in the proximal tubule via the sodium-phosphate cotransporter in the luminal membrane [3,4]. This transporter uses the favorable inward concentration gradient for sodium (the cell sodium concentration is less than 25 mEq/L, well below the 145 mEq/L concentration in the tubular lumen) to drive the active reabsorption of phosphate from the tubular lumen into the cell. Phosphate depletion leads to increased gene expression and synthesis of new transporters, thereby enhancing the uptake of filtered phosphate into the cell [4].

EVALUATION — The cause of hypophosphatemia is often evident from the history (table 1) (see "Hypophosphatemia: Causes of hypophosphatemia"). If, however, the diagnosis is not apparent, then measurement of urinary phosphate excretion should be helpful. Phosphate excretion can be measured either from a 24-hour urine collection or by calculation of the fractional excretion of filtered phosphate (FEPO4) from a random urine specimen.

In patients with hypophosphatemia:

A 24-hour urine phosphate excretion less than 100 mg or a FEPO4 less than 5 percent indicates appropriate low renal phosphate excretion, suggesting that the hypophosphatemia is caused by internal redistribution (eg, refeeding syndrome, acute respiratory alkalosis) or decreased intestinal absorption (eg, chronic antacid therapy, steatorrhea). (See "Hypophosphatemia: Causes of hypophosphatemia", section on 'Internal redistribution' and "Hypophosphatemia: Causes of hypophosphatemia", section on 'Decreased intestinal absorption'.)

A 24-hour urine phosphate excretion greater than or equal to 100 mg or a FEPO4 greater than or equal to 5 percent indicates renal phosphate wasting, suggesting that the hypophosphatemia is caused by hyperparathyroidism, vitamin D deficiency, or a variety of other conditions. (See "Hypophosphatemia: Causes of hypophosphatemia", section on 'Increased urinary excretion'.)

The formula used to calculate the FEPO4 (calculator 1) is the same as that for the fractional excretion of sodium (FENa):

 FEPO4  =  [UPO4  x  PCr  x  100]  ÷  [PPO4  x  UCr]

where U and P refer to the urine and plasma concentrations of phosphate (PO4) and creatinine (Cr).

Low phosphate excretion — In the setting of hypophosphatemia, daily phosphate excretion should be less than 100 mg and the FEPO4 should be well below 5 percent (normal value is 5 to 20 percent) if the kidney is responding normally and renal phosphate wasting is not the cause of the hypophosphatemia. A review of the basic aspects of renal phosphate handling is presented separately. (See "Hypophosphatemia: Causes of hypophosphatemia".)

The differential diagnosis of hypophosphatemia with an appropriately low urinary FEPO4 (or 24-hour urinary phosphate excretion) includes increased cellular uptake (internal redistribution) and reduced net intestinal absorption (table 1):

Increased cell entry is more likely if the patient has received glucose or insulin infusions (as in refeeding or the treatment of uncontrolled diabetes mellitus) or has acute respiratory alkalosis (as in patients with hyperventilation).

In the absence of these problems, the most likely cause of the hypophosphatemia is decreased intestinal absorption of phosphate. Several mechanisms may promote a high fecal excretion of phosphate, including increased intestinal transit and secretions (as seen with chronic diarrhea), intestinal phosphate binding by calcium, magnesium, or aluminum to form insoluble salts (as observed with chronic antacid therapy), or inhibition of intestinal phosphate transport (as occurs with niacin therapy) [5,6].

Inappropriately high phosphate excretion — Urinary phosphate excretion above 100 mg/day or a FEPO4 above 5 percent is indicative of renal phosphate wasting in patients with hypophosphatemia. This problem is usually due either to hyperparathyroidism or to a renal tubular defect, both of which impair phosphate reabsorption by diminishing the activity of the sodium-phosphate cotransporters (NaPi-IIa and NaPi-IIc) in the proximal tubule (table 1) [7]. (See "Hypophosphatemia: Causes of hypophosphatemia", section on 'Increased urinary excretion'.)

Hypophosphatemia can be seen with either primary or secondary hyperparathyroidism. The triad of hypercalcemia, hypophosphatemia, and urinary phosphate wasting is often present in primary hyperparathyroidism. By contrast, hypocalcemia is a major stimulus for hypersecretion of parathyroid hormone in secondary disease. Hypophosphatemia and urinary phosphate wasting in a patient without hypercalcemia should prompt an evaluation for vitamin D deficiency. (See "Etiology of hypercalcemia" and "Etiology of hypocalcemia in adults" and "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment".)

Persistent hyperparathyroidism and hypophosphatemia can also occur after successful kidney transplantation due both to residual parathyroid hormone hypersecretion by hyperplastic parathyroid glands and to persistently elevated plasma levels of fibroblast growth factor 23 (FGF23), a bone-derived phosphaturic hormone that is markedly elevated in patients with kidney disease. (See "Kidney transplantation in adults: Persistent hyperparathyroidism after kidney transplantation".)

Tubular defects, which are relatively rare, can occur either as an isolated impairment in proximal phosphate transport (as seen in hypophosphatemic rickets or tumor-induced osteomalacia) or as a generalized defect in proximal function (called the Fanconi syndrome) (see "Hereditary hypophosphatemic rickets and tumor-induced osteomalacia"). The Fanconi syndrome is typically accompanied by clinical evidence of other abnormalities in proximal reabsorption, including glucosuria (at a normal plasma glucose concentration), hypouricemia, aminoaciduria, and a hyperchloremic metabolic acidosis due to urinary bicarbonate wasting. Among the major causes of the Fanconi syndrome are cystinosis, Wilson's disease, multiple myeloma (in which filtered light chains are toxic to the proximal tubule), heavy metal toxicity, and medications (particularly nucleotide analog reverse transcriptase inhibitors, such as tenofovir, and ifosfamide). (See "Etiology and diagnosis of distal (type 1) and proximal (type 2) renal tubular acidosis", section on 'Proximal (type 2) RTA'.)

Isolated urinary phosphate wasting is rare but can be observed in patients receiving ferric carboxymaltose therapy for treatment of iron deficiency anemia [8], in children with certain genetic mutations leading to vitamin D-resistant rickets, or in adults with oncogenic osteomalacia, a condition characterized by the overproduction of phosphaturic substances from a mesenchymal tumor (usually a hemangiopericytoma). (See "Hypophosphatemia: Causes of hypophosphatemia", section on 'Vitamin D deficiency or resistance' and "Hypophosphatemia: Causes of hypophosphatemia", section on 'Primary renal phosphate wasting'.)

Diseases characterized by urinary phosphate wasting, such as hereditary forms of hypophosphatemic rickets and oncogenic osteomalacia, result from excess production of the phosphaturic hormone FGF23. Clinical clues that support the presence of one of these disorders as a cause for persistent hypophosphatemia include skeletal deformities, bone pain associated with severe osteopenia, progressive muscle weakness, history of nontraumatic fractures, a high urinary phosphate excretion in the absence of other signs of generalized proximal tubular dysfunction (eg, renal tubular acidosis, glucosuria, aminoaciduria, uricosuria), and a low or inappropriately normal plasma calcitriol (1,25-dihydroxyvitamin D) level. Typically, hypophosphatemia results in stimulation of calcitriol production, which in turn would raise serum phosphate by increasing intestinal phosphate absorption and, perhaps, via bone resorption. Thus, low or normal calcitriol levels in the setting of persistent hypophosphatemia would be counterintuitive. A more extensive discussion on the clinical features and diagnosis of phosphate wasting syndromes and vitamin D metabolism is provided elsewhere. (See "Hereditary hypophosphatemic rickets and tumor-induced osteomalacia", section on 'Tumor-induced osteomalacia' and "Overview of vitamin D", section on 'Metabolism'.)

TREATMENT — While overt symptoms of hypophosphatemia rarely occur unless the serum phosphate concentration is less than 2 mg/dL (0.64 mmol/L), some evidence suggests that even mild hypophosphatemia may be associated with poor clinical outcomes [9]. Serious symptoms such as muscle weakness and rhabdomyolysis are generally not observed until the serum phosphate concentration falls below 1 mg/dL (0.32 mmol/L) [10,11]. (See "Hypophosphatemia: Clinical manifestations of phosphate depletion".)

For these reasons, most hypophosphatemic patients will not require therapy other than that aimed at the underlying cause. As examples:

Hypophosphatemia occurring during the correction of diabetic ketoacidosis will correct spontaneously with normal dietary intake. Trials of routine phosphate supplementation have not shown benefit, but such therapy may be warranted in patients with severe symptomatic hypophosphatemia. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis", section on 'Serum phosphate' and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section on 'Phosphate depletion'.)

Patients who have hypophosphatemia due to gastrointestinal losses should correct spontaneously once there is resolution of the underlying cause (eg, diarrhea, chronic antacid therapy, or vitamin D deficiency which should be treated with vitamin D supplementation). Specific recommendations for vitamin D supplementation are presented elsewhere. (See "Hypophosphatemia: Causes of hypophosphatemia" and "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment".)

Phosphate repletion regimens — Our approach to phosphate repletion takes into account the serum phosphate concentration, the presence or absence of overt symptoms of hypophosphatemia, and whether the patient can take oral therapy. If possible, we prefer oral rather than intravenous phosphate therapy since intravenous repletion can lead to hyperphosphatemia that may result in serious complications such as hypocalcemia, acute kidney injury, and arrhythmias. (See 'Intravenous dosing' below.)

We suggest the following approach:

In asymptomatic patients with a serum phosphate less than 2.0 mg/dL (0.64 mmol/L), we give oral phosphate therapy since many of these patients have myopathy and weakness that are not clinically apparent

The treatment of symptomatic patients varies with the severity of the hypophosphatemia:

We treat with oral phosphate if the serum phosphate is 1.0 to 1.9 mg/dL (0.32 to 0.63 mmol/L)

We treat with intravenous phosphate if the serum phosphate is less than 1.0 mg/dL (0.32 mmol/L) and switch to oral replacement when the serum phosphate exceeds 1.5 mg/dL (0.48 mmol/L)

We stop phosphate repletion when the serum phosphate is greater than or equal to 2.0 mg/dL (0.64 mmol/L) unless there is an indication for chronic therapy such as persistent urinary phosphate wasting

Oral repletion is most often achieved with a combined preparation of sodium and potassium phosphate; sodium phosphate is preferred for intravenous therapy.

Oral dosing — When oral dosing is used, we initiate therapy with 30 to 80 mmol of phosphate per day in divided doses. Phosphate may also be supplemented with skim milk, which contains approximately 15 mmol of phosphate per 480 mL serving.

The following regimen is a reasonable approach [12]:

If the serum phosphate is greater than or equal to 1.5 mg/dL (0.48 mmol/L), 1 mmol/kg of elemental phosphorus (minimum of 40 mmol and a maximum of 80 mmol) can be given in three to four divided doses over a 24-hour period.

If the serum phosphate is less than 1.5 mg/dL (0.48 mmol/L), 1.3 mmol/kg of elemental phosphorus (up to a maximum of 100 mmol) can be given in three to four divided doses over a 24-hour period.

Patients with severe obesity may receive the maximal initial doses or an adjusted dose based upon their height and weight (calculator 2).

Patients with a reduced glomerular filtration rate should receive approximately one-half of the suggested initial dose.

The serum phosphate concentration should be rechecked 2 to 12 hours following the last of the divided doses to determine whether repeated doses are required. If so, the same approach may be reapplied.

Oral phosphate supplements (tablets and powders) contain varying ratios of sodium and potassium phosphate. Serious medication errors have occurred due to confusion among preparations and lack of uniformity of units on product labels and when ordering. Thus, an oral phosphate supplement should be selected with consideration of its potassium and sodium content and dosed according to mmol of phosphate. Commonly used oral potassium phosphate-sodium phosphate supplements include 250 mg (8 mmol) of phosphate per tablet.

Intravenous dosing — Intravenous phosphate is potentially dangerous since it can precipitate with calcium and produce a variety of adverse effects including hypocalcemia due to binding of calcium, kidney failure due to calcium phosphate precipitation in the kidneys, and possibly fatal arrhythmias.

If intravenous therapy is necessary in patients with severe symptomatic hypophosphatemia or an inability to take oral therapy, we suggest a dose that varies depending upon the severity of the hypophosphatemia and the weight of the patient. We suggest the following regimen [13,14]:

If the serum phosphate concentration is greater than or equal to 1.25 mg/dL (0.40 mmol/L), we give 0.08 to 0.24 mmol/kg over six hours (up to a maximum total dose of 30 mmol)

If the serum phosphate concentration is less than 1.25 mg/dL (0.40 mmol/L), we give 0.25 to 0.50 mmol/kg over 8 to 12 hours (up to a maximum total dose of 80 mmol)

Other investigators have advocated a more aggressive approach since, in critically ill patients receiving nutritional support, lower doses similar to those above were not effective. This strategy was evaluated in a study of 79 critically ill trauma patients with hypophosphatemia [15]. The following algorithm was used for dosing:

If the serum phosphate was 2.3 to 3.0 mg/dL (0.73 to 0.96 mmol/L), 0.32 mmol/kg was given

If the serum phosphate was 1.6 to 2.2 mg/dL (0.51 to 0.72 mmol/L), 0.64 mmol/kg was given

If the serum phosphate was less than 1.6 mg/dL (0.50 mmol/L or less), 1.0 mmol/kg was given

Each dose was rounded to the nearest 7.5 mmol for ease of preparation and was infused at 7.5 mmol per hour. If hypophosphatemia persisted on subsequent days, additional doses were given according to this strategy. On day 3, the serum phosphate was normal in all 79 patients. This dosing regimen appeared safe; mild hyperphosphatemia was noted only eight times in 237 patient-days, and there were no instances of hypocalcemia.

However, none of the patients in this study had kidney function impairment, a setting in which aggressive replacement should generally be avoided. In addition, we do not usually give phosphate replacement when the serum phosphate is above 2.0 mg/dL (0.64 mmol/L).

The serum phosphate concentration should be monitored every six hours when intravenous phosphate is given, and the patient should be switched to oral replacement when the serum phosphate concentration reaches 1.5 mg/dL (0.48 mmol/L) [16].

Urinary phosphate wasting — Hypophosphatemia due to persistent urinary phosphate wasting is more difficult to treat than other causes of hypophosphatemia since raising the serum phosphate concentration with phosphate supplements will result in a further increase in phosphate excretion that minimizes the elevation in serum phosphate.

Another possible approach to the treatment of urinary phosphate wasting is the administration of dipyridamole. The observation that acute administration of dipyridamole increases renal phosphate reabsorption in animals and humans prompted a prospective study evaluating its efficacy in 64 patients with idiopathic increased urinary phosphate losses and mild hypophosphatemia [17]. Exclusion criteria included hypercalcemia, a history of cardiovascular disease, a glomerular filtration rate of less than 70 mL/min per 1.73 m2, and others that were primarily focused on identifying patients with specific causes of phosphate wasting.

The administration of dipyridamole (75 mg four times daily) significantly increased serum phosphate levels in 80 percent of patients, with the maximum effect occurring after nine months of therapy. Serum levels of parathyroid hormone and calcium were unchanged, but the concentration of calcitriol (1,25-dihydroxyvitamin D) was significantly decreased. In two subsequent studies, dipyridamole had no effect in six patients with X-linked hypophosphatemia [18], and it increased serum phosphate levels in 11 patients with hypophosphatemia due to phosphate wasting following kidney transplantation [19].

Further studies are required to determine the role of dipyridamole in patients with hypophosphatemia due to urinary phosphate wasting. Based upon the available evidence, some but not all of the authors and reviewers of this topic suggest a trial of dipyridamole (75 mg four times daily), primarily in patients who have symptoms that might be attributable to hypophosphatemia (eg, muscle weakness, rhabdomyolysis).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Fluid and electrolyte disorders in adults".)

SUMMARY AND RECOMMENDATIONS

Evaluation – The etiology of hypophosphatemia is often evident from the history. If, however, the diagnosis is not apparent, then measurement of urinary phosphate excretion should be helpful. Phosphate excretion can be measured either from a 24-hour urine collection or by calculation of the fractional excretion of filtered phosphate (FEPO4) (calculator 1) from a random urine specimen. (See 'Evaluation' above.)

Low phosphate excretion – In hypophosphatemic patients, daily phosphate excretion should be less than 100 mg and the FEPO4 should be well below 5 percent if the kidney is responding normally and renal phosphate wasting is not the cause of the hypophosphatemia. The differential diagnosis of hypophosphatemia with an appropriately low FEPO4 includes increased cellular uptake and reduced net intestinal absorption. (See 'Low phosphate excretion' above and "Hypophosphatemia: Causes of hypophosphatemia".)

High phosphate excretion – Urinary phosphate excretion above 100 mg/day or a FEPO4 above 5 percent is indicative of renal phosphate wasting in patients with hypophosphatemia. This problem is due either to hyperparathyroidism or to a renal tubular defect, both of which impair proximal phosphate reabsorption by diminishing the activity of the sodium-phosphate cotransporters. (See 'Inappropriately high phosphate excretion' above and "Hypophosphatemia: Causes of hypophosphatemia", section on 'Increased urinary excretion'.)

Treatment – Symptoms of hypophosphatemia rarely occur unless the serum phosphate concentration is less than 2 mg/dL (0.64 mmol/L). For these reasons, most hypophosphatemic patients will not require therapy other than that aimed at the underlying cause. (See 'Treatment' above.)

Approach – In patients with hypophosphatemia and a serum phosphate less than 2.0 mg/dL (0.64 mmol/L), we suggest phosphate repletion (Grade 2C). Even if these patients are not overtly symptomatic, they may have myopathy and weakness that are not clinically apparent. (See 'Phosphate repletion regimens' above.)

-In asymptomatic patients with a serum phosphate less than 2.0 mg/dL (0.64 mmol/L), we give oral phosphate therapy.

-The treatment of symptomatic patients varies with the severity of the hypophosphatemia. We treat with oral phosphate if the serum phosphate is 1.0 to 1.9 mg/dL (0.32 to 0.63 mmol/L). We treat with intravenous (IV) phosphate if the serum phosphate is less than 1.0 mg/dL (0.32 mmol/L) and switch to oral replacement when the serum phosphate exceeds 1.5 mg/dL (0.48 mmol/L).

-We stop phosphate repletion when the serum phosphate is greater than or equal to 2.0 mg/dL (0.64 mmol/L) unless there is an indication for chronic therapy such as persistent urinary phosphate wasting.

Oral dosing – When oral phosphate is used, the following regimen is a reasonable approach (see 'Oral dosing' above):

-If the serum phosphate is greater than or equal to 1.5 mg/dL (0.48 mmol/L), 1 mmol/kg of elemental phosphorus (minimum of 40 mmol and a maximum of 80 mmol) can be given in three to four divided doses over a 24-hour period.

-If the serum phosphate is less than 1.5 mg/dL (0.48 mmol/L), 1.3 to 1.4 mmol/kg of elemental phosphorus (up to a maximum of 100 mmol) can be given in three to four divided doses over a 24-hour period.

IV dosing – IV phosphate is potentially dangerous since it can precipitate with calcium and produce a variety of adverse effects including hypocalcemia due to binding of calcium, kidney failure due to calcium phosphate precipitation in the kidneys, and possibly fatal arrhythmias.

If IV therapy is necessary, we use a dose that depends upon the severity of the hypophosphatemia and the weight of the patient (see 'Intravenous dosing' above):

-If the serum phosphate concentration is greater than or equal to 1.25 (0.40 mmol/L), we give 0.08 to 0.24 mmol/kg over six hours (up to a maximum total dose of 30 mmol).

-If the serum phosphate concentration is less than 1.25 mg/dL (0.40 mmol/L), we give 0.25 to 0.50 mmol/kg over 8 to 12 hours (up to a maximum total dose of 80 mmol).

The serum phosphate concentration should be monitored every six hours when intravenous phosphate is given, and the patient should be switched to oral replacement when the serum phosphate concentration reaches 1.5 mg/dL (0.48 mmol/L). (See 'Intravenous dosing' above.)

ACKNOWLEDGMENT — The authors and UpToDate thank Dr. Zalman Agus, who contributed to earlier versions of this topic review.

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