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Overview of the causes and treatment of hyperphosphatemia

Overview of the causes and treatment of hyperphosphatemia
Authors:
Jason R Stubbs, MD
Alan S L Yu, MB, BChir
Section Editor:
Stanley Goldfarb, MD
Deputy Editor:
Albert Q Lam, MD
Literature review current through: Jun 2022. | This topic last updated: Jun 28, 2021.

INTRODUCTION — Phosphate is an inorganic molecule consisting of a central phosphorus atom and four oxygen atoms. In the steady state, the serum phosphate concentration is primarily determined by the ability of the kidneys to excrete dietary phosphate. The diagnostic approach to hyperphosphatemia involves elucidating why phosphate entry into the extracellular fluid exceeds the degree to which it can be excreted in order to maintain normal plasma levels.

A broad overview of the causes and treatment of hyperphosphatemia is presented in this topic. Detailed discussions of renal osteodystrophy and the treatment of hyperphosphatemia in patients with chronic kidney disease (CKD) are found elsewhere:

(See "Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)".)

(See "Management of hyperphosphatemia in adults with chronic kidney disease".)

(See "Management of secondary hyperparathyroidism in adult dialysis patients".)

CAUSES OF HYPERPHOSPHATEMIA — Renal excretion is so efficient in normal subjects that balance can be maintained with only a minimal rise in serum phosphate concentration even if phosphorus intake is increased to as much as 4000 mg/day (130 mmol/day). Phosphorus intake above 4000 mg/day (130 mmol/day) causes only small elevations in serum phosphate concentrations as long as the intake is distributed over the course of the day. If, however, an acute phosphate load is given over several hours, transient hyperphosphatemia will ensue.

The diagnostic approach to hyperphosphatemia involves elucidating why phosphate entry into the extracellular fluid exceeds the degree to which it can be excreted or why the renal threshold for phosphate excretion is increased above normal. There are four general circumstances in which this occurs (table 1):

Acute phosphate load

Acute extracellular shift of phosphate

Acute or chronic kidney disease

A primary increase in tubular phosphate reabsorption

Acute phosphate load — A phosphate load sufficient to overwhelm renal capacity for excretion can be derived from either endogenous or exogenous sources. Since phosphate is the major intracellular anion, any cause of marked tissue breakdown can lead to release of intracellular phosphate into the extracellular fluid. The ensuing hyperphosphatemia may then induce potentially symptomatic hypocalcemia due to calcium-phosphate precipitation in the tissues. Examples of marked tissue breakdown include tumor lysis syndrome, muscle necrosis (rhabdomyolysis), and, rarely, marked hemolysis or transfusion of stored blood.

Tumor lysis syndrome — Tumor lysis syndrome is most often caused by cytotoxic therapy (but can occasionally occur spontaneously) in patients with a large burden of a tumor characterized by rapid cell turnover, such as lymphomas (particularly Burkitt lymphoma and non-Hodgkin lymphoma) and certain leukemias [1]. In addition to release of phosphate, this syndrome is also associated with the release of potassium, purines (which can be metabolized to uric acid), and cell proteins (which can be metabolized to urea). Thus, hyperkalemia, hyperuricemia (which may lead to acute kidney injury [AKI]), and azotemia are other common metabolic complications [2,3]. (See "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology and risk factors".)

Rhabdomyolysis — Similar considerations apply to rhabdomyolysis except that myoglobin is also released from the damaged cells [4,5]. The severity of the hyperphosphatemia and hypocalcemia may be increased if heme pigment-induced AKI ensues. In these patients, resolution of the kidney injury can lead to hypercalcemia as the serum phosphate concentration falls and the tissue calcium-phosphate deposits are mobilized [5]. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)", section on 'Treatment'.)

Exogenous phosphate — Hyperphosphatemia from exogenous sources is most commonly induced by the ingestion of large amounts of phosphate-containing laxatives [6-9]. Fleet's Phospho-Soda (which is no longer available over the counter), for example, contains 132 mg (4.25 mmol) of inorganic phosphate per mL. As a result, 20 mL taken over three to six hours can cause severe, even fatal, hyperphosphatemia and hypocalcemia. Less commonly, hyperphosphatemia has been reported in patients receiving high-dose fosphenytoin for the treatment of seizures [10].

In addition to absorption of the excess phosphate associated with phosphate-containing laxatives, volume contraction (due to diarrhea) and mild kidney function impairment (due to decreased kidney perfusion) may contribute to hyperphosphatemia in this setting. A review of the literature suggests that patients with underlying chronic kidney disease (CKD) are at particularly high risk for hyperphosphatemia due to phosphate-containing medications [6].

Acute phosphate nephropathy — There are a number of reports describing acute or subacute kidney injury (called acute phosphate nephropathy or phosphate nephropathy) occurring after the ingestion of sodium-phosphate laxatives (solution or tablets) as bowel preparation for colonoscopy [11-14]. This is discussed elsewhere. (See "Acute phosphate nephropathy".)

Acute extracellular shift of phosphate — Massive cellular shifts of phosphate out of the cells is a rare cause of hyperphosphatemia but has been documented with lactic acidosis and diabetic ketoacidosis (or severe hyperglycemia alone) [15-17]. In addition to promoting a shift of phosphate out of cells, metabolic acidosis can diminish glycolysis and therefore cellular phosphate utilization, resulting in an increase in the serum phosphate.

For unclear reasons, other forms of acidosis are less likely to be associated with hyperphosphatemia. In the case of lactic acidosis, concurrent tissue hypoxia and cell death is likely to further contribute to a decreased consumption and increased release of phosphate from cells. In the case of diabetic ketoacidosis, decreased cellular phosphate uptake due to insulin deficiency may contribute to the hyperphosphatemia. However, such patients are usually phosphate depleted, resulting from phosphaturia associated with the osmotic diuresis induced by hyperglycemia [17]. The phosphate deficiency in these patients will typically be unmasked (leading to hypophosphatemia) by the administration of insulin. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis", section on 'Serum phosphate'.)

Acute or chronic kidney disease — The filtered load of phosphorus is approximately 4 to 8 g/day (130 to 194 mmol/day). If, for example, the glomerular filtration rate (GFR) is 180 L/day (125 mL/min) and the phosphorus concentration is 4 mg/dL (1.3 mmol/L), then the filtered load will be 7.2 g/day. Only 5 to 20 percent of the filtered phosphorus is normally excreted, with most being reabsorbed in the proximal tubule [18,19]. The normal physiologic regulation of renal phosphate excretion is described elsewhere in detail; briefly, the following factors are involved (see "Hypophosphatemia: Causes of hypophosphatemia", section on 'Increased urinary excretion'):

Serum phosphate concentration – Hyperphosphatemia can directly diminish proximal tubular phosphate reabsorption via suppression of sodium-phosphate cotransporters in the luminal membrane that mediate reabsorption of filtered phosphate.

Parathyroid hormone – Parathyroid hormone (PTH) increases phosphate excretion by diminishing activity of sodium-phosphate cotransporters.

Phosphatonins – Similar to PTH, phosphatonins such as fibroblast growth factor 23 (FGF23) and secreted frizzled related protein-4 (sFRP-4) enhance urinary phosphate excretion by suppressing the luminal expression of sodium-phosphate cotransporters.

An acute or chronic reduction in GFR will initially diminish phosphate filtration and excretion. Nevertheless, phosphate balance can initially be maintained in such patients by decreasing proximal phosphate reabsorption under the influence of increased secretion of PTH and FGF23. Once the GFR falls below 20 to 25 mL/min, however, phosphate reabsorption is thought to be maximally suppressed, and urinary excretion may no longer keep pace with phosphate intake. At this point, hyperphosphatemia occurs, increasing the filtered load and reestablishing phosphate balance. (See "Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)".)

Increased tubular reabsorption of phosphate — In addition to a reduction in GFR, phosphate excretion can also be diminished by an increase in proximal phosphate reabsorption. This usually occurs in patients with otherwise normal kidney function who have one of the following conditions:

Hypoparathyroidism — Either deficient PTH secretion or renal resistance to PTH (pseudohypoparathyroidism) results in increased phosphate reabsorption and leads to hyperphosphatemia. These patients also have hypocalcemia due to reduced bone resorption and urinary calcium losses. (See "Etiology of hypocalcemia in adults".)

Treatment with calcium and vitamin D (or calcitriol [1,25-dihydroxyvitamin D, the most active metabolite of vitamin D]) lowers the serum phosphate concentration, although not always to the normal range. How this occurs is not clear, although two potential mechanisms include the following: calcium and vitamin D therapy increase the serum calcium concentration, which may directly diminish phosphate transport in the proximal tubule; calcitriol stimulates FGF23 production by bone, which could lead to a suppression of phosphate reabsorption by the proximal tubule.

Acromegaly — Hyperphosphatemia occurs in some patients with acromegaly. It is presumably due to direct stimulation of phosphate reabsorption by growth hormones or insulin-like growth factor I [20]. (See "Causes and clinical manifestations of acromegaly".)

Bisphosphonates — Bisphosphonates, primarily etidronate, can cause mild hyperphosphatemia [21,22]. This effect is mediated in part by direct stimulation of renal phosphate reabsorption [21].

FGFR inhibitors — The majority of cancer patients treated with fibroblast growth factor receptor (FGFR) inhibitors, such as erdafitinib, infigratinib, and pemigatinib, develop hyperphosphatemia [23,24]. This class effect is due to inhibition of fibroblast growth factor 23 (FGF23) signaling. FGF23 normally maintains systemic phosphate balance by stimulating urinary phosphate excretion; thus, blockade of FGF23 signaling enhances phosphate reabsorption in the proximal tubule, potentially resulting in hyperphosphatemia. This is discussed in greater detail elsewhere. (See "Chemotherapy nephrotoxicity and dose modification in patients with kidney impairment: Molecularly targeted agents and immunotherapies", section on 'FGFR inhibitors'.)

Vitamin D toxicity — Hyperphosphatemia may be associated with vitamin D toxicity. Vitamin D increases intestinal phosphate and calcium absorption, and the rise in serum calcium concentration diminishes urinary phosphate excretion, both by inhibiting PTH secretion and, in many cases, by impairing kidney function (in part due to direct renal vasoconstriction).

Familial tumoral calcinosis — Familial tumoral calcinosis is a rare autosomal recessive disorder characterized by hyperphosphatemia due to an increase in proximal tubular phosphate reabsorption, often in association with increased serum calcitriol concentrations [25]. The underlying defect that was first described was a mutation in the GALNT3 gene, which encodes a glycosyltransferase that is thought to prevent the degradation of FGF23 [26,27]. Gene mutations in FGF23 and Klotho (the FGF23 co-receptor) have also been described [28-31]. It is postulated that inactivating mutations in either the GALNT3 or FGF23 genes could lead to deficiency of circulating intact FGF23, which is a promoter of renal phosphate excretion [26]. In addition, FGF23 requires Klotho to bind to its receptor; therefore, a deficiency in Klotho could lead to a state of FGF23 end-organ resistance [32,33]. FGF23 and Klotho are discussed in detail elsewhere. (See "Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)", section on 'Fibroblast growth factor 23'.)

Familial tumoral calcinosis appears to be the mirror image of X-linked and autosomal dominant hypophosphatemic rickets in which increased activity of FGF23 causes a primary increase in renal phosphate excretion. The gold standard for diagnosis of familial tumoral calcinosis is genetic sequencing from whole blood samples. Detailed information regarding genetic testing for this disorder can be found here. (See "Hereditary hypophosphatemic rickets and tumor-induced osteomalacia".)

Serum calcium and PTH concentrations are typically within the normal range in patients with familial tumoral calcinosis. The tendency of phosphate to complex with calcium and cause hypocalcemia appears to be counterbalanced by increased production of 1,25-dihyroxyvitamin D and perhaps hyperphosphatemia-induced stimulation of calcium reabsorption in the distal nephron. The combination of hyperphosphatemia and normocalcemia results in a high calcium-phosphate product and calcium-phosphate deposition in the skin and subcutaneous tissues [34].

Lowering the serum phosphate concentration by dietary restriction and phosphate binders, which impair intestinal phosphate absorption, often results in resolution of these deposits [25,35]. If this is ineffective, increasing urinary phosphate excretion by the chronic administration of acetazolamide may be beneficial [36].

Pseudohyperphosphatemia — Spurious hyperphosphatemia due to interference with analytical methods may rarely occur in patients with hyperglobulinemia (any type of immunoglobulin in excess quantity), hyperlipidemia, hemolysis, and hyperbilirubinemia [37-40]. Among these conditions, the most common is hyperglobulinemia due to multiple myeloma, Waldenström macroglobulinemia, or monoclonal gammopathy [37,38]. Extreme pseudohyperphosphatemia due to therapy with high-dose liposomal amphotericin B has also been reported [41], as has spurious hyperphosphatemia due to sample contamination with recombinant tissue plasminogen activator or heparin [42,43]. Phosphate can be determined accurately by use of alternative analysis methods [41].

TREATMENT OF HYPERPHOSPHATEMIA — The approach to therapy differs in acute and chronic hyperphosphatemia. Acute severe hyperphosphatemia with symptomatic hypocalcemia can be life-threatening. The hyperphosphatemia usually resolves within 6 to 12 hours if kidney function is intact. If kidney function is intact, phosphate excretion can be increased by saline infusion, although this can further reduce the serum calcium concentration by dilution. Hemodialysis may be indicated in patients with symptomatic hypocalcemia, particularly if kidney function is impaired.

Chronic hyperphosphatemia — Chronic hyperphosphatemia requiring therapy occurs in patients with chronic kidney disease (CKD) and familial tumoral calcinosis. Treatment consists of diminishing intestinal phosphate absorption by a low-phosphate diet and phosphate binders. (See "Management of hyperphosphatemia in adults with chronic kidney disease" and "Management of secondary hyperparathyroidism in adult dialysis patients".)

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

Hyperphosphatemia results when phosphate entry into the extracellular fluid exceeds the rate at which it can be excreted. This occurs when there is a large phosphate load over a short period of time (which may be from endogenous or exogenous sources), cellular shift of phosphate from the cells to the extracellular fluid, acute or chronic kidney disease (CKD), and as a result of a primary increase in proximal phosphate reabsorption (table 1). (See 'Introduction' above.)

Increased extracellular phosphate from endogenous sources occurs in tumor lysis syndrome, muscle necrosis (rhabdomyolysis), and, rarely, marked hemolysis or transfusion of stored blood. Lactic acidosis and diabetic ketoacidosis (or severe hyperglycemia alone) may also cause increased mobilization of intracellular phosphate into the extracellular fluid. (See 'Acute phosphate load' above.)

An acute exogenous phosphate load may result from the ingestion of a large amount of a phosphate-containing laxative. Volume contraction (due to diarrhea) and mild kidney function impairment (due to decreased kidney perfusion) may contribute to hyperphosphatemia. (See 'Exogenous phosphate' above.)

Acute or chronic kidney disease is a common cause of diminished phosphate excretion. Urinary excretion may not keep pace with phosphate intake when the glomerular filtration rate (GFR) falls below 20 to 25 mL/min. (See 'Acute or chronic kidney disease' above.)

Increased proximal phosphate reabsorption occurs in patients with hypoparathyroidism or acromegaly, during treatment with bisphosphonates, fibroblast growth factor receptor (FGFR) inhibitors, or vitamin D, and due to a heritable condition called familial tumoral calcinosis. (See 'Increased tubular reabsorption of phosphate' above.)

Pseudohyperphosphatemia may rarely be caused by interference with analytical methods in patients with hyperglobulinemia, hyperlipidemia, hemolysis, and hyperbilirubinemia and has been reported with high-dose liposomal amphotericin B, recombinant tissue plasminogen activator, and heparin. (See 'Pseudohyperphosphatemia' above.)

Severe hyperphosphatemia with symptomatic hypocalcemia can be life-threatening. Phosphate excretion can be increased by saline infusion if kidney function is intact. Hemodialysis may be indicated in patients with symptomatic hypocalcemia, particularly if kidney function is impaired. (See 'Treatment of hyperphosphatemia' above.)

Chronic hyperphosphatemia occurs in patients with CKD and familial tumoral calcinosis. Treatment consists of diminishing intestinal phosphate absorption by a low-phosphate diet and phosphate binders. (See 'Chronic hyperphosphatemia' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Zalman S Agus, MD, who contributed to an earlier version of this topic review.

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