Hyperphosphatemia
- Article Author:
- Rajeev Goyal
- Article Editor:
- Ishwarlal Jialal
- Updated:
- 6/25/2020 11:55:32 AM
- For CME on this topic:
- Hyperphosphatemia CME
- PubMed Link:
- Hyperphosphatemia
Introduction
Phosphate is an abundant mineral found in the body. The body store of phosphate is 500 to 800 g, with 85% of the total body phosphate present in crystals of hydroxyapatite in the bone — about 10% found in muscles and bones in association with proteins, carbohydrates, and lipids. The rest gets distributed in various compounds in the extracellular fluid (ECF) and intracellular fluid (ICF). Phosphate is predominantly an intracellular anion.
The normal plasma inorganic phosphate (Pi )concentration in an adult is 2.5 to 4.5 mg/dl, and men have a slightly higher concentration than women. In children, the normal range is 4 to 7 mg/dl. A plasma phosphate level higher than 4.5 mg/dL is hyperphosphatemia. Phosphate plays an essential role in many biological functions such as the formation of ATP, cyclic AMP, phosphorylation of proteins, etc. Phosphate is also present in nucleic acids and acts as an important intracellular buffer.
Normal adult dietary phosphate intake is around 1000 mg/day. 90% of this is absorbed primarily in the jejunum. In the small intestine, phosphate is absorbed both actively and by passive paracellular diffusion. Active absorption is through sodium-dependent phosphate co-transporter type IIb (NPT2b).
Kidneys excrete ninety percent of the daily phosphate load while the gastrointestinal tract excretes the remainder. As phosphorus is not significantly bound to albumin, most of it gets filtered at the glomerulus. Therefore, the number of functional nephrons plays a significant role in phosphorus homeostasis; 75% of filtered phosphorus is reabsorbed in the proximal tubule, approximately 10% in the distal tubule, and 15% is lost in the urine. In the luminal side of the proximal tubule, the primary phosphorus transporter is the Type II Na/Pi co-transporter (NPT-2a). The activity of this transporter is increased by low serum phosphorus and 1,25(OH)2 vitamin D, increasing reabsorption of phosphorus. Renal tubular phosphorus reabsorption also increases by volume depletion, chronic hypocalcemia, metabolic alkalosis, insulin, estrogen, thyroid hormone, and growth hormone. Tubular reabsorption of phosphorus decreases by parathyroid hormone, phosphatonins, acidosis, hyperphosphatemia, chronic hypercalcemia, and volume expansion.
Phosphorus is transported out of the renal cell by a phosphate-anion exchanger located in the basolateral membrane.
Phosphate homeostasis is under direct hormonal influence of calcitriol, PTH, and phosphatonins, including fibroblast growth factor 23 (FGF-23). Receptors for Vitamin D, FGF-23, PTH, and calcium-sensing receptor (CaSR) also play an important role in phosphate homeostasis. Serum phosphate level is maintained through a complex interaction between intestinal phosphate absorption, renal phosphate handling, and the transcellular movement of phosphate that occurs between intracellular fluid and bone storage pool. A transient shift of phosphate into the cells is also stimulated by insulin and respiratory alkalosis.
Sodium-dependent Pi co-transporters
Absorption of phosphate is mediated by the brush border sodium-dependent Pi co-transporters (NPT), which depend on the Na/K-dependent ATPase. There are three classes of these co-transporters:
Type I Na/Pi co-transporter (NPT1): It gets expressed on the renal brush border membrane of the proximal tubule.
Type II Na/Pi co-transporters: These include three closely related isoforms, namely NPT2a, NPT2c, and NPT2b. NPT2a and NPT2c are both exclusively expressed on the brush border membrane of the renal proximal tubules, while NPT2b is expressed in several tissues, including lung and small intestine, but not the kidney.
Type III Na/Pi co-transporters: These are cell surface retroviral receptors that are ubiquitously expressed and are localized to every segment of the nephron at the basolateral membrane and mediate cellular Pi balance.
Parathyroid hormone (PTH)
Parathyroid hormone (PTH) is an important hormone that controls calcium and phosphate concentration through stimulation of renal tubular calcium reabsorption and bone resorption. PTH also stimulates the conversion of 25- hydroxyvitamin D to 1,25 dihydroxy vitamin D in renal tubular cells, which promotes intestinal calcium absorption as well as bone turnover.
Parathyroid hormone is synthesized, processed, and stored in parathyroid cells. Parathyroid hormone is secreted by exocytosis within seconds after induction of hypocalcemia. In circulation, parathyroid hormone is rapidly taken up by the liver and kidney, where it is cleaved into active amino- and inactive carboxyl-terminal fragments that are then cleared by the kidney. Intact parathyroid hormone has a plasma half-life of two to four minutes.
Any change in ionized calcium concentration gets sensed by calcium-sensing receptor (CaSR) on the surface of parathyroid cells, Increase in calcium activates these receptors, which inhibit parathyroid hormone secretion and decreases renal tubular reabsorption of calcium through second messengers.
Hypocalcemia, induced by increased phosphate levels, can also produce these effects. However, changes in phosphate concentration should be significant to produce substantial changes in serum calcium. Hyperphosphatemia can also directly stimulate parathyroid hormone synthesis as well as parathyroid cellular proliferation
Several drugs, such as penicillin, corticosteroids, some diuretics, furosemide, and thiazides, can induce hyperphosphatemia as an adverse reaction.
1, 25 dihydroxycholecalciferol (1, 25 DHCC)
1, 25 dihydroxycholecalciferol is the activated form of Vitamin D. It increases intestinal phosphate absorption by enhancing the expression of NPT2b transporter and stimulates renal phosphate absorption by increasing expression of NPT2a and NPT2c in the proximal tubule. 1,25 DHCC also enhances FGF23 production. The 1,25(OH)2D also suppresses the synthesis of PTH and enhances FGF23 production. [1]
Fibroblast growth factor 23 (FGF23)
FGF23 is a phosphatonin that is produced primarily by osteocytes and to a lesser extent, by osteoblasts. It is a hormone which consists of 251 amino acid residues, including a signal peptide comprising 24 amino acids.
It inhibits renal tubular reabsorption of phosphate. FGF23 exerts its effects by binding to the FGFR1-Klotho complex. Alpha Klotho serves as a co-receptor. FGF23 suppresses NPT2a and NPT2c expression at the proximal renal tubules, thereby inhibiting renal phosphate reabsorption.[2][3] FGF23 also reduces the circulatory level of 1,25(OH)2D by decreasing the expression of 1-alpha-hydroxylase and increasing the expression of 24-hydroxylase.
Etiology
Renal failure is the most common cause of hyperphosphatemia. A glomerular filtration rate of less than 30 mL/min significantly reduces the filtration of inorganic phosphate, increasing its serum level.
Other less common causes include a high intake of phosphorus or increased renal reabsorption.
High intake of phosphate can result due to excessive use of phosphate-containing laxatives or enemas, and vitamin D intoxication. Vitamin D increases intestinal phosphate absorption.
Hypoparathyroidism, acromegaly, and thyrotoxicosis enhance renal phosphate reabsorption resulting in hyperphosphatemia.
Hyperphosphatemia can also be due to genetic causes. Several genetic deficiencies can lead to hypoparathyroidism, pseudohypoparathyroidism, and decreased FGF-23 activity.
Pseudohyperphosphatemia is a laboratory artifact sometimes seen in patients with hyperglobulinemia, hyperlipidemia, and hyperbilirubinemia. This artifact is due to interference in phosphate assay.
Epidemiology
Researched revealed that the incidence of hyperphosphataemia was 12% in all patients at admission to a tertiary care hospital, excluding patients with end-stage renal disease (ESRD), with acute kidney injury (AKI) or whose phosphate did not get measured at admission.[4]
Hyperphosphatemia is a common laboratory abnormality encountered by nephrologists. In patients with ESRD, the prevalence of hyperphosphatemia varies from 50 to 74%.[5]
In a study, researchers found that among children with oncologic disorders who received liposomal amphotericin, nearly 45% of children developed hyperphosphatemia.[6]
Pathophysiology
Hyperphosphatemia, in general, can be caused due to:
- Excessive phosphate load
- Decreased renal excretion
- Transcellular shifting
- Hypoparathyroidism and pseudohypoparathyroidism
1. Excessive phosphate load:
An acute increase in phosphate load can be due to exogenous or endogenous causes. Phosphate being the major intracellular anion, massive tissue breakdown due to any cause can lead to the release of intracellular phosphate into the extracellular fluid. Massive tissue breakdown can result from rhabdomyolysis, tumor lysis syndrome, or severe hemolysis.
- Tumor lysis syndrome: Tumor lysis syndrome is caused mostly due to cytotoxic therapy in patients with conditions of rapid cell turnover, such as lymphomas and leukemias. Lysis of cells leads to the release of phosphate, causing hyperphosphatemia, accompanied by hyperuricemia, hyperkalemia, and hypocalcemia.
- Exogenous phosphate: This is most commonly due to the ingestion of large amounts of phosphate-containing laxatives.
- Vitamin D Intoxication: Vitamin D intoxication increases intestinal absorption of dietary phosphate and calcium.
2. Decreased renal excretion:
As discussed above, 90% of daily phosphate load gets excreted by kidneys, a decrease in renal function causes decreased secretion and increased retention of phosphate.
High serum phosphate levels are seen only in the late stages of chronic kidney disease. Activation of compensatory mechanisms, including an increase in fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) secretion, prevent an increase in serum phosphate during the early stages of CKD. Both FGF 23 and PTH increase fractional excretion of phosphate per functioning nephron, compensating for the progressive loss of functioning nephron mass. As CKD progresses, these mechanisms are unable to overcome the input of phosphate from dietary intake, leading to hyperphosphatemia.[7]
Renal failure also results in reduced synthesis of calcitriol and secondary hyperparathyroidism, causing increased osteoclastic bone reabsorption and release of calcium and phosphate into the circulation. Metabolic acidosis in renal failure can also contribute to hyperphosphataemia by the cellular shift of phosphate from cells.
Tumor Calcinosis: Tumoral calcinosis is a rare syndrome characterized by calcium salt deposition in different periarticular soft tissue regions. It primarily manifests during childhood or adolescence as painless, firm, tumor-like masses around the joints such as hips shoulders and elbows. They can also present with painful hyperostosis in the long bones, e.g., the tibia. Recessive mutations in UDP-N-acetyl-alpha-D-galactosamine: polypeptide N-acetylgalactosaminyl-transferase 3 (GALNT3) and fgf23 cause deficiency of FGF23, reducing renal phosphate excretion and causing hyperphosphatemia. Mutations in Klotho results in FGF23 resistance resulting in decreased activity and hyperphosphatemia.[8]
GALNT3 is responsible for the O-glycosylation of FGF23, which is essential for the secretion of biologically active intact FGF23. Homozygous or compound heterozygous GALNT3 mutations result in defects in the post-translational modification of FGF23, producing tumoral calcinosis. Mutations in the FGF23 coreceptor alpha-Klotho gene leads to end-organ resistance to FGF23.[2]
3. Transcellular shift: Lactic acidosis and diabetic ketoacidosis can, rarely, cause massive cellular shifts of phosphate out of the cells.
4. Pseudohypoparathyroidism (PHP): This is a rare condition characterized by a resistance to PTH at its receptor. Its manifestations include low serum calcium, high serum phosphate, and inappropriately high PTH levels.
PTH resistance can result from impaired cAMP generation, from accelerated cAMP degradation, or impaired cAMP-dependent protein kinase activation. Impaired production of cAMP and the defects in the Gsa protein, which couples PTH1Receptor to adenylyl cyclase, are most common. As this signal transduction pathway is used by many G-protein–coupled receptors(GPCRs), reduced responsiveness to numerous other hormones, including thyroid-stimulating hormone (TSH), is also seen.[9]
Hypoparathyroidism: This is a rare disease that results in hypocalcemia. The most common cause is an injury to or removal of the parathyroid gland during anterior neck surgery. Symptoms include paresthesias, muscle cramps, seizures, and laryngospasm.
It can also result from mutations in the autoimmune regulator gene (AIRE) gene resulting in hypoparathyroidism, mucocutaneous candidiasis, adrenal insufficiency, and malabsorption. AIRE plays a role in shaping central immunological tolerance by building the thymic microarchitecture, facilitating the negative selection of T cells in the thymus, and inducing a specific subset of regulatory T cells. The mutation in this gene leads to a form of hypoparathyroidism called autoimmune polyglandular failure type 1 (APS1), also called autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED). In this disease, hypoparathyroidism is usually the first of multiple autoimmune endocrine disorders to appear.[10][11]
Albright hereditary osteodystrophy (AHO): Defects include short stature, shortened fourth metacarpals and other bones of the hands and feet, rounded face, obesity, dental hypoplasia, and soft-tissue calcifications/ossifications and cognitive impairment. Patients with Pseudohypoparathyroidism have AHO and PTH resistance resulting in hypocalcemia and hyperphosphatemia. Patients with pseudo-pseudo hypoparathyroidism (pseudo PHP) have an AHO phenotype but no impairment in mineral metabolism, i.e., normal calcium and phosphate levels.
History and Physical
Most patients are asymptomatic. The underlying pathologies contribute to symptoms.
The clinician should check for features of Albright hereditary osteodystrophy (AHO).
The ensuing hyperphosphatemia may induce potentially symptomatic hypocalcemia due to calcium-phosphate precipitation in the tissues. Calcifications can also be present in skin, soft tissue, and periarticular regions. Prolonged bone demineralization can lead to bone fractures.
CNS features include delirium, coma, seizures, neuromuscular hyperexcitability, (Chvostek’s sign and Trousseau’s phenomenon), hyperreflexia, muscle cramping (e.g., carpopedal spasm) or tetany.
Cardiovascular changes include hypotension and heart failure.
Hyperphosphatemia results in deposits of calcium-phosphate complexes throughout the body; this results in vascular calcification and arteriosclerosis, producing systolic hypertension, widened pulse pressure, and subsequent left ventricular hypertrophy.
Ocular manifestations include band-shaped keratopathy, cataracts, red-eye, or conjunctivitis.
Evaluation
Repeat phosphate estimation should take place to confirm hyperphosphatemia.
Several factors affect the levels of serum phosphate. Serum phosphate exhibits a marked circadian rhythm, with a peak around 3:00 am and a nadir around 11:00 am. As hemodialysis removes phosphate, the timing between sampling and the last dialysis session is also important.[12][13]
As there is intraindividual variation in phosphate levels in CKD patients, the clinician should take serial measurements before deciding on phosphate lowering treatment. Serum phosphate level and Urinary total phosphate excretion are not reliable markers of the state of body phosphate load. Serum phosphate does not rise above normal until the glomerular filtration rate falls below 30 ml/min per 1.73 m^2.
Fractional phosphate excretion is a better marker and reflects the body’s adaptation to excrete increasing amounts of phosphate per remaining functional nephron.
Renal function tests, vitamin D, Serum calcium, and PTH levels also require assay. An increased BUN and creatinine with normal or elevated PTH and low calcium levels suggest renal insufficiency. PTH-based diagnostic approach should serve to evaluate hyperphosphatemia that is not due to kidney failure. Vitamin D intoxication characteristically demonstrates high calcium and phosphate levels and an increase in vitamin D levels.
Marked hyperphosphatemia with accompanying hypocalcemia and hyperkalemia and hyperuricemia suggests tumor lysis syndrome. Creatine phosphokinase levels and serum uric acid are elevated in rhabdomyolysis, while tumor lysis syndrome shows normal or marginally elevated creatine kinase and markedly elevated serum uric acid.
Patients with normal renal function require urinary phosphate assessment. These levels can help in differentiating between increased renal reabsorption ( extracellular fluid volume contraction and tumoral calcinosis) and extrarenal causes (rhabdomyolysis, laxative or enema use or phosphate toxicity)
Tumoral calcinosis characteristically demonstrates hyperphosphatemia and elevated or normal serum 1,25-dihydroxy vitamin D and calcitriol levels with normal serum calcium, alkaline phosphatase, and PTH concentrations.
X-ray imaging may demonstrate metastatic calcifications.
For blood phosphate estimation, serum or plasma is an option. For plasma, lithium heparin is the agent of choice as anticoagulants such as EDTA, oxalate, and citrate may interfere with the formation of the phosphomolybdate complex in routine assays.
Urine samples can be collected in plain bottles. Acidified urine is also useful to reduce the formation of insoluble calcium phosphate complexes. A 24-hour urine collection should accompany a paired serum sample for the calculation of renal tubular absorption of phosphate.
The most common measurement of serum inorganic phosphate is the reaction of phosphate ions with ammonium molybdate, in acidic pH, to form a colorless phosphomolybdate complex that can be measured directly by ultraviolet (UV) absorption at 340 nm, or after reduction to colored molybdenum blue at 600 to 700 nm. Currently, no reference method exists for the measurement of serum phosphate.
Monitoring
As per KDIGO guidelines, serum phosphate, along with calcium, intact parathyroid hormone (iPTH), and 25-hydroxyvitamin D levels are estimated in all patients with an estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m^2.
If the estimated glomerular filtration rate (eGFR) is between 30 to 59 mL/min/1.73 m^2, serum phosphate, and calcium should be measured every 6 to 12 months. In patients with estimated eGFR 15 to 29 mL/min/1.73 m^2, serum phosphate and calcium require assessment every three to six months.[14]
Treatment / Management
The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines for the management of hyperphosphatemia suggest that, in dialysis patients, phosphate levels require lowering toward the normal range; however, there is no given specific target level. In chronic kidney disease patients not receiving dialysis, serum phosphate level require maintenance in the normal range (i.e., under 4.5 mg/dL [1.45 mmol/L]). There are several strategies to control phosphate levels.
Acute hyperphosphatemia: If renal function is good, renal phosphate excretion can increase through extracellular volume expansion by saline infusion and diuretics.
Dietary Restriction: Dietary restriction of phosphate is effective both in predialysis and in dialysis patients. KDIGO recommends a daily phosphate intake of 800 to 1000 mg/d with a daily protein intake of 1.2 g/kg body weight. Also, it is reasonable to consider phosphate sources (e.g., animal, vegetable, additives) in making dietary recommendations. Severe protein restriction can cause malnutrition and, eventually, poorer outcomes.[15]
If renal function is impaired, it is an indication for hemodialysis.
Phosphate Binders:
In patients with persistently or progressively elevated phosphate despite dietary phosphate restriction, phosphate binders are the agent of choice. These are also used, concurrently with dietary restriction, when phosphate levels at presentation are very high (greater than 6 mg/dl)
Phosphate binders reduce the absorption of dietary phosphate in the gastrointestinal tract, by exchanging the anion phosphate with an active cation (carbonate, acetate, oxyhydroxide, and citrate) to form a nonabsorbable compound that gets excreted in the feces.
Aluminum-based agents are amongst the most effective and best tolerated. But doubts regarding their potential to cause aluminum toxicity, presenting with encephalopathy, osteomalacia, microcytic anemia, and premature death, have discouraged their prolonged use.
Calcium-based binders
Calcium-based binders (e.g., calcium carbonate and calcium acetate) are effective and do not have adverse effects associated with aluminum-based agents. However, they can lead to a positive calcium balance, which can aggravate the development of ectopic calcification in the media and intima of arterial vessels, a major contributing factor for the excess cardiovascular mortality observed in CKD patients.
Magnesium carbonate
Magnesium carbonate effectively reduces serum phosphate levels and shows good gastrointestinal tolerance. It also reduces vascular calcification by interfering with hydroxyapatite formation.
Sevelamer
Sevelamer is a crosslinked polymer which exchanges phosphate with HCl or carbonate in the gastrointestinal tract. The phosphate-laden polymer gets excreted in the feces. Both sevelamer hydrochloride (HCl) and sevelamer carbonate are options. Besides controlling hyperphosphatemia, sevelamer also improves endothelial function, binds bile salts, resulting in a significant reduction in serum total cholesterol and low-density lipoprotein cholesterol. However, this action may interfere with the absorption of fat and fat-soluble vitamins.
Lanthanum Carbonate
It is a chewable, calcium-free phosphate binder, which uses metal lanthanum for phosphate chelation. Lanthanum carbonate binds phosphate to form the nonabsorbable compound lanthanum phosphate.
Ferric Citrate
Ferric citrate exchanges citrate with phosphate in the gastrointestinal tract to form ferric phosphate, which is insoluble and excreted in the feces. An additional advantage with ferric citrate is that it increases serum ferritin, reducing the need for intravenous iron and erythropoietin stimulating agents in chronic kidney disease.
Sucroferric Oxyhydroxide
Sucroferric oxyhydroxide is a chewable, iron-based phosphate binder. A lower dose helps in better compliance. As iron gets excreted as part of the phosphate complex, it does not cause iron overload.
Drugs targeting intestinal phosphate transporters
Nicotinic Acid and Nicotinamide
These drugs lower sodium-dependent intestinal phosphate absorption via a reduction in NaPi2b expression. The degree of reduction is modest. Adverse effects included flushing, nausea, diarrhea, thrombocytopenia, and accumulation of potentially toxic metabolites.
Tenapanor
Tenapanor inhibits sodium/hydrogen ion-exchanger isoform 3 (NHE3), which plays a role in secondary active phosphate absorption. It thus reduces intestinal sodium and phosphate absorption.
Renal replacement Therapies:
Both peritoneal and hemodialysis remove phosphate, but the amount of phosphate absorbed from a normal diet is for more than that removed by any of these dialysis methods. Recommendations are for more intensive dialysis to improve phosphate removal.[16]
Management of Secondary Hyperparathyroidism:
For better control of hyperphosphatemia, control of secondary hyperparathyroidism is essential, using vitamin D metabolites and the calcium-sensing receptor agonists. Calcitriol or synthetic vitamin D analogs should not be given unless the serum phosphate concentration is < 5.5 mg/dL and the serum calcium is less than 9.5 mg/dL, as these agents can increase the serum calcium and phosphate, leading to metastatic and vascular calcification in patients with hyperphosphatemia before treatment.
For all dialysis patients, the target serum levels of phosphate should be between 3.5 and 5.5 mg/dL (1.13 to 1.78 mmol/L). Serum levels of corrected total calcium should be maintained lower than 9.5 mg/dL (less than 2.37 mmol/L). The values of the parathyroid hormone (PTH) should remain less than two to nine times the upper limit for the PTH assay.[17]
Differential Diagnosis
- Pseudohyperphosphatemia: It may be due to paraproteinemia caused by Waldenstrom macroglobulinemia, multiple myeloma or monoclonal gammopathy of unknown significance.
- Vitamin D intoxication
- Rhabdomyolysis
- Tumor lysis syndrome
- Pseudohypoparathyroidism
Prognosis
Hyperphosphatemia, in general, is an asymptomatic condition. Mortality is mostly due to underlying conditions.
Short term complications of hyperphosphatemia include tetany due to hypocalcemia. There can also be deposition of calcium/phosphate in soft tissues, subcutaneous tissues, and joints.
Increased serum phosphate is associated with increased mortality among dialysis patients. Research has shown that phosphate is a potential biomarker to predict mortality and reflect disease severity in critically ill patients receiving continuous renal replacement therapy.[18]
Acute phosphate nephropathy, due to mineral and bone disorder of the recipient, has been reported to cause graft failure in the renal transplant recipients.[19]
In a study in ICU patients, researchers found that altered phosphate levels were associated with worse morbidity and mortality.[20]
Complications
Increased serum phosphate is associated with increased mortality among dialysis patients.
In chronic kidney disease (CKD) patients, cardiovascular disease is the most common cause of death, due in part to excess vascular calcification. Amongst dialysis patients, vascular calcification is detected in more than 80 percent of patients by computed tomography (CT) scan. Hyperphosphatemia, along with hypercalcemia and high PTH concentration, induces a phenotypic switch of vascular smooth muscle cells to osteoblast-like cells and local inflammation, leading to medial calcification. Microcalcifications of coronary arteries may increase the vulnerability of the atheromatous plaque to mechanical stress imposed by blood pressure. Calcification of large vessels like the aorta increases arterial stiffness, causing hypertension and increased pulse pressure.[21][22]
Hyperphosphatemia complexes serum calcium, decreasing the levels of ionized calcium, and triggering the release of PTH, resulting in secondary hyperparathyroidism; this causes high bone turnover state, releasing calcium from the bone, to normalize the serum calcium level.
Elevated phosphate levels also inhibit 1-alpha hydroxylase, a renal enzyme required for activation of Vitamin D. The decrease of active vitamin D results in decreased intestinal absorption of calcium, decreased renal calcium and phosphate reabsorption, and impaired bone mineralization. Over months to years, bone density decreases and can cause abnormal bone architecture. Clinically, chronic hyperphosphatemia can manifest as bone pain and fractures.
Hyperphosphatemia, when due to tumor lysis syndrome, also correlates with increased potassium and increased release of purines and proteins, potentially causing an increase in uric acid and urea. Therefore, hyperuricemia and azotemia are common metabolic complications of tumor lysis syndrome.
In Rhabdomyolysis, myoglobin released from damaged tissue can cause heme pigment induced acute kidney injury.
In patients with acute kidney injury, hypercalcemia can occur during recovery due to the mobilization of tissue calcium phosphate deposits in response to a fall in serum phosphate levels.
Enhancing Healthcare Team Outcomes
Hyperphosphatemia can have a delayed diagnosis, as most patients remain asymptomatic. However, as the regulation of phosphate intricately links to calcium regulation, hyperphosphatemia can have significant effects on overall calcium phosphate homeostasis.
The key is to manage and treat the condition with an interprofessional team.
As the condition is more common in patients with renal disorders, nephrologists commonly encounter this condition in their clinical practice. However, a large number of specialists, including endocrinologists, pediatricians, pathologists, and radiologists play an essential role in its management.
The evaluation of hyperphosphatemia needs to have a broad vision, as several factors can affect phosphate levels.
The most crucial management action is the treatment of the underlying cause. The immediate management involves reducing the phosphate load in the body, either by promoting urinary excretion or by hemodialysis.
Several phosphate binders are also available and useful in patients with renal failure.