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Hyperphosphatemia

Updated : January 12, 2024





Background

Phosphate is a plentiful mineral mainly located in bones as hydroxyapatite crystals, making up about 85% of its content. The normal range for plasma inorganic phosphate concentration in adults is upto 4.5 mg/dl, and if it exceeds 4.5 mg/dl, it leads to hyperphosphatemia. Phosphate is involved in many important biological functions, such as the production of ATP and protein phosphorylation.

The absorption of phosphate occurs primarily in the jejunum via the sodium-dependent phosphate co-transporter type IIb (NPT2b), and 90% of the daily phosphate load is excreted by the kidneys, while the rest is eliminated by the gastrointestinal tract. The regulation of phosphate levels is primarily influenced by hormones such as calcitriol, PTH, and phosphatonins. Phosphate is absorbed through the sodium-dependent Pi co-transporters.

PTH regulates calcium and phosphate levels by promoting renal tubular calcium reabsorption and bone resorption. The calcium-sensing receptor (CaSR) detects changes in ionized calcium concentration and inhibits parathyroid hormone secretion, leading to decreased renal tubular calcium reabsorption. Hyperphosphatemia can directly stimulate parathyroid hormone synthesis and cellular proliferation, and certain medications can cause hyperphosphatemia as an adverse effect.

 

 

Epidemiology

Hyperphosphatemia is a common medical condition that nephrologists often come across. In a tertiary care hospital, 12% of patients at admission, excluding those with end-stage renal disease, acute kidney injury, or unmeasured phosphate levels, had hyperphosphatemia. The prevalence of hyperphosphatemia in patients with ESRD varies from 50% to 74%.

A recent study found that almost 45% of children with cancer treated with liposomal amphotericin developed hyperphosphatemia. This condition occurs when there is an excess of phosphate in the bloodstream and causes symptoms such as bone pain, muscle cramps, and abnormal heart rhythms.

Liposomal amphotericin is a potent medication used to treat fungal infections in children with cancer, but it has been linked to several adverse effects, including hyperphosphatemia. Healthcare providers must be aware of this potential side effect and monitor the phosphate levels of children prescribed this medication to prevent or manage hyperphosphatemia.

 

 

Anatomy

 

 

Pathophysiology

Hyperphosphatemia is a medical condition with high levels of phosphate in the blood. This can be caused by various factors, including excessive phosphate intake, decreased kidney function, and shifting of phosphate from cells to the bloodstream. Excessive phosphate intake can result from tissue breakdown due to certain medical conditions, including tumor lysis syndrome, rhabdomyolysis, severe hemolysis, and ingesting substantial amounts of phosphate-comprising laxatives or vitamin D supplements.

A decrease in kidney function can also lead to hyperphosphatemia since the kidneys play a critical role in filtering and excreting excess phosphate from the body. This is often seen in patients with chronic kidney disease (CKD) and is associated with secondary hyperparathyroidism, reduced calcitriol synthesis, and improved osteoclastic bone reabsorption. Metabolic acidosis in renal failure can also promote hyperphosphatemia by causing the release of phosphate from cells.

Tumor calcinosis is a rare condition that can cause hyperphosphatemia. This condition is characterized by the deposition of calcium salts in soft tissue regions and is primarily seen in children and adolescents. Recessive mutations in the fgf23 and GALNT3 genes cause a deficiency of fibroblast growth factor 23 (FGF23), leading to reduced renal phosphate excretion and hyperphosphatemia. Mutations in the Klotho gene can also result in FGF23 resistance and cause hyperphosphatemia.

In rare cases, diabetic ketoacidosis and lactic acidosis can cause significant cellular shifts of phosphate out of the cells, leading to abnormal phosphate levels in the bloodstream. Pseudohypoparathyroidism is an uncommon condition characterized by resistance to parathyroid hormone (PTH) at its receptor. This results in high serum phosphate, low serum calcium and inappropriately high PTH levels. The most common cause of PTH resistance is impaired cAMP production and defects in the Gsa protein.

Reduced responsiveness to numerous other hormones, including thyroid-stimulating hormone (TSH), is also observed since many G-protein–coupled receptors use this signal transduction pathway. Hypoparathyroidism is a rare condition that causes low calcium levels and is usually caused by injury or exclusion of the parathyroid gland in neck surgery. Symptoms include seizures, muscle cramps, and laryngospasm. The AIRE gene mutation can also lead to mucocutaneous candidiasis, hypoparathyroidism, adrenal insufficiency, and malabsorption.

This gene plays a critical role in determining central immunological tolerance and facilitating the adverse selection of T cells in the thymus. A mutation in this gene results in hypoparathyroidism called autoimmune polyglandular failure type 1 (APS1) or autoimmune polyendocrinopathy candidiasis ectodermal dystrophy. Hypoparathyroidism is often the first of multiple autoimmune endocrine disorders to appear in this disease.

 

 

Etiology

Hyperphosphatemia, characterized by elevated levels of inorganic phosphate in the blood, is commonly associated with renal failure, mainly when the glomerular filtration rate (GFR) is less than 30 mL/min. In such cases, the kidneys are less efficient in filtering out phosphate from the blood, resulting in its accumulation. However, there are several other less common causes of hyperphosphatemia.

One such cause is a high intake of phosphorus, which can result from the excessive use of phosphate-containing laxatives or enemas, as well as vitamin D intoxication. Vitamin D increases phosphate absorption in the intestines, leading to its accumulation in the blood. Hypoparathyroidism, thyrotoxicosis, and acromegaly can also enhance renal phosphate reabsorption, contributing to hyperphosphatemia. In some cases, hyperphosphatemia may also be caused by genetic deficiencies.

For example, hypoparathyroidism, pseudohypoparathyroidism, and decreased fibroblast growth factor 23 (FGF-23) activity can all lead to elevated levels of phosphate in the blood. It is worth noting that hyperphosphatemia can also be a laboratory artifact, particularly in patients with conditions such as hyperlipidemia, hyperglobulinemia, and hyperbilirubinemia. In such cases, the interference in the phosphate assay can lead to falsely elevated phosphate levels in the blood, a condition known as pseudo hyperphosphatemia.

 

 

Genetics

 

 

Prognostic Factors

Hyperphosphatemia is typically a condition that does not present with prominent symptoms, and mortality rates are usually attributable to underlying health conditions. However, short-term complications can occur, such as tetany resulting from low calcium levels and the deposition of calcium and phosphate in soft tissues, subcutaneous tissues, and joints.

Elevated levels of serum phosphate have been linked to increased mortality rates in patients undergoing dialysis. Additionally, phosphate may serve as a potential biomarker for predicting mortality rates and reflecting the severity of illness in critically ill patients receiving continuous renal replacement therapy.

In renal transplant recipients, acute phosphate nephropathy, caused by mineral and bone disorders, has been found to cause graft failure. A study of ICU patients revealed that altered phosphate levels were associated with greater morbidity and mortality rates.

 

 

Clinical History

Clinical History

Hyperphosphatemia is caused by an abnormally high concentration of phosphate in the blood. It is often asymptomatic, but acute cases may result in symptoms such as muscle cramps, tingling, and numbness, caused by hypocalcemia. Other symptoms include joint and bone pain, rash, and itching.

Generally, patients report symptoms related to the underlying cause of hyperphosphatemia, which could be uremic symptoms such as fatigue, shortness of breath, anorexia, nausea, vomiting, and sleep disturbances. Obtaining information related to the causes of hyperphosphatemia is important, and historical clues such as a history of kidney disease, cancer, endocrinopathies, trauma, burns, prolonged immobilization, metabolic or hematologic disorders, and ischemic bowel should be considered.

It is also crucial to review medication history as certain medications like oral phosphate binders, antacids, laxatives, potassium phosphate, bisphosphonates, enemas, hyperalimentation, or nutritional supplements may contribute to the development of hyperphosphatemia.

 

 

Physical Examination

Physical Examination

While no specific physical examination findings are unique to hyperphosphatemia, acute cases may present with hypotension and signs of hypocalcemia, such as positive Chvostek or Trousseau signs, hyperreflexia, carpopedal spasm, or seizures. One possible ocular sign of hyperphosphatemia is the development of cataracts. However, the condition affects the cardiovascular and nervous systems more commonly.

The nervous system signs and symptoms of hyperphosphatemia are diverse and can be debilitating. Patients with hyperphosphatemia may experience altered mental status, delirium, muscle cramping, tetany, coma, obtundation, convulsions, seizures, and neuromuscular hyperexcitability can manifest as Chvostek and Trousseau signs.

Additionally, patients may report experiencing paresthesias, particularly around the mouth and distal extremities. Hyperphosphatemia can cause a range of central nervous system and neuromuscular symptoms that can significantly impact a patient’s quality of life. It is important for healthcare providers to consider hyperphosphatemia as a potential cause of these symptoms and to initiate appropriate diagnostic and treatment measures to manage the condition.

 

 

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Differential Diagnoses

  • Vitamin D intoxication
  • Rhabdomyolysis
  • Pseudohypoparathyroidism
  • Tumor lysis syndrome
  • Pseudohyperphosphatemia

 

 

Laboratory Studies

 

 

Imaging Studies

 

 

Procedures

 

 

Histologic Findings

 

 

Staging

 

 

Treatment Paradigm

Phosphate Binders

When patients have persistently high phosphate levels despite dietary restrictions, phosphate binders are often prescribed as the preferred treatment. These binders are also used with dietary restrictions when initial phosphate levels are high, greater than 6 mg/dl. Phosphate binders work by decreasing the absorption of dietary phosphate in the gastrointestinal tract.

They accomplish this by swapping the anion phosphate with an active cation such as carbonate, acetate, oxyhydroxide, or citrate. This exchange creates a nonabsorbable compound that is eliminated through feces. While aluminum-based phosphate binders are considered the most effective and well-tolerated agents, concerns about the potential for aluminum toxicity have limited their long-term use.

Prolonged exposure to these agents can result in encephalopathy, osteomalacia, microcytic anemia, and premature death. Aluminum toxicity can be particularly harmful to patients with chronic kidney disease as they cannot excrete aluminum effectively. Because of this, aluminum-based phosphate binders should only be used as a last resort and for short periods under strict medical supervision.

Calcium-based binders

Calcium-based binders, such as calcium acetate and calcium carbonate, are highly effective in managing high phosphorus levels in individuals with chronic kidney disease (CKD). Compared to aluminum-based agents, these binders have fewer adverse effects. However, it is important to note that using calcium-based binders can result in a positive calcium balance in the body, which may contribute to ectopic calcification in the media and intima of arterial vessels. This major factor contributes to the excess cardiovascular mortality observed in CKD patients.

Ectopic calcification occurs when calcium is deposited in tissues that do not normally belong, such as blood vessels. In individuals with CKD, the kidneys cannot effectively remove excess calcium from the body. As a result, calcium can accumulate in the blood vessels, leading to calcified plaques that can narrow the arteries and increase the risk of cardiovascular disease. While calcium-based binders are effective in managing phosphorus levels, they should be used with caution in individuals with CKD who have high levels of calcium in their blood or a history of cardiovascular disease.

Magnesium carbonate

Magnesium carbonate is an effective agent for lowering serum phosphate levels and is well-tolerated by the gastrointestinal system. In addition, it can prevent hydroxyapatite formation, thus reducing the risk of vascular calcification.

Lanthanum Carbonate

It is a type of phosphate binder that can be chewed and does not contain calcium. It utilizes the metal lanthanum to trap phosphate. By binding with phosphate, lanthanum carbonate creates lanthanum phosphate, which the body cannot absorb.

Ferric Citrate

Ferric citrate works by replacing citrate with phosphate in the gastrointestinal tract, resulting in the formation of insoluble ferric phosphate that is then eliminated from the body through feces. Notably, ferric citrate also enhances serum ferritin levels, which can reduce the reliance on intravenous iron and erythropoietin-stimulating agents for individuals with chronic kidney disease.

 

 

by Stage

 

 

by Modality

 

 

Chemotherapy

 

 

Radiation Therapy

 

 

Surgical Interventions

 

 

Hormone Therapy

 

 

Immunotherapy

 

 

Hyperthermia

 

 

Photodynamic Therapy

 

 

Stem Cell Transplant

 

 

Targeted Therapy

 

 

Palliative Care

 

 

Medication

 

 

 

aluminum hydroxide 

Administer 300 to 600 mg orally thrice daily between meals and bedtime

Ulcer
Administer 5 to 30ml orally between meals and at bedtime



sucroferric oxyhydroxide 

Initial dose: 500 mg orally thrice a day with each meal
Titration and maintenance
Titrate the dosage in decrements or increments of 500 mg (i.e., 1 tablet) per day as necessary, until an adequate blood phosphorus level (5.5 mg/dL) is attained. Regular monitoring is then required.
Titration can begin as soon as one week after therapy begins, and it can thereafter be adjusted as needed at weekly intervals.
According to clinical trials, patients needed 3–4 tablets (1,500–2,000 mg/day) on average.
In a Phase 3 clinical study, patients with ESRD received a maximum daily dosage of six tablets (3,000 mg/day).



tetraferric tricitrate decahydrate 

with CKD on dialyisis
:

Initial dose: 420 mg (i.e., 2 tablets) orally 3 times a day with the meals
Monitor the serum phosphorus levels at 1-week intervals and alter dosage in decreasing or increasing of one to two tablets a day when necessary to keep serum phosphorus at desired levels.
should not exceed more than 12 tablets a day



 

aluminum hydroxide 

Administer 50 to 150 mg/kg/day orally divided every 4 to 6 hours
To maintain phosphorous within a normal range, titrate the dosage



 

Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK551586/

 

Hyperphosphatemia

Updated : January 12, 2024




Phosphate is a plentiful mineral mainly located in bones as hydroxyapatite crystals, making up about 85% of its content. The normal range for plasma inorganic phosphate concentration in adults is upto 4.5 mg/dl, and if it exceeds 4.5 mg/dl, it leads to hyperphosphatemia. Phosphate is involved in many important biological functions, such as the production of ATP and protein phosphorylation.

The absorption of phosphate occurs primarily in the jejunum via the sodium-dependent phosphate co-transporter type IIb (NPT2b), and 90% of the daily phosphate load is excreted by the kidneys, while the rest is eliminated by the gastrointestinal tract. The regulation of phosphate levels is primarily influenced by hormones such as calcitriol, PTH, and phosphatonins. Phosphate is absorbed through the sodium-dependent Pi co-transporters.

PTH regulates calcium and phosphate levels by promoting renal tubular calcium reabsorption and bone resorption. The calcium-sensing receptor (CaSR) detects changes in ionized calcium concentration and inhibits parathyroid hormone secretion, leading to decreased renal tubular calcium reabsorption. Hyperphosphatemia can directly stimulate parathyroid hormone synthesis and cellular proliferation, and certain medications can cause hyperphosphatemia as an adverse effect.

 

 

Hyperphosphatemia is a common medical condition that nephrologists often come across. In a tertiary care hospital, 12% of patients at admission, excluding those with end-stage renal disease, acute kidney injury, or unmeasured phosphate levels, had hyperphosphatemia. The prevalence of hyperphosphatemia in patients with ESRD varies from 50% to 74%.

A recent study found that almost 45% of children with cancer treated with liposomal amphotericin developed hyperphosphatemia. This condition occurs when there is an excess of phosphate in the bloodstream and causes symptoms such as bone pain, muscle cramps, and abnormal heart rhythms.

Liposomal amphotericin is a potent medication used to treat fungal infections in children with cancer, but it has been linked to several adverse effects, including hyperphosphatemia. Healthcare providers must be aware of this potential side effect and monitor the phosphate levels of children prescribed this medication to prevent or manage hyperphosphatemia.

 

 

 

 

Hyperphosphatemia is a medical condition with high levels of phosphate in the blood. This can be caused by various factors, including excessive phosphate intake, decreased kidney function, and shifting of phosphate from cells to the bloodstream. Excessive phosphate intake can result from tissue breakdown due to certain medical conditions, including tumor lysis syndrome, rhabdomyolysis, severe hemolysis, and ingesting substantial amounts of phosphate-comprising laxatives or vitamin D supplements.

A decrease in kidney function can also lead to hyperphosphatemia since the kidneys play a critical role in filtering and excreting excess phosphate from the body. This is often seen in patients with chronic kidney disease (CKD) and is associated with secondary hyperparathyroidism, reduced calcitriol synthesis, and improved osteoclastic bone reabsorption. Metabolic acidosis in renal failure can also promote hyperphosphatemia by causing the release of phosphate from cells.

Tumor calcinosis is a rare condition that can cause hyperphosphatemia. This condition is characterized by the deposition of calcium salts in soft tissue regions and is primarily seen in children and adolescents. Recessive mutations in the fgf23 and GALNT3 genes cause a deficiency of fibroblast growth factor 23 (FGF23), leading to reduced renal phosphate excretion and hyperphosphatemia. Mutations in the Klotho gene can also result in FGF23 resistance and cause hyperphosphatemia.

In rare cases, diabetic ketoacidosis and lactic acidosis can cause significant cellular shifts of phosphate out of the cells, leading to abnormal phosphate levels in the bloodstream. Pseudohypoparathyroidism is an uncommon condition characterized by resistance to parathyroid hormone (PTH) at its receptor. This results in high serum phosphate, low serum calcium and inappropriately high PTH levels. The most common cause of PTH resistance is impaired cAMP production and defects in the Gsa protein.

Reduced responsiveness to numerous other hormones, including thyroid-stimulating hormone (TSH), is also observed since many G-protein–coupled receptors use this signal transduction pathway. Hypoparathyroidism is a rare condition that causes low calcium levels and is usually caused by injury or exclusion of the parathyroid gland in neck surgery. Symptoms include seizures, muscle cramps, and laryngospasm. The AIRE gene mutation can also lead to mucocutaneous candidiasis, hypoparathyroidism, adrenal insufficiency, and malabsorption.

This gene plays a critical role in determining central immunological tolerance and facilitating the adverse selection of T cells in the thymus. A mutation in this gene results in hypoparathyroidism called autoimmune polyglandular failure type 1 (APS1) or autoimmune polyendocrinopathy candidiasis ectodermal dystrophy. Hypoparathyroidism is often the first of multiple autoimmune endocrine disorders to appear in this disease.

 

 

Hyperphosphatemia, characterized by elevated levels of inorganic phosphate in the blood, is commonly associated with renal failure, mainly when the glomerular filtration rate (GFR) is less than 30 mL/min. In such cases, the kidneys are less efficient in filtering out phosphate from the blood, resulting in its accumulation. However, there are several other less common causes of hyperphosphatemia.

One such cause is a high intake of phosphorus, which can result from the excessive use of phosphate-containing laxatives or enemas, as well as vitamin D intoxication. Vitamin D increases phosphate absorption in the intestines, leading to its accumulation in the blood. Hypoparathyroidism, thyrotoxicosis, and acromegaly can also enhance renal phosphate reabsorption, contributing to hyperphosphatemia. In some cases, hyperphosphatemia may also be caused by genetic deficiencies.

For example, hypoparathyroidism, pseudohypoparathyroidism, and decreased fibroblast growth factor 23 (FGF-23) activity can all lead to elevated levels of phosphate in the blood. It is worth noting that hyperphosphatemia can also be a laboratory artifact, particularly in patients with conditions such as hyperlipidemia, hyperglobulinemia, and hyperbilirubinemia. In such cases, the interference in the phosphate assay can lead to falsely elevated phosphate levels in the blood, a condition known as pseudo hyperphosphatemia.

 

 

 

 

Hyperphosphatemia is typically a condition that does not present with prominent symptoms, and mortality rates are usually attributable to underlying health conditions. However, short-term complications can occur, such as tetany resulting from low calcium levels and the deposition of calcium and phosphate in soft tissues, subcutaneous tissues, and joints.

Elevated levels of serum phosphate have been linked to increased mortality rates in patients undergoing dialysis. Additionally, phosphate may serve as a potential biomarker for predicting mortality rates and reflecting the severity of illness in critically ill patients receiving continuous renal replacement therapy.

In renal transplant recipients, acute phosphate nephropathy, caused by mineral and bone disorders, has been found to cause graft failure. A study of ICU patients revealed that altered phosphate levels were associated with greater morbidity and mortality rates.

 

 

Clinical History

Hyperphosphatemia is caused by an abnormally high concentration of phosphate in the blood. It is often asymptomatic, but acute cases may result in symptoms such as muscle cramps, tingling, and numbness, caused by hypocalcemia. Other symptoms include joint and bone pain, rash, and itching.

Generally, patients report symptoms related to the underlying cause of hyperphosphatemia, which could be uremic symptoms such as fatigue, shortness of breath, anorexia, nausea, vomiting, and sleep disturbances. Obtaining information related to the causes of hyperphosphatemia is important, and historical clues such as a history of kidney disease, cancer, endocrinopathies, trauma, burns, prolonged immobilization, metabolic or hematologic disorders, and ischemic bowel should be considered.

It is also crucial to review medication history as certain medications like oral phosphate binders, antacids, laxatives, potassium phosphate, bisphosphonates, enemas, hyperalimentation, or nutritional supplements may contribute to the development of hyperphosphatemia.

 

 

Physical Examination

While no specific physical examination findings are unique to hyperphosphatemia, acute cases may present with hypotension and signs of hypocalcemia, such as positive Chvostek or Trousseau signs, hyperreflexia, carpopedal spasm, or seizures. One possible ocular sign of hyperphosphatemia is the development of cataracts. However, the condition affects the cardiovascular and nervous systems more commonly.

The nervous system signs and symptoms of hyperphosphatemia are diverse and can be debilitating. Patients with hyperphosphatemia may experience altered mental status, delirium, muscle cramping, tetany, coma, obtundation, convulsions, seizures, and neuromuscular hyperexcitability can manifest as Chvostek and Trousseau signs.

Additionally, patients may report experiencing paresthesias, particularly around the mouth and distal extremities. Hyperphosphatemia can cause a range of central nervous system and neuromuscular symptoms that can significantly impact a patient’s quality of life. It is important for healthcare providers to consider hyperphosphatemia as a potential cause of these symptoms and to initiate appropriate diagnostic and treatment measures to manage the condition.

 

 

Differential Diagnoses

  • Vitamin D intoxication
  • Rhabdomyolysis
  • Pseudohypoparathyroidism
  • Tumor lysis syndrome
  • Pseudohyperphosphatemia

 

 

 

 

 

 

 

 

 

 

 

 

Phosphate Binders

When patients have persistently high phosphate levels despite dietary restrictions, phosphate binders are often prescribed as the preferred treatment. These binders are also used with dietary restrictions when initial phosphate levels are high, greater than 6 mg/dl. Phosphate binders work by decreasing the absorption of dietary phosphate in the gastrointestinal tract.

They accomplish this by swapping the anion phosphate with an active cation such as carbonate, acetate, oxyhydroxide, or citrate. This exchange creates a nonabsorbable compound that is eliminated through feces. While aluminum-based phosphate binders are considered the most effective and well-tolerated agents, concerns about the potential for aluminum toxicity have limited their long-term use.

Prolonged exposure to these agents can result in encephalopathy, osteomalacia, microcytic anemia, and premature death. Aluminum toxicity can be particularly harmful to patients with chronic kidney disease as they cannot excrete aluminum effectively. Because of this, aluminum-based phosphate binders should only be used as a last resort and for short periods under strict medical supervision.

Calcium-based binders

Calcium-based binders, such as calcium acetate and calcium carbonate, are highly effective in managing high phosphorus levels in individuals with chronic kidney disease (CKD). Compared to aluminum-based agents, these binders have fewer adverse effects. However, it is important to note that using calcium-based binders can result in a positive calcium balance in the body, which may contribute to ectopic calcification in the media and intima of arterial vessels. This major factor contributes to the excess cardiovascular mortality observed in CKD patients.

Ectopic calcification occurs when calcium is deposited in tissues that do not normally belong, such as blood vessels. In individuals with CKD, the kidneys cannot effectively remove excess calcium from the body. As a result, calcium can accumulate in the blood vessels, leading to calcified plaques that can narrow the arteries and increase the risk of cardiovascular disease. While calcium-based binders are effective in managing phosphorus levels, they should be used with caution in individuals with CKD who have high levels of calcium in their blood or a history of cardiovascular disease.

Magnesium carbonate

Magnesium carbonate is an effective agent for lowering serum phosphate levels and is well-tolerated by the gastrointestinal system. In addition, it can prevent hydroxyapatite formation, thus reducing the risk of vascular calcification.

Lanthanum Carbonate

It is a type of phosphate binder that can be chewed and does not contain calcium. It utilizes the metal lanthanum to trap phosphate. By binding with phosphate, lanthanum carbonate creates lanthanum phosphate, which the body cannot absorb.

Ferric Citrate

Ferric citrate works by replacing citrate with phosphate in the gastrointestinal tract, resulting in the formation of insoluble ferric phosphate that is then eliminated from the body through feces. Notably, ferric citrate also enhances serum ferritin levels, which can reduce the reliance on intravenous iron and erythropoietin-stimulating agents for individuals with chronic kidney disease.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

aluminum hydroxide 

Administer 300 to 600 mg orally thrice daily between meals and bedtime

Ulcer
Administer 5 to 30ml orally between meals and at bedtime



sucroferric oxyhydroxide 

Initial dose: 500 mg orally thrice a day with each meal
Titration and maintenance
Titrate the dosage in decrements or increments of 500 mg (i.e., 1 tablet) per day as necessary, until an adequate blood phosphorus level (5.5 mg/dL) is attained. Regular monitoring is then required.
Titration can begin as soon as one week after therapy begins, and it can thereafter be adjusted as needed at weekly intervals.
According to clinical trials, patients needed 3–4 tablets (1,500–2,000 mg/day) on average.
In a Phase 3 clinical study, patients with ESRD received a maximum daily dosage of six tablets (3,000 mg/day).



tetraferric tricitrate decahydrate 

with CKD on dialyisis
:

Initial dose: 420 mg (i.e., 2 tablets) orally 3 times a day with the meals
Monitor the serum phosphorus levels at 1-week intervals and alter dosage in decreasing or increasing of one to two tablets a day when necessary to keep serum phosphorus at desired levels.
should not exceed more than 12 tablets a day



aluminum hydroxide 

Administer 50 to 150 mg/kg/day orally divided every 4 to 6 hours
To maintain phosphorous within a normal range, titrate the dosage



 

 

https://www.ncbi.nlm.nih.gov/books/NBK551586/