Case Study 1

An 11-year-old girl recently diagnosed with acute myeloid leukemia. After the third chemotherapy course, consisting of cytarabine, mitoxantrone, and intrathecal methotrexate, she was admitted to the hospital because of septic shock during febrile neutropenia. She was treated with meropenem and vancomycin, and blood cultures were positive for Streptococcus mitis . Because of persistent fever, the central venous catheter was removed. Nevertheless, the fever persisted and a chest computed tomography (CT) was performed, which revealed multiple abnormalities suggestive of pulmonary aspergillosis, which was confirmed by bronchoalveolar lavage. On day 5 of admission, she was started on amphotericin B, 5 mg/kg in glucose 5%. Because of the persisting neutropenia, granulocyte colony-stimulating factor (G-CSF) was administered. Fever disappeared with neutrophil recovery approximately 5 days after the start of G-CSF and amphotericin B.

Repeated blood tests showed normal renal function (creatinine 0.4 mg/dL, urea 15 mg/dL). Potassium supplementation was started because of hypokalemia. While phosphate concentrations were low at 2 mg/dL on day 5, they rose spontaneously from day 7 and laboratory tests showed progressive hyperphosphatemia, with a maximum of 7 mg/dL.

What is the most likely cause of the hyperphosphatemia observed in this patient?

  • A.


  • B.

    Pseudohyperphosphatemia due to amphoticin B

  • C.

    Vitamin D intoxication

  • D.

    Increased phosphate intake

The correct answer is B

Comment: Serum phosphate concentration is mainly affected by dietary intake and renal excretion of phosphate. Phosphate homeostasis is regulated by the phosphaturic hormones fibroblast growth factor-23 (FGF23) and parathyroid hormone, as well as by growth hormone and vitamin D. Other sources of phosphate include leakage of intracellular phosphate during tumor lysis, rhabdomyolysis, or hemolysis or a transcellular shift of phosphate during diabetic ketoacidosis or lactate acidosis.

The differential diagnosis of hyperphosphatemia can be divided into four major groups: (1) increased phosphate intake, (2) transcellular phosphate shift, (3) diminished phosphate excretion, and (4) pseudohyperphosphatemia. The patient in this case received no dietary phosphate supplements or phosphate-containing laxatives. The underlying malignancy was in remission and there were no signs of rhabdomyolysis or hemolysis. There was also no transcellular phosphate shift by diabetic ketoacidosis or lactic acidosis.

Laboratory investigations excluded renal insufficiency, and tubular reabsorption of phosphate was normal (87%). Hypoparathyroidism leading to increased tubular reabsorption of phosphate was ruled out. Growth analysis showed no signs of growth hormone excess, although growth hormone concentration was not measured.

Having excluded all in vivo causes, pseudohyperphosphatemia, that is, an artifact during the measurement of phosphate, was considered. This in vitro phenomenon has been reported for immunoglobulins, hyperlipidemia, and hyperbilirubinemia. Although there is an ongoing debate on the clinical relevance of some of these interferences, the influence of elevated levels of paraproteins by Waldenstrom macroglobulinemia and multiple myeloma is well established. Also, sample hemolysis is known to interfere with the laboratory phosphate assay.

In this case, triglyceride and bilirubin concentrations were normal, as were immunoglobulins. Samples from this patient were nonhemolytic. Analysis was therefore extended to medications known to cause pseudohyperphosphatemia, such as heparin and a tissue plasminogen activator. Another drug, which has been linked to interference of the laboratory phosphate assay, is liposomal amphotericin B, an antimycotic antibiotic. In our patient, hyperphosphatemia was first noted 2 days after liposomal amphotericin B had been prescribed for treatment of pulmonary aspergillosis. Therefore, this drug was considered the most probable culprit of the hyperphosphatemia.

Case Study 2

You receive a critical laboratory value on a patient with serum phosphorus level of 5.9 mg/dL.

Which of the following conditions MOST likely cussed the elevated serum phosphorus level? (Select all that apply)

  • A.

    Renal insufficiency

  • B.

    Tumor lysis syndrome

  • C.


  • D.


  • E.


The correct answers are A, B, and D

Comment: Normal serum phosphorus is between 3 and 4.5 mg/dL. The patient is experiencing hyperphosphatemia. Potential causes can include renal insufficiency, hypoparathyroidism, and tumor lysis syndrome. Malnutrition and hyperparathyroidism are causes for hypophosphatemia.

Case Study 3

A 14-year-old patient with renal insufficiency has recently been diagnosed with hyperphosphatemia.

What foods should the patient avoid to further worsening of high phosphorus levels? (Select all that apply)

  • A.

    Collard greens

  • B.

    Chicken and beef

  • C.


  • D.


The correct answer is B

Comment: Phosphorous is found in bones and is used for activation of vitamins/minerals. In renal insufficiency, the kidneys are unable to excrete phosphorus and it continues to build up in the blood. Fish, nuts, pumpkin, pork, beef, chicken, and squash are all rich in phosphorous.

Case Study 4

The physician is reviewing the clinical manifestations for hyperphosphatemia.

What would you expect to find on this patient’s clinical findings? (Select all that apply)

  • A.


  • B.


  • C.

    Negative Trousseau sign

  • D.

    Shortened ST interval

  • E.

    Prolonged QT interval

The correct answers are A, B, and E

Comment: Clinical manifestations you can see with high phosphorous levels are decreased heart rate, hypotension, diminished peripheral pulses, high risk for bleeding, irritable skeletal muscles, hyperactive deep tendon reflexes, prolonged QT intervals, and prolonged ST interval. We will not see negative Trousseau sign, negative Chvostek sign, and shortened ST interval.

Case Study 5

Which dietary recommendations would you provide to this patient? (Select all that apply)

  • A.

    Avoid laxative and enema medications

  • B.

    Increase intake of calcium-rich foods

  • C.

    Decease intake of phosphorous-rich foods

  • D.

    Avoid phosphate-binding medications

The correct answers are A, B, and C

Comment: Calcium and phosphorus have an inverse relationship. If the phosphorous is high, the calcium is low. The patient will need to decrease their phosphorous intake and increase their calcium intake. It is also important to discontinue laxative and enema medications as these medications cause phosphorous excess. Discontinuing phosphate-binding medications can cause an increase in phosphorus.

Case Study 6

Which of the following laboratory abnormalities would you expect to see in patients with hyperphosphatemia? (Select all that apply)

  • A.


  • B.


  • C.


  • D.


The correct answers are A and D

Comment: Phosphorous also has an inverse relationship with calcium and potassium. If the phosphorous is high, the calcium and potassium will be low. 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 adenosine triphosphate (ATP), cyclic adenosine monophosphate (cAMP), 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. Ninety percent 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 cotransporter type IIb (NPT2b).

Kidneys excrete 90% 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 cotransporter (NPT2a). 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 (PTH), 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.

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-hydroxy vitamin D to 1,25 dihydroxy vitamin D in renal tubular cells, which promotes intestinal calcium absorption as well as bone turnover. Any changes in ionized calcium concentration gets sensed by 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 (DHCC) 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.

FGF23 is a phosphatonin that is produced primarily by osteocytes and, to a lesser extent, by osteoblasts. It is a hormone that 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 coreceptor. FGF23 suppresses NPT2a and NPT2c expression at the proximal renal tubules, thereby inhibiting renal phosphate reabsorption. 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.

Renal failure is the most common cause of hyperphosphatemia. A glomerular filtration rate of less than 30 mL/min significantly reduces the filtration of Pi, 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.

Case Study 7

Patients with hyperphosphatemia may present with which symptoms?

  • A.

    Muscle cramps, tetany, and periorbital numbness

  • B.


  • C.

    Migraine, persistent dizziness

  • D.

    Pallor, skin discoloration

The correct answer is A

Comment: Most patients with hyperphosphatemia are asymptomatic. However, some may experience hypocalcemic symptoms, including muscle cramps, tetany, and perioral numbness or tingling. Other possible symptoms include bone and joint pain, pruritus, and rash. More often, patients report symptoms related to the underlying cause of the hyperphosphatemia.

Case Study 8

Which might be suggestive of renal failure, hypoparathyroidism, and pseudohypoparathyroidism as a cause of hyperphosphatemia?

  • A.

    Relatively low levels of intact parathyroid hormone (PTH)

  • B.

    High serum calcium and phosphate levels

  • C.

    Low levels of PTH and vitamin D

  • D.

    Low serum calcium levels with high phosphate levels

The correct answer is D

Comment: Low serum calcium levels along with high phosphate levels are observed with renal failure, hypoparathyroidism, and pseudohypoparathyroidism. Blood urea nitrogen (BUN) and creatinine values can also help to determine whether renal failure is the cause of hyperphosphatemia.

Relatively low levels of intact PTH along with normal renal function can be found in patients with primary or acquired hypoparathyroidism. High serum calcium and increased phosphate levels are observed with vitamin D intoxication and milk-alkali syndrome. Low levels of PTH and vitamin D are seen in milk-alkali syndrome.

Case Study 9

How often should serum levels of phosphate and calcium be assessed in patients with chronic kidney disease (CKD)?

  • A.

    Every 6 to 12 months in patients with stage 3 CKD

  • B.

    Every 1 to 2 months among patients with stage 4 CKD

  • C.

    Every 3 to 6 months in all patients with CKD, regardless of stage

  • D.

    Every 1 to 3 months in patients with stage 3 CKD

The correct answer is A

Comment: In patients with CKD, the development of metabolic bone disease involves a complex interaction of phosphate, calcium, and parathyroid hormone (PTH). As such, serial assessments of all three parameters are recommended in patients with CKD stage G3a-G5D to guide treatment. According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, reasonable monitoring intervals are as follows :

  • CKD G3a-G3b—Serum phosphate and calcium, every 6 to 12 months; PTH, based on baseline level and CKD progression

  • CKD G4—Serum phosphate and calcium, every 3 to 6 months; PTH, every 6 to 12 months

  • CKD G5, including G5D—Serum phosphate and calcium, every 1 to 3 months; PTH, every 3 to 6 months

Case Study 10

When should phosphate-lowering therapies be initiated in patients with chronic kidney disease (CKD)?

  • A.

    In all circumstances, unless contraindicated

  • B.

    Upon initiation of dialysis

  • C.

    Only in patients with progressive or persistent hyperphosphatemia

  • D.

    To those with glomerular filtration rate (GFR) less than 8 to 10 mL/min/1.73 m 2

The correct answer is C

Comment: In earlier releases of the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines , clinicians were advised to maintain phosphate in the normal range in patients with CKD. However, while acknowledging that preventing, rather than treating, hyperphosphatemia may be beneficial in patients with advanced CKD, the working group believes more data are needed to ascertain the risk/benefit ratio. Thus, current recommendations suggest phosphate-lowering therapies be administered to patients with progressive or persistent hyperphosphatemia only.

Case Study 11

What role do dietary interventions play in the management of phosphate levels in patients with chronic kidney disease (CKD)?

  • A.

    Dietary phosphate restriction is no longer recommended

  • B.

    Dietary phosphate intake should be limited in all patients with advanced CKD (stages 3 to 5)

  • C.

    Dietary phosphate restriction should only be used in conjunction with phosphate-lowering therapies

  • D.

    Dietary phosphate intake should be limited in all patients with CKD regardless of stage

The correct answer is B

Comments: Restricting dietary phosphate is an important practice for patients with advanced CKD and it is one of the strategies for correcting hyperphosphatemia. However, it is a complex and challenging task, and diet alone is often insufficient and unreliable for keeping phosphate concentrations within the recommended range. Consequently, many patients are advised to restrict dietary phosphate intake in addition to adequate dialysis and phosphate-lowering therapies.

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 fibroblast growth factor 23 (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.

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.

Approximately, kidneys excrete 90% of daily phosphate load; 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 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.

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 hyperphosphatemia by the cellular shift of phosphate from cells. Lactic acidosis and diabetic ketoacidosis can rarely cause massive cellular shifts of phosphate out of the cells.

Pseudohypoparathyroidism (PHP) 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 cyclic adenosine monophosphate (cAMP) generation, accelerated cAMP degradation, or impaired cAMP-dependent protein kinase activation. Impaired production of cAMP and the defects in the Gsa protein, which couples PTH1 receptor 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.

Hypoparathyroidism is also 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 (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.

Albright hereditary osteodystrophy (AHO) findings 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-pseudohypoparathyroidism (pseudo PHP) have an AHO phenotype but no impairment in mineral metabolism, that is, normal calcium and phosphate levels.

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 levels 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.

If renal function is good, renal phosphate excretion can increase through extracellular volume expansion by saline infusion and diuretics. Dietary restriction of phosphate is effective both in predialysis and in dialysis patients. KDIGO recommends a daily phosphate intake of 800 to 1000 mg/dL 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. If renal function is impaired, it is an indication for hemodialysis.

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 (> 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 (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 effectively reduces serum phosphate levels and shows good gastrointestinal tolerance. It also reduces vascular calcification by interfering with hydroxyapatite formation.

Sevelamer is a cross-linked polymer that exchanges phosphate with hydrochloride (HCl) or carbonate in the gastrointestinal tract. The phosphate-laden polymer gets excreted in the feces. Both sevelamer 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 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 exchanges citrate with phosphate in the gastrointestinal tract to form ferric phosphate, which is insoluble and excreted in the feces. An additional advantage of ferric citrate is that it increases serum ferritin, reducing the need for intravenous iron and erythropoietin stimulating agents in chronic kidney disease.

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.

Nicotinic acid and nicotinamide are drugs used in lowering sodium-dependent intestinal phosphate absorption via a reduction in NaPi-IIb expression. The degree of reduction is modest. Adverse effects included flushing, nausea, diarrhea, thrombocytopenia, and accumulation of potentially toxic metabolites.

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.

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.

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 less than 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 and 1.78 mmol/L). Serum levels of corrected total calcium should be maintained lower than 9.5 mg/dL (< 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.


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Sep 9, 2023 | Posted by in NEPHROLOGY | Comments Off on Hyperphosphatemia

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