Hypophosphatemia%20-and-%20hyperphosphatemia Diagnosis

• A decrease in serum phosphate should be distinguished from a decrease in total body storage of phosphate (phosphate deficiency)
• The extracellular fluid contains <5% of total body phosphorus
• Depending on renal function, serum phosphate may be normal or high in profound intracellular deficiency
• Serum phosphate may be low even when intracellular phosphate is normal following a sudden movement of extracellular phosphate

• Normal adult range: 2.45-4.5 mg/dL (0.81-1.45 mmol/L)

• Patient is usually asymptomatic
• Serum phosphate 0.75-1.0 mmol/L (2.2-3 mg/dL)

• Usually asymptomatic
• Serum phosphate 0.5-0.7 mmol/L (1.5-2.2 mg/dL)

• Patient is usually symptomatic
• Serum phosphate <0.3-0.5 mmol/L (<1-1.5 mg/dL)

• Hypophosphatemia may be transient and reflect intracellular shift with minimal clinical consequences
• In most cases of intracellular shift of phosphate, serum phosphate normalizes once the cause is managed

Conditions that accelerate intracellular uptake of phosphate

• Any cause of hyperventilation (eg sepsis, anxiety, pain, etc)
• Intravenous (IV) glucose administration
• Insulin therapy
• Administration of catecholamines and beta-receptor agonists
• Leukemic blast crisis
• Administration of erythropoietin or GCS-F
• Postsurgery or after trauma
• Thyrotoxic periodic paralysis

• Severe deprivation of dietary phosphate
• Chronic diarrhea and steatorrhea
• Vitamin D deficiency and resistance
• Phosphate absorption inhibition caused by antacids, phosphate binders, niacin

• Hyperparathyroidism
• Vitamin D deficiency and resistance
• Hypophosphatemic rickets that is hereditary
• Oncogenic osteomalacia
• Fanconi syndrome
• Use of Acetazolamide, Tenofovir, Iron (IV), chemotherapeutic agents

• Patients with CKD has elevated risk in having hyperphosphatemia
• In the early stages of CKD, there is a gradual decrease in filtered phosphate load that causes phosphate retention
• The retention of phosphate stimulates fibroblast growth factor-23 (FGF-23) and parathyroid hormone (PTH) secretion, that causes increased renal fractional excretion of phosphate by decreasing tubular phosphate reabsorption
• Production of dihydroxyvitamin D is suppressed by FGF-23, thereby decreasing intestinal phosphate absorption which causes elevated PTH levels, resulting in the development of secondary hyperparathyroidism
• The continued decline in renal function causes development of hyperphosphatemia due to insufficient renal excretion despite high levels of PTH and FGF-23