Hypophosphatemia%20-and-%20hyperphosphatemia Diagnosis
Diagnosis
Hypophosphatemia
- 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)
Classification
Mild Hypophosphatemia
- 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)
Evaluation
- 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
Hyperphosphatemia in Chronic Kidney Disease (CKD) Patients
- 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