From the Guidelines
Hypophosphatemia is primarily caused by decreased intestinal absorption, increased urinary excretion, or internal redistribution of phosphate within the body, with common causes including malnutrition, vitamin D deficiency, and certain medications. The causes of low phosphate levels can be multifaceted, involving various mechanisms and underlying conditions. According to the most recent and highest quality study available, 1, the main mechanisms behind hypophosphatemia include:
- Decreased intestinal absorption, which can be due to malnutrition, vitamin D deficiency, chronic alcoholism, and malabsorption syndromes.
- Increased urinary excretion, often associated with certain medications like diuretics, hyperparathyroidism, and renal tubular disorders such as Fanconi syndrome.
- Internal redistribution of phosphate, which occurs during refeeding syndrome, respiratory alkalosis, hungry bone syndrome after parathyroidectomy, and treatment of diabetic ketoacidosis.
Other factors that can contribute to hypophosphatemia include severe burns, sepsis, and certain cancers. Treatment of hypophosphatemia depends on identifying and addressing the underlying cause, with options ranging from oral phosphate supplements for mild cases to intravenous phosphate replacement for severe or symptomatic cases. Monitoring phosphate levels during correction is crucial to prevent overcorrection and hyperphosphatemia.
Key considerations in managing hypophosphatemia, as highlighted by 1 and 1, include the use of oral phosphorus and active vitamin D in patients with X-linked hypophosphatemia, adjusting doses based on clinical and biochemical responses, and preventing nephrocalcinosis by keeping calciuria levels within the normal range. Additionally, 1 emphasizes the importance of avoiding hypercalcemia and using a dialysate calcium concentration between 1.25 and 1.50 mmol/L in patients with CKD stage G5D.
In clinical practice, as noted by 1 and 1, managing hypophosphatemia may involve dietary phosphate restriction, the use of phosphate binders, and addressing secondary causes such as vitamin D deficiency and phosphate wasting. The goal is to maintain normal phosphate levels, prevent complications, and improve patient outcomes.
From the FDA Drug Label
Hypophosphatemia should be avoided during periods of total parenteral nutrition (TPN), or other lengthy periods of intravenous infusions It has been suggested that patients receiving TPN receive 20 mEq phosphate (13 mmol phosphate)/1000 kcal from dextrose. Serum phosphate levels should be regularly monitored and appropriate amounts of phosphate should be added to the infusions to maintain normal serum phosphate levels
The causes of low phosphate (hypophosphatemia) are not directly stated in the provided drug labels. However, it can be inferred that total parenteral nutrition (TPN) and lengthy periods of intravenous infusions may lead to hypophosphatemia if not properly managed with phosphate supplementation.
- Key factors to consider:
From the Research
Causes of Hypophosphatemia
- Inadequate intake of phosphate
- Decreased intestinal absorption of phosphate
- Excessive urinary excretion of phosphate
- Shift of phosphate from the extracellular to the intracellular compartments 4
- Renal phosphate wasting due to genetic or acquired renal disorders 4, 5
- Vitamin D deficiency hyperparathyroidism 4
- Oncogenic osteomalacia 4
- Fanconi syndrome 4
- X-linked hypophosphatemic rickets 4
Clinical Settings Associated with Hypophosphatemia
- Refeeding after malnutrition or starvation 6, 5
- Alcoholism 6, 5, 7
- Diabetic ketoacidosis 5, 7
- Postoperative period 8
- Gram-negative septicemia 8
- Use of certain medications such as antacids, diuretics, and steroids 8
- Malignancy 7
- Renal failure 7
- Chronic obstructive pulmonary disease 7