causes of hypophosphatemia

causes of hypophosphatemia

The causes of hypophosphatemia should be organized by decreased intake and GI losses, transcellular shift, and increased renal phosphate wasting. Since phosphorus is a common constituent of food, decreased dietary intake is a rare cause of hypophosphatemia. However, malabsorption or increased colonic secretion from diarrhea can result in hypophosphatemia. Some cases of hypophosphatemia occur with chronic overuse of phosphorus binders or calcium-, magnesium-, or aluminum-containing antacids that block phosphorus absorption. Pharmaceutical niacin causes a modest reduction in serum phosphorus (0.3 mg/dL, 0.1 mmol/L), which is thought to be due to decreased GI absorption.

Increased renal phosphate excretion is a common cause of hypophosphatemia. Since PTH decreases renal phosphorus absorption by decreasing sodium-phosphate cotransporter activity in the proximal tubule, primary hyperparathyroidism is the prototypical example of renal phosphorous wasting. A unique form of hyperparathyroidism can occur after a kidney transplant. Patients with significant secondary hyperparathyroidism prior to transplant often have prolonged hypophosphatemia because they are unable to adequately suppress PTH following the transplant. In others, the hypophosphatemia persists despite normal PTH. In a series of 27 living donor transplants, FGF-23 was found to correlate best with post-transplant phosphorus levels.

Vitamin D deficiency can lead to hypocalcemia. This causes secondary hyperparathyroidism, which decreases serum phosphorus. This is made worse by decreased dietary phosphorus absorption from the lack of vitamin D.

Generalized dysfunction in the proximal tubule, Fanconi syndrome, is characterized by hypophosphatemia, in addition to glucosuria, proximal renal tubular acidosis, hypokalemia, and aminoaciduria.

Autosomal dominant hypophosphatemic rickets causes renal wasting of phosphorus. Patients are unable to mineralize bones so they end up with soft bones. It is due to an inability to inactivate FGF-23, which results in increased renal phosphorus wasting. A similar phenotype is seen in X-linked hypophosphatemic rickets ; however, in this condition, there is an inactivating mutation of PHEX, which normally decreases the expression of FGF-23.

The last major cause of hypophosphatemia is transcellular shift, where phosphorus is either shifted into cells or taken up by bones. The former occurs with increases in insulin. Refeeding syndrome occurs in patients with total body phosphorus depletion, who then undergo a fast of 2 to 3 days. When they resume eating, the sudden increase in carbohydrates causes a release of insulin which shifts glucose, potassium, and phosphorus into cells. Phosphorus, which is already somewhat depleted, is rapidly consumed with the conversion of glucose to glucose 6-phosphate.

Respiratory alkalosis reliably causes a shift of phosphorus into cells.

The other sudden cause of hypophosphatemia is hungry bone syndrome, which occurs in patients with significant secondary or tertiary hyperparathyroidism, which is then corrected by surgical removal of the parathyroid glands. This triggers a sudden drop in PTH and rapid remineralization of osteoid throughout the skeleton, causing sudden drops in serum calcium, phosphorus, magnesium, and potassium.


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