Abstract

This chapter focuses on two main types of phosphate homeostasis disorders: hypophosphatemia and hyperphosphatemia. Hypophosphatemia refers to serum phosphorus concentrations of less than 2.5 mg/dl. Several pathophysiological conditions may increase excretion of phosphorus in the urine. Some of these conditions are characterized by elevated levels of circulating parathyroid hormone (PTH). Because PTH decreases phosphorus reabsorption by the kidney, modest to marked elevations of this hormone may increase urinary excretion of this anion. Decreased tubular reabsorption of phosphorus may also occur without increased levels of PTH and may be because of changes in the reabsorption of salt and water, or because of renal tubular defects specific for the reabsorption of certain solutes or phosphorus. Hypophosphatemia may also occur in the diuretic phase of acute tubular necrosis or in post-obstructive diuresis, presumably owing to a combination of high levels of PTH and decreased tubular reabsorption of salt and water. Hyperphosphatemia is said to occur when serum phosphorus concentration exceeds 5 mg/dl in adults. It should be remembered that in children and adolescents, serum levels of phosphorus of up to 6 mg/dl may be physiological. The most frequent cause of hyperphosphatemia is decreased excretion of phosphorus in the urine as a consequence of a fall in glomerular filtration rate. However, increases in serum phosphorus can also occur as a result of increased entry into the extracellular fluid because of excessive intake of phosphorus or increased release of phosphorus from tissue breakdown.

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