Moshe Levi Mordecai Popovtzer

The physiologic concentration of serum phosphorus (phosphate) in normal adults ranges from 2.5 to 4.5 mg/dL (0.80-1.44 mmol/L). A diurnal variation occurs in serum phosphorus of 0.6 to 1.0 mg/dL, the lowest concentration occurring between 8 AM and 11 AM. A seasonal variation also occurs; the highest serum phosphorus concentration is in the summer and the lowest in the winter. Serum phosphorus concentration is markedly higher in growing children and adolescents than in adults, and it is also increased during pregnancy [1,2].

Of the phosphorus in the body, 80% to 85% is found in the skeleton. The rest is widely distributed throughout the body in the form of organic phosphate compounds. In the extracellular fluid, including in serum, phosphorous is present mostly in the inorganic form. In serum, more than 85% of phosphorus is present as the free ion and less than 15% is protein-bound.

Phosphorus plays an important role in several aspects of cellular metabolism, including adenosine triphosphate synthesis, which is the source of energy for many cellular reactions, and 2,3-diphosphoglycerate concentration, which regulates the dissociation of oxygen from hemoglobin. Phosphorus also is an important component of phospholipids in cell membranes. Changes in phosphorus content, concentration, or both, modulate the activity of a number of metabolic pathways.

Major determinants of serum phosphorus concentration are dietary intake and gastrointestinal absorption of phosphorus, urinary excretion of phosphorus, and shifts between the intracellular and extracellular spaces. Abnormalities in any of these steps can result either in hypophosphatemia or hyperphosphatemia [3-7].

The kidney plays a major role in the regulation of phosphorus homeostasis. Most of the inorganic phosphorus in serum is ultrafil-terable at the level of the glomerulus. At physiologic levels of serum phosphorus and during a normal dietary phosphorus intake, approximately 6 to 7 g/d of phosphorous is filtered by the kidney. Of that amount, 80% to 90% is reabsorbed by the renal tubules and the rest is excreted in the urine. Most of the filtered phosphorus is reabsorbed in the proximal tubule by way of a sodium gradient-dependent process (Na-Pj cotransport) located on the apical brush border membrane [8-10]. Recently two distinct Na-Pi cotransport proteins have been cloned from the kidney

(type I and type II Na-Pj cotransport proteins). Most of the hormonal and metabolic factors that regulate renal tubular phosphate reabsorption, including alterations in dietary phosphate content and parathyroid hormone, have been shown to modulate the proximal tubular apical membrane expression of the type II Na-Pj cotransport protein [11-16].

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