Part of “CHAPTER 67 – DISEASES OF ABNORMAL PHOSPHATE METABOLISM“

Treatment of the myriad of diseases that characteristically display hyperphosphatemia or hypophosphatemia depends on determining the mechanism underlying their pathogenesis. The cause can almost always be ascertained by assessment of the clinical setting, determination of renal function, measurement of urinary phosphate excretion, and analysis of arterial carbon dioxide tension and pH. Therapy is aimed at correcting both the serum phosphate concentration and the associated complications.

Theoretically, elevated serum phosphate levels may be reduced by decreasing the TmP, increasing the GFR, or diminishing the phosphate load (exogenous or endogenous). There are no generally available pharmacologic means of acutely altering the GFR or reducing the TmP. However, chronic use of drugs, such as acetazolamide, which decreases TmP and induces phosphaturia, is effective as ancillary treatment of disorders such as tumoral calcinosis. Nevertheless, regulation of hyperphosphatemia is most often achieved by reducing the renal phosphate load. In tumoral calcinosis and chronic renal failure, such an effect is obtained by restricting the dietary phosphate intake or by administering calcium carbonate or aluminum hydroxide. Alternative strategies for management of load-dependent hyperphosphatemia include the administration of intravenous calcium or intravenous glucose and insulin. The consequence of such intervention is sequestration of phosphate in bone or soft tissues. Dialysis can also be used for the acute management of load-dependent disorders or for the chronic maintenance of phosphate overload, such as that which complicates chronic renal failure. In the latter condition, phosphate binders are essential.71,72