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Chapter 7: Disorders of Phosphorus Balance: Hyperphosphatemia and Hypophosphatemia

Prior to rounding on your dialysis shift you are stopped by the dietician in the hall. She recently met with one of your patients and shows you their laboratory results: serum calcium concentration 10.5 mg/dL, serum phosphorus concentration 7.5 mg/dL, and PTH level 40 pg/mL. The patient is currently on calcium acetate two tablets with meals three times a day. She asks what you would like to do to better control the hyperphosphatemia. Which of the choices below is the best answer?

A. Start paricalcitol

B. Begin cinacalcet

C. Shorten the patient’s dialysis time

D. Discontinue calcium acetate and start sevelamer hydrochloride

E. Order a dose of alendronate

The answer is D. Given the elevated serum calcium concentration, hyperphosphatemia and a suppressed PTH the best option would be to stop the calcium-containing binder and switch to a noncalcium-containing binder. Paricalcitol would not be optimal given the suppressed PTH and hypercalcemia. Cinacalcet would also not be a good option given the suppressed PTH. Alendronate would also not be a good option given the suppressed PTH.

A 35-year-old woman was previously well until 5 years previously when she began to develop a series of fractures with minimal or no trauma. Laboratory evaluation revealed a serum phosphorus concentration of 0.8 mg/dL with a markedly elevated fractional excretion of phosphate and a normal serum calcium concentration. Which of the following tests would you order next?



C. FGF-23

D. 1,25(OH)2 vitamin D3

E. Bone biopsy

The answer is C. An FGF-23 level would be the next test to order. The patient has severe hypophosphatemia and urinary phosphate wasting likely as a result of oncogenic osteomalacia. Severe hypophosphatemia is seen in patients with this disorder due to removal of sodium phosphate cotransporters from the luminal membrane of the proximal tubule and a decrease in 1,25 dihydroxyvitamin D3 concentration due to downregulation of 1α-hydroxylase and upregulation of 24-hydroxylase mediated by FGF-23. PTH generally does not cause severe hypophosphatemia because renal phosphate loses are to some degree mitigated by the actions of PTH on bone and intestine. PTH upregulates 1α-hydroxylase and increases intestinal calcium reabsorption. The same is true of PTHrP. 1,25(OH)2 vitamin D3 level would not be the best option. Bone biopsy is not the best option at this early point in the evaluation.


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