Post-renal transplantation hypophosphatemia


An understanding of the pathophysiologic mechanisms of post-renal transplant (PRT) bone disease is of important clinical significance. Although bone disease occurs after all solid organ transplantation, the cumulative skeletal fracture rate remains high in PRT subjects while reaching a plateau with other transplantations. One major difference in the pathophysiology of PRT bone disease is, perhaps, due to persistent renal phosphorus (Pi) wasting. Novel phosphaturic agents have recently been suggested to participate in the development of bone disease in PRT subjects. However, it is unclear as of yet whether these factors alone or in conjunction with excess parathyroid hormone (PTH) secretion play a key role in the development of negative Pi balance and consequent bone disease in this population. In this review, I present a natural history of PRT hypophosphatemia and persistent renal Pi leak, provide pathophysiologic insight into these developments, and discuss the difficulty in diagnosing these phenotypes in both adult and pediatric populations.

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The author would like to acknowledge Ms. Hadley Armstrong for her primary role in the preparation and editorial review of this manuscript.


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Correspondence to Khashayar Sakhaee.

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Sakhaee, K. Post-renal transplantation hypophosphatemia. Pediatr Nephrol 25, 213–220 (2010).

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  • Bone disease
  • Hypophosphatemia
  • Phosphorus wasting
  • Post-renal transplantation