Post-renal transplantation hypophosphatemia

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)213-220
Number of pages8
JournalPediatric Nephrology
Volume25
Issue number2
DOIs
StatePublished - Feb 2010

Fingerprint

Hypophosphatemia
Kidney Transplantation
Bone Diseases
Kidney
Transplants
Organ Transplantation
Natural History
Parathyroid Hormone
Phosphorus
Population
Transplantation
Pediatrics
Phenotype

Keywords

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

ASJC Scopus subject areas

  • Nephrology
  • Pediatrics, Perinatology, and Child Health
  • Medicine(all)

Cite this

Post-renal transplantation hypophosphatemia. / Sakhaee, Khashayar.

In: Pediatric Nephrology, Vol. 25, No. 2, 02.2010, p. 213-220.

Research output: Contribution to journalArticle

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