Tertiary excess of fibroblast growth factor 23 and hypophosphatemia following kidney transplantation

Authors


Myles Wolf, MD, MMSc, Division of Nephrology and Hypertension, University of Miami, Miller School of Medicine, 1120 NW 14th St., CRB 819, Miami, FL 33136, USA
Tel.: 305 243 7760
Fax: 305 243 8914
E-mail: mwolf2@med.miami.edu

Abstract

Seeherunvong W, Wolf M. Tertiary excess of fibroblast growth factor 23 and hypophosphatemia following kidney transplantation.
Pediatr Transplantation 2011: 15:37–46. © 2010 John Wiley & Sons A/S.

Abstract:  Hypophosphatemia caused by inappropriate urinary phosphate wasting is a frequent metabolic complication of the early period following kidney transplantation. Although previously considered to be caused by tertiary hyperparathyroidism, recent evidence suggests a primary role for persistently elevated circulating levels of the phosphorus-regulating hormone, FGF23. In the setting of a healthy renal allograft, markedly increased FGF23 levels from the dialysis period induce renal phosphate wasting and inhibition of calcitriol production, which contribute to hypophosphatemia. While such tertiary FGF23 excess and resultant hypophosphatemia typically abates within the first few weeks to months post-transplant, some recipients manifest persistent renal phosphate wasting. Furthermore, increased FGF23 levels have been associated with increased risk of kidney disease progression, cardiovascular disease, and death outside of the transplant setting. Whether tertiary FGF23 excess is associated with adverse transplant outcomes is unknown. In this article, we review the physiology of FGF23, summarize its relationship with hypophosphatemia after kidney transplantation, and speculate on its potential impact on long-term outcomes of renal allograft recipients.

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