FGF-23 and sFRP-4 in chronic kidney disease and post-renal transplantation

Sangeeta Pande, Cynthia S. Ritter, Marcos Rothstein, Karen Wiesen, John Vassiliadis, Rajiv Kumar, Susan C. Schiavi, Eduardo Slatapolsky, Alex J. Brown

Research output: Contribution to journalArticle

71 Scopus citations

Abstract

Background: The phosphatonins fibroblast growth factor-23 (FGF-23) and FRP-4 are inhibitors of tubular phosphate reabsorption that may play a role in the hyperphosphatemia associated with chronic kidney disease (CKD) or in the hypophosphatemia associated with renal transplants. Methods: Plasma FGF-23, FRP-4, phosphorus and parathyroid hormone were measured in patients at all stages of CKD. Phosphate regulation of FGF-23 and secreted frizzled related protein-4 (sFRP-4) was examined in end-stage renal disease patients in the presence and absence of therapeutic phosphate binder usage. In renal transplant patients, plasma FGF-23, sFRP-4 and phosphorus concentrations were determined before and 4-5 days after transplantation. Results: Plasma FGF-23 correlated with creatinine clearance (r2 = -0.584, p < 0.0001) and plasma phosphorus (r2 = 0.347, p < 0.001) in CKD patients and with plasma phosphorus (r2 = 0.448, p <0.001) in end-stage renal disease patients. Phosphate binder withdrawal increased FGF-23 levels. In kidney transplant patients, dramatic decreases in FGF-23 (-88.8 ± 5.4%) and phosphorus (-64 ± 10.2%) were observed by 4-5 days post-transplantation. In patients with post-transplant hypophosphatemia, FGF-23 levels correlated inversely with plasma phosphorus (r2 = 0.661, p < 0.05). sFRP-4 levels did not change with creatinine clearance or hyperphosphatemia in CKD or end-stage renal disease patients, and no relation was noted between post-transplant sFRP-4 levels and hypophosphatemia. Conclusions: In CKD, FGF-23 levels rose with decreasing creatinine clearance rates and increasing plasma phosphorus levels, and rapidly decreased post-transplantation suggesting FGF-23 is cleared by the kidney. Residual FGF-23 may contribute to the hypophosphatemia in post-transplant patients.

Original languageEnglish (US)
Pages (from-to)p23-p32
JournalNephron - Physiology
Volume104
Issue number1
DOIs
StatePublished - Aug 1 2006

    Fingerprint

Keywords

  • Fibroblast growth factor-23
  • Hyperparathyrodiism
  • Hypophosphatemia
  • Kidney disease
  • Matrix extracellular phosphoglycoprotein
  • Parathyroid hormone
  • Phosphate
  • Phosphatonin
  • Renal transplantation
  • Secreted frizzled related protein-4

ASJC Scopus subject areas

  • Physiology
  • Nephrology
  • Physiology (medical)

Cite this

Pande, S., Ritter, C. S., Rothstein, M., Wiesen, K., Vassiliadis, J., Kumar, R., Schiavi, S. C., Slatapolsky, E., & Brown, A. J. (2006). FGF-23 and sFRP-4 in chronic kidney disease and post-renal transplantation. Nephron - Physiology, 104(1), p23-p32. https://doi.org/10.1159/000093277