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FGF-23 and sFRP-4 in chronic kidney disease and post-renal transplantation.
Nephron Physiol. 2006; 104(1):p23-32.NP

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.

Authors+Show Affiliations

Renal Division, Washington University School of Medicine, St. Louis, Mo. 63110, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16691036

Citation

Pande, Sangeeta, et al. "FGF-23 and sFRP-4 in Chronic Kidney Disease and Post-renal Transplantation." Nephron. Physiology, vol. 104, no. 1, 2006, pp. p23-32.
Pande S, Ritter CS, Rothstein M, et al. FGF-23 and sFRP-4 in chronic kidney disease and post-renal transplantation. Nephron Physiol. 2006;104(1):p23-32.
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), p23-32.
Pande S, et al. FGF-23 and sFRP-4 in Chronic Kidney Disease and Post-renal Transplantation. Nephron Physiol. 2006;104(1):p23-32. PubMed PMID: 16691036.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - FGF-23 and sFRP-4 in chronic kidney disease and post-renal transplantation. AU - Pande,Sangeeta, AU - Ritter,Cynthia S, AU - Rothstein,Marcos, AU - Wiesen,Karen, AU - Vassiliadis,John, AU - Kumar,Rajiv, AU - Schiavi,Susan C, AU - Slatapolsky,Eduardo, AU - Brown,Alex J, Y1 - 2006/05/10/ PY - 2005/02/11/received PY - 2006/02/02/accepted PY - 2006/5/13/pubmed PY - 2006/9/29/medline PY - 2006/5/13/entrez SP - p23 EP - 32 JF - Nephron. Physiology JO - Nephron Physiol VL - 104 IS - 1 N2 - 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. SN - 1660-2137 UR - https://www.unboundmedicine.com/medline/citation/16691036/FGF_23_and_sFRP_4_in_chronic_kidney_disease_and_post_renal_transplantation_ L2 - https://www.karger.com?DOI=10.1159/000093277 DB - PRIME DP - Unbound Medicine ER -