ArticleNephron. Physiology2006
FGF-23 and sFRP-4 in chronic kidney disease and post-renal transplantation.
Article in Nephron. Physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 107 citations in OpenAlex.
- Early control of PTH and FGF23 in normophosphatemic CKD patients: a new target in CKD-MBD therapy?Clinical journal of the American Society of Nephrology : CJASN · 2010Trial
- The Calcified Vasculature in Chronic Kidney Disease Secretes Factors that Inhibit Bone Mineralization.JBMR plus · 2022Article
- Hyperphosphatemia with elevated serum PTH and FGF23, reduced 1,25(OH)BMC nephrology · 2021Article
- Mineral and Bone Disease in Kidney Transplant Recipients.Current osteoporosis reports · 2018Review
- Status of vitamin D and parameters of calcium homeostasis in renal transplant recipients in Nepal: a cross sectional study.BMC nephrology · 2018Observational
- The Use of Vitamin D Metabolites and Analogues in the Treatment of Chronic Kidney Disease.Endocrinology and metabolism clinics of North America · 2017Review
- Stimulation of fibroblast growth factor 23 by metabolic acidosis requires osteoblastic intracellular calcium signaling and prostaglandin synthesis.American journal of physiology. Renal physiology · 2017Article
- FGF23 is associated with early post-transplant hypophosphataemia and normalizes faster than iPTH in living donor renal transplant recipients: a longitudinal follow-up study.Clinical kidney journal · 2016Article
- Serum fibroblast growth factor-23 and incident hypertension: the Atherosclerosis Risk in Communities (ARIC) Study.Journal of hypertension · 2016Article
- Renal Clearance of Mineral Metabolism Biomarkers.Journal of the American Society of Nephrology : JASN · 2016Article
- A Prospective Cohort Study of Mineral Metabolism After Kidney Transplantation.Transplantation · 2016Observational
- Mineral and bone disorder after kidney transplantation.World journal of transplantation · 2015Review
- Tumor-Induced Osteomalacia.Translational endocrinology & metabolism · 2015Article
- The use of fibroblast growth factor 23 testing in patients with kidney disease.Clinical journal of the American Society of Nephrology : CJASN · 2014Review
- FGF23 and mineral metabolism in the early post-renal transplantation period.Pediatric nephrology (Berlin, Germany) · 2013Article
- Renal phosphate handling: Physiology.Indian journal of endocrinology and metabolism · 2013Article
- Insights from genetic disorders of phosphate homeostasis.Seminars in nephrology · 2013Review
- Update on fibroblast growth factor 23 in chronic kidney disease.Kidney international · 2012Review
- Metabolic acidosis increases fibroblast growth factor 23 in neonatal mouse bone.American journal of physiology. Renal physiology · 2012Article
- Fibroblast growth factor 23 contributes to diminished bone mineral density in childhood inflammatory bowel disease.BMC gastroenterology · 2012Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe 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.
methodsPlasma 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.
resultsPlasma 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.
conclusionsIn 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.
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