Biochemistry and Molecular Biology
Volume 5, Issue 2, June 2020, Pages: 12-17
Received: Apr. 7, 2020;
Accepted: Apr. 22, 2020;
Published: Apr. 28, 2020
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Ayse Senelmis, Department of Medical Biochemistry, Gazi University, Faculty of Medicine, Ankara, Turkey
Ozge Tugce Pasaoglu, Faculty of Health Science, Gazi University, Ankara, Turkey
Ozant Helvaci, Department of Internal Medicine (Nephrology), Faculty of Medicine, Gazi University, Ankara, Turkey
Ulver Derici, Department of Internal Medicine (Nephrology), Faculty of Medicine, Gazi University, Ankara, Turkey
Hatice Pasaoglu, Department of Medical Biochemistry, Gazi University, Faculty of Medicine, Ankara, Turkey
Aim of the study: Chronic kidney disease is characterized by elevated iFGF-23 level, which is known to regulate phosphate, little is known about the relationship between iFGF-23 and phosphate homeostasis in posttransplant patients, however. We will look at the iFGF-23 level and correlate it with sKlotho, and 1,25 (OH)2 D3 Vitamin in posttransplant patients. Material and methods: This study was conducted using 60 kidney transplant patients. 34 healthy subjects enrolled as a control group. Blood samples were withdrawn for measuring the levels of serum iFGF-23, sKlotho, 1,25 (OH)2 D3 Vitamin, Calcium, Phosphorus, iPTH, 25 (OH) D vitamin. CKD-EPI is used to calculate GFR. Results: iFGF-23 levels were elevated in the posttransplant period compared with healthy subjects. iFGF-23 levels were measured as 263.64±153.08 pg/ml in transplant patients and 155.05±73.40 pg/ml within the control group. sKlotho levels were measured as 2.82±1.76 ng/ml and 3.72±3.59 ng/ml in transplant patients and control groups respectively. 1,25 (OH)2 D3 Vitamin levels were measured as 49.56±13.73 pg/ml and 48.42±12.13 pg/ml in transplant patients and control group respectively. The results of this study revealed a significant correlation between iFGF-23 and sKlotho both in transplant patients and in the control group. Conclusions: Significantly elevated iFGF-23 and iPTH level accompanied by decreased GFR activity suggests a progressive deficiency in phosphate homeostasis.
Ozge Tugce Pasaoglu,
Serum iFGF-23, sKlotho, and 1,25 (OH)2 D3 Vitamin Levels in Kidney Transplant, Biochemistry and Molecular Biology.
Vol. 5, No. 2,
2020, pp. 12-17.
Bergwitz, C. and H. Juppner, Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23. Annu Rev Med, 2010. 61: p. 91-104.
Gutierrez, O., et al., Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. J Am Soc Nephrol, 2005. 16 (7): p. 2205-15.
Prasad, N., et al., FGF23 is associated with early post-transplant hypophosphataemia and normalizes faster than iPTH in living donor renal transplant recipients: a longitudinal follow-up study. Clin Kidney J, 2016. 9 (5): p. 669-76.
Hu, M. C. and O. W. Moe, Klotho as a potential biomarker and therapy for acute kidney injury. Nat Rev Nephrol, 2012. 8 (7): p. 423-9.
Kurosu, H., et al., Regulation of fibroblast growth factor-23 signaling by klotho. J Biol Chem, 2006. 281 (10): p. 6120-3.
Sawires, H. K., et al., Serum klotho: relation to fibroblast growth factor-23 and other regulators of phosphate metabolism in children with chronic kidney disease. Nephron, 2015. 129 (4): p. 293-9.
Wolf, M., Update on fibroblast growth factor 23 in chronic kidney disease. Kidney Int, 2012. 82 (7): p. 737-47.
Ambuhl, P. M., et al., Metabolic aspects of phosphate replacement therapy for hypophosphatemia after renal transplantation: impact on muscular phosphate content, mineral metabolism, and acid/base homeostasis. Am J Kidney Dis, 1999. 34 (5): p. 875-83.
Green, J., et al., Evidence for a PTH-independent humoral mechanism in post-transplant hypophosphatemia and phosphaturia. Kidney Int, 2001. 60 (3): p. 1182-96.
Saito, H., et al., Human fibroblast growth factor-23 mutants suppress Na+-dependent phosphate co-transport activity and 1alpha, 25-dihydroxyvitamin D3 production. J Biol Chem, 2003. 278 (4): p. 2206-11.
Tony, E., et al., Serum changes in fibroblast growth factor-23 and in parameters of phosphorus metabolism after renal transplantation. Journal of The Egyptian Society of Nephrology and Transplantation, 2018. 18 (2): p. 46-56.
Bleskestad, I. H., et al., Soluble Klotho and intact fibroblast growth factor 23 in long-term kidney transplant patients. Eur J Endocrinol, 2015. 172 (4): p. 343-50.
Economidou, D., et al., FGF-23 Levels before and after Renal Transplantation. J Transplant, 2009. 2009: p. 379082.
Tomida, K., et al., Dialysis vintage and parathyroid hormone level, not fibroblast growth factor-23, determines chronic-phase phosphate wasting after renal transplantation. Bone, 2012. 51 (4): p. 729-736.
Saddadi, F., et al., Impact of FGF23 level on calcium and phosphorus levels in post-renal transplantation. J Renal Inj Prev, 2017. 6 (2): p. 99-102.
Sánchez Fructuoso, A. I., et al., Role of fibroblast growth factor 23 (FGF23) in the metabolism of phosphorus and calcium immediately after kidney transplantation. Transplantation proceedings, 2012. 44 (9): p. 2551-2554.
Mehrotra, S., R. K. Sharma, and M. R. Patel, Vitamin D, 1, 25-Dihydroxyvitamin D, FGF23, and Graft Function after Renal Transplantation. Indian J Nephrol, 2019. 29 (4): p. 242-247.
Komaba, H., M. Koizumi, and M. Fukagawa, Parathyroid resistance to FGF23 in kidney transplant recipients: back to the past or ahead to the future? Kidney Int, 2010. 78 (10): p. 953-5.
Krajisnik, T., et al., Parathyroid Klotho and FGF-receptor 1 expression decline with renal function in hyperparathyroid patients with chronic kidney disease and kidney transplant recipients. Kidney International, 2010. 78 (10): p. 1024-1032.
Dhayat, N. A., et al., Parathyroid Hormone and Plasma Phosphate Are Predictors of Soluble α-Klotho Levels in Adults of European Descent. J Clin Endocrinol Metab, 2020. 105 (4).
Olauson, H., et al., Parathyroid-specific deletion of Klotho unravels a novel calcineurin-dependent FGF23 signaling pathway that regulates PTH secretion. PLoS genetics, 2013. 9 (12): p. e1003975-e1003975.
Cianciolo, G., et al., Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy. American Journal of Nephrology, 2016. 43 (6): p. 397-407.
Tan, S.-J., et al., Mineral adaptations following kidney transplantation. Transplant International, 2017. 30 (5): p. 463-473.
Kim, H. R., et al., Circulating sKlotho Levels in CKD and Relationship to Progression. American Journal of Kidney Diseases, 2013. 61 (6): p. 899-909.
Seiler, S., et al., Plasma Klotho is not related to kidney function and does not predict adverse outcome in patients with chronic kidney disease. Kidney International, 2013. 83 (1): p. 121-128.
Ben-Dov, I. Z., et al., The parathyroid is a target organ for FGF23 in rats. J Clin Invest, 2007. 117 (12): p. 4003-8.
Meir, T., et al., Parathyroid hormone activates the orphan nuclear receptor Nurr1 to induce FGF23 transcription. Kidney Int, 2014. 86 (6): p. 1106-15.