Biochemistry and Molecular Biology

| Peer-Reviewed |

Serum iFGF-23, sKlotho, and 1,25 (OH)2 D3 Vitamin Levels in Kidney Transplant

Received: Apr. 07, 2020    Accepted: Apr. 22, 2020    Published: Apr. 28, 2020
Views:       Downloads:

Share This Article

Abstract

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 Blood samples were withdrawn for measuring the levels of serum iFGF-23, sKlotho, 1,25 (OH)2 D3 Vitamin, Calcium, Phosphorus, iPTH, 25 (OH) D vitamin.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.

DOI 10.11648/j.bmb.20200502.11
Published in Biochemistry and Molecular Biology ( Volume 5, Issue 2, June 2020 )
Page(s) 12-17
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

iFGF-23, sKlotho, 1, 25 (OH)2 D3, Kidney Transplantation

References
[1] Bergwitz, C. and H. Juppner, Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23. Annu Rev Med, 2010. 61: p. 91-104.
[2] 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.
[3] 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.
[4] 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.
[5] Kurosu, H., et al., Regulation of fibroblast growth factor-23 signaling by klotho. J Biol Chem, 2006. 281 (10): p. 6120-3.
[6] 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.
[7] Wolf, M., Update on fibroblast growth factor 23 in chronic kidney disease. Kidney Int, 2012. 82 (7): p. 737-47.
[8] 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.
[9] 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.
[10] 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.
[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.
[12] 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.
[13] Economidou, D., et al., FGF-23 Levels before and after Renal Transplantation. J Transplant, 2009. 2009: p. 379082.
[14] 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.
[15] 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.
[16] 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.
[17] 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.
[18] 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.
[19] 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.
[20] 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).
[21] 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.
[22] Cianciolo, G., et al., Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy. American Journal of Nephrology, 2016. 43 (6): p. 397-407.
[23] Tan, S.-J., et al., Mineral adaptations following kidney transplantation. Transplant International, 2017. 30 (5): p. 463-473.
[24] 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.
[25] 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.
[26] 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.
[27] Meir, T., et al., Parathyroid hormone activates the orphan nuclear receptor Nurr1 to induce FGF23 transcription. Kidney Int, 2014. 86 (6): p. 1106-15.
Cite This Article
  • APA Style

    Ayse Senelmis, Ozge Tugce Pasaoglu, Ozant Helvaci, Ulver Derici, Hatice Pasaoglu. (2020). Serum iFGF-23, sKlotho, and 1,25 (OH)2 D3 Vitamin Levels in Kidney Transplant. Biochemistry and Molecular Biology, 5(2), 12-17. https://doi.org/10.11648/j.bmb.20200502.11

    Copy | Download

    ACS Style

    Ayse Senelmis; Ozge Tugce Pasaoglu; Ozant Helvaci; Ulver Derici; Hatice Pasaoglu. Serum iFGF-23, sKlotho, and 1,25 (OH)2 D3 Vitamin Levels in Kidney Transplant. Biochem. Mol. Biol. 2020, 5(2), 12-17. doi: 10.11648/j.bmb.20200502.11

    Copy | Download

    AMA Style

    Ayse Senelmis, Ozge Tugce Pasaoglu, Ozant Helvaci, Ulver Derici, Hatice Pasaoglu. Serum iFGF-23, sKlotho, and 1,25 (OH)2 D3 Vitamin Levels in Kidney Transplant. Biochem Mol Biol. 2020;5(2):12-17. doi: 10.11648/j.bmb.20200502.11

    Copy | Download

  • @article{10.11648/j.bmb.20200502.11,
      author = {Ayse Senelmis and Ozge Tugce Pasaoglu and Ozant Helvaci and Ulver Derici and Hatice Pasaoglu},
      title = {Serum iFGF-23, sKlotho, and 1,25 (OH)2 D3 Vitamin Levels in Kidney Transplant},
      journal = {Biochemistry and Molecular Biology},
      volume = {5},
      number = {2},
      pages = {12-17},
      doi = {10.11648/j.bmb.20200502.11},
      url = {https://doi.org/10.11648/j.bmb.20200502.11},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.bmb.20200502.11},
      abstract = {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.},
     year = {2020}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Serum iFGF-23, sKlotho, and 1,25 (OH)2 D3 Vitamin Levels in Kidney Transplant
    AU  - Ayse Senelmis
    AU  - Ozge Tugce Pasaoglu
    AU  - Ozant Helvaci
    AU  - Ulver Derici
    AU  - Hatice Pasaoglu
    Y1  - 2020/04/28
    PY  - 2020
    N1  - https://doi.org/10.11648/j.bmb.20200502.11
    DO  - 10.11648/j.bmb.20200502.11
    T2  - Biochemistry and Molecular Biology
    JF  - Biochemistry and Molecular Biology
    JO  - Biochemistry and Molecular Biology
    SP  - 12
    EP  - 17
    PB  - Science Publishing Group
    SN  - 2575-5048
    UR  - https://doi.org/10.11648/j.bmb.20200502.11
    AB  - 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.
    VL  - 5
    IS  - 2
    ER  - 

    Copy | Download

Author Information
  • Department of Medical Biochemistry, Gazi University, Faculty of Medicine, Ankara, Turkey

  • Faculty of Health Science, Gazi University, Ankara, Turkey

  • Department of Internal Medicine (Nephrology), Faculty of Medicine, Gazi University, Ankara, Turkey

  • Department of Internal Medicine (Nephrology), Faculty of Medicine, Gazi University, Ankara, Turkey

  • Department of Medical Biochemistry, Gazi University, Faculty of Medicine, Ankara, Turkey

  • Section