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Hemodiyaliz Hastalarında Serum FGF-23 ve Sklerostin Düzeyleri: Kemik Mineral Dansitesi ve Kırık Riski ile İlişkisi

Year 2026, Volume: 16 Issue: 1, 110 - 115, 23.01.2026
https://doi.org/10.33631/sabd.1794625

Abstract

Amaç: Bu çalışmada hemodiyaliz hastalarında serum fibroblast büyüme faktörü-23 (FGF-23) ve sklerostin düzeylerinin sağlıklı kontroller ile karşılaştırılması ve bu biyobelirteçlerin kemik mineral dansitesi (KMD) ve kırık riski ile ilişkilerinin incelenmesi amaçlanmıştır.
Gereç ve Yöntemler: Çalışmaya 40 hemodiyaliz hastası ve yaş-cinsiyet açısından eşleştirilmiş 26 sağlıklı kontrol olmak üzere toplam 66 birey dahil edildi. Demografik, klinik ve biyokimyasal veriler kaydedildi. Serum FGF-23 ve sklerostin düzeyleri ELISA yöntemiyle ölçüldü. KMD, lomber omurga ve femur boynunda DXA ile değerlendirildi; kırık riski FRAX skorlarıyla hesaplandı. Korelasyon ve çok değişkenli regresyon analizlerine ek olarak, gruplar arası karşılaştırmalar uygun istatistiksel testlerle yapıldı ve kategorik değişkenler ki-kare analizi ile değerlendirildi.
Bulgular: Hemodiyaliz hastalarında serum FGF-23 (p<0,001) ve sklerostin (p<0,001) düzeyleri kontrollerden anlamlı derecede yüksekti. Lomber omurga ve femur KMD değerleri hemodiyaliz grubunda daha düşüktü (sırasıyla p=0,004 ve p=0,006). FRAX majör osteoporotik kırık (p=0,002) ve kalça kırığı risk skorları (p=0,001) ise anlamlı olarak daha yüksekti. FGF-23 ve sklerostin, serum fosfat (p=0,002 ve p=0,004) ve PTH (p=0,01 ve p=0,009) ile pozitif; lomber KMD ile negatif (p=0,01 ve p=0,008) korelasyon gösterdi. Çok değişkenli regresyon analizlerinde fosfat (p=0,01) ve PTH (p=0,008), FGF-23 için; fosfat (p=0,02) ve lomber KMD (p=0,01) ise sklerostin için bağımsız belirleyiciler olarak bulundu.
Sonuç: Hemodiyaliz hastalarında artmış FGF-23 ve sklerostin düzeyleri, azalmış KMD ve artmış kırık riski ile karakterizedir. Bu biyobelirteçler, kronik böbrek hastalığında kemik kırılganlığının değerlendirilmesinde densitometrik ölçümlere ek katkı sağlayabilir.

References

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  • 2. Navriya SC, Yadav OK, Shettar A, Singh M, Jain J, Kumar S, et al. Safety, feasibility, and efficacy of surgical intervention for Urolithiasis in patients with chronic kidney disease: A systematic review. World J Nephrol. 2025;14(3):105288. doi:10.5527/wjn.v14.i3.105288.
  • 3. Wung CH, Liu HY, Tsai TT, Chen JJ. Effects of anti-osteoporotic drugs in patients with chronic kidney disease: a systemic review and network meta-analysis of bone mineral density, clinical fracture rate and renal function. Front Pharmacol. 2025;16:1569744. doi:10.3389/fphar.2025.1569744. 4. Natale P, Green SC, Ruospo M, Craig JC, Vecchio M, Elder GJ, et al. Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD). Cochrane Database Syst Rev. 2025;6(6):Cd006023. doi:10.1002/14651858.CD006023.pub4.
  • 5. Hou YC, Lu CL, Lu KC. Mineral bone disorders in chronic kidney disease. Nephrology (Carlton). 2018;23 Suppl 4:88-94. doi:10.1111/nep.13457.
  • 6. Razzaque MS, Lanske B. The emerging role of the fibroblast growth factor-23-klotho axis in renal regulation of phosphate homeostasis. J Endocrinol. 2007;194(1):1-10. doi:10.1677/joe-07-0095.
  • 7. Czaya B, Faul C. The role of fibroblast growth factor 23 in inflammation and anemia. Int J Mol Sci. 2019;20(17).4195. doi:10.3390/ijms20174195.
  • 8. Jimbo R, Shimosawa T. Cardiovascular risk factors and chronic kidney disease-FGF23: a key molecule in the cardiovascular disease. Int J Hypertens. 2014;2014:381082. doi:10.1155/2014/381082.
  • 9. Clarke BL, Drake MT. Clinical utility of serum sclerostin measurements. BoneEy reports. 2013;2:361. doi:10.1038/bonekey.2013.95.
  • 10. Omran A, Atanasova D, Landgren F, Magnusson P. Sclerostin: from molecule to clinical biomarker. Int J Mol Sci. 2022;23(9):4751. doi: 10.3390/ijms23094751.
  • 11. Chiu SH, Wu WT. Sclerostin and cardiovascular risk: evaluating the cardiovascular safety of romosozumab in osteoporosis treatment. 2024;12(12):4751. doi:10.3390/biomedicines12122880.
  • 12. Lloret MJ, Fusaro M. Evaluating osteoporosis in chronic kidney disease: both bone quantity and quality matter. 2024;13(4): doi:10.3390/jcm13041010.
  • 13. Asadipooya K, Abdalbary M, Ahmad Y, Kakani E, Monier-Faugere MC, El-Husseini A. Bone quality in CKD patients: current concepts and future directions - Part I. Kidney Dis (Basel). 2021;7(4):268-77. doi:10.1159/000515534.
  • 14. Alobaidi S. Emerging biomarkers and advanced diagnostics in chronic kidney disease: early detection through multi-omics and AI. Diagnostics (Basel). 2025;15(10):1225. doi:10.3390/diagnostics15101225.
  • 15. Cannata-Andia JB, Roman-Garcia P, Hruska K. The connections between vascular calcification and bone health. Nephrol Dial Transplant. 2011;26(11):3429-36. doi:10.1093/ndt/gfr591.
  • 16. Shen Y, Yu C. The bone-vascular axis: a key player in chronic kidney disease associated vascular calcification. Kidney Dis (Basel). 2024;10(6):545-57. doi:10.1159/000541280.
  • 17. Lee WT, Fang YW, Chen M. Serum intact fibroblast growth factor 23 levels are negatively associated with bone mineral density in chronic hemodialysis patients. J Clin Med. 2023;12(4):1550. doi:10.3390/jcm12041550.
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  • 19. Li GH, Robinson-Cohen C, Sahni S, Au PC, Tan KC, Kung AW, et al. Association of genetic variants related to serum calcium levels with reduced bone mineral density. J Clin Endocrinol Metab. 2020;105(3):e328-36. doi:10.1210/clinem/dgz088.
  • 20. Eskandari Naji H, Ghorbanihaghjo A, Argani H, Raeisi S, Safa J, Alirezaei AH, et al. Serum sTWEAK and FGF-23 Levels in Hemodialysis and Renal Transplant Patients. Int J Organ Transplant Med. 2017;8(2):110-6.
  • 21. Vogt I, Haffner D, Leifheit-Nestler M. FGF23 and phosphate-cardiovascular toxins in CKD. Toxins (Basel). 2019;11(11):647. doi:10.3390/toxins11110647.
  • 22. Komaba H. Roles of PTH and FGF23 in kidney failure: a focus on nonclassical effects. Clin Exp Nephrol. 2023;27(5):395-401. doi:10.1007/s10157-023-02336-y.
  • 23. Isakova T, Wahl P, Vargas GS, Gutiérrez OM, Scialla J, Xie H, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int. 2011;79(12):1370-8. doi:10.1038/ki.2011.47.
  • 24. Delanaye P, Cavalier E, Bouquegneau A, Khwaja A. Sclerostin levels in CKD patients: an important, but not definitive, step on the way to clinical use. Kidney Int. 2015;88(6):1221-3. doi:10.1038/ki.2015.258.
  • 25. Laster M, Pereira RC, Noche K, Gales B, Salusky IB, Albrecht LV. Sclerostin, Osteocytes, and Wnt Signaling in Pediatric Renal Osteodystrophy. 2023;15(19):4127. doi:10.3390/nu15194127.
  • 26. Gómez-Islas VE, García-Fong KR, Aguilar-Fuentes RE, Hernández-Castellanos S, Pherez-Farah A, Méndez-Bribiesca SA, et al. Evaluation of bone densitometry by dual-energy x-ray absorptiometry as a fracture prediction tool in women with chronic kidney disease. Bone Rep. 2020;13:100298. doi:10.1016/j.bonr.2020.100298.
  • 27. Wu PY, Chen SC, Lin YC, Chen PC, Chung WS, Huang YC, et al. Role of fracture risk assessment tool and bone turnover markers in predicting all-cause and cardiovascular mortality in hemodialysis patients. Front Med (Lausanne). 2022;9:891363. doi:10.3389/fmed.2022.891363.
  • 28. Moysés RM, Schiavi SC. Sclerostin, Osteocytes, and Chronic Kidney Disease - Mineral Bone Disorder. Seminars in dialysis. 2015;28(6):578-86.10.1111/sdi.12415.

Serum FGF-23 and Sclerostin Levels in Hemodialysis Patients: Associations with Bone Mineral Density and Fracture Risk

Year 2026, Volume: 16 Issue: 1, 110 - 115, 23.01.2026
https://doi.org/10.33631/sabd.1794625

Abstract

Aim: This study aimed to evaluate serum fibroblast growth factor-23 (FGF-23) and sclerostin levels in hemodialysis patients compared with healthy controls, and to investigate their associations with bone mineral density (BMD) and fracture risk..
Material and methods: A total of 66 participants were included: 40 patients undergoing maintenance hemodialysis and 26 age- and sex-matched healthy controls. Demographic, clinical, and biochemical parameters were recorded. Serum FGF-23 and sclerostin were measured using ELISA. BMD was assessed at the lumbar spine and femoral neck using DXA, and fracture risk was estimated using FRAX scores. In addition to correlation and multivariate regression analyses, between-group comparisons were performed using appropriate statistical tests, and categorical variables were evaluated with chi-square analysis.
Results: Hemodialysis patients had significantly higher serum FGF-23 (p<0.001) and sclerostin (p<0.001) levels compared with controls. Lumbar spine and femoral BMD values were significantly lower in the hemodialysis group (p=0.004 and p=0.006, respectively), while FRAX major osteoporotic and hip fracture risk scores were significantly higher (p=0.002 and p=0.001, respectively). FGF-23 and sclerostin showed positive correlations with phosphate (p=0.002 and p=0.004) and PTH (p=0.01 and p=0.009), and negative correlations with lumbar BMD (p=0.01 and p=0.008). In multivariate regression, phosphate (p=0.01) and PTH (p=0.008) were independent determinants of FGF-23, while phosphate (p=0.02) and lumbar BMD (p=0.01) were independent determinants of sclerostin.
Conclusion: Elevated FGF-23 and sclerostin levels, along with reduced BMD and increased fracture risk, characterize hemodialysis patients. These biomarkers may complement densitometric measures in evaluating bone fragility in chronic kidney disease.

Ethical Statement

This cross-sectional study was approved by the Clinical Research Ethics Committee of Duzce University (Approval number: 2022/163) and conducted in accordance with the principles of the Declaration of Helsinki. Written informed consent was obtained from all participants prior to enrollment. This study was conducted as part of the medical specialty thesis of Feyza Bircan under the supervision and academic responsibility of Kürşad Öneç

References

  • 1. Bello AK, Alrukhaimi M, Ashuntantang GE, Basnet S, Rotter RC, Douthat WG, et al. Complications of chronic kidney disease: current state, knowledge gaps, and strategy for action. Kidney international supplements. 2017;7(2):122-9. doi:10.1016/j.kisu.2017.07.007.
  • 2. Navriya SC, Yadav OK, Shettar A, Singh M, Jain J, Kumar S, et al. Safety, feasibility, and efficacy of surgical intervention for Urolithiasis in patients with chronic kidney disease: A systematic review. World J Nephrol. 2025;14(3):105288. doi:10.5527/wjn.v14.i3.105288.
  • 3. Wung CH, Liu HY, Tsai TT, Chen JJ. Effects of anti-osteoporotic drugs in patients with chronic kidney disease: a systemic review and network meta-analysis of bone mineral density, clinical fracture rate and renal function. Front Pharmacol. 2025;16:1569744. doi:10.3389/fphar.2025.1569744. 4. Natale P, Green SC, Ruospo M, Craig JC, Vecchio M, Elder GJ, et al. Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD). Cochrane Database Syst Rev. 2025;6(6):Cd006023. doi:10.1002/14651858.CD006023.pub4.
  • 5. Hou YC, Lu CL, Lu KC. Mineral bone disorders in chronic kidney disease. Nephrology (Carlton). 2018;23 Suppl 4:88-94. doi:10.1111/nep.13457.
  • 6. Razzaque MS, Lanske B. The emerging role of the fibroblast growth factor-23-klotho axis in renal regulation of phosphate homeostasis. J Endocrinol. 2007;194(1):1-10. doi:10.1677/joe-07-0095.
  • 7. Czaya B, Faul C. The role of fibroblast growth factor 23 in inflammation and anemia. Int J Mol Sci. 2019;20(17).4195. doi:10.3390/ijms20174195.
  • 8. Jimbo R, Shimosawa T. Cardiovascular risk factors and chronic kidney disease-FGF23: a key molecule in the cardiovascular disease. Int J Hypertens. 2014;2014:381082. doi:10.1155/2014/381082.
  • 9. Clarke BL, Drake MT. Clinical utility of serum sclerostin measurements. BoneEy reports. 2013;2:361. doi:10.1038/bonekey.2013.95.
  • 10. Omran A, Atanasova D, Landgren F, Magnusson P. Sclerostin: from molecule to clinical biomarker. Int J Mol Sci. 2022;23(9):4751. doi: 10.3390/ijms23094751.
  • 11. Chiu SH, Wu WT. Sclerostin and cardiovascular risk: evaluating the cardiovascular safety of romosozumab in osteoporosis treatment. 2024;12(12):4751. doi:10.3390/biomedicines12122880.
  • 12. Lloret MJ, Fusaro M. Evaluating osteoporosis in chronic kidney disease: both bone quantity and quality matter. 2024;13(4): doi:10.3390/jcm13041010.
  • 13. Asadipooya K, Abdalbary M, Ahmad Y, Kakani E, Monier-Faugere MC, El-Husseini A. Bone quality in CKD patients: current concepts and future directions - Part I. Kidney Dis (Basel). 2021;7(4):268-77. doi:10.1159/000515534.
  • 14. Alobaidi S. Emerging biomarkers and advanced diagnostics in chronic kidney disease: early detection through multi-omics and AI. Diagnostics (Basel). 2025;15(10):1225. doi:10.3390/diagnostics15101225.
  • 15. Cannata-Andia JB, Roman-Garcia P, Hruska K. The connections between vascular calcification and bone health. Nephrol Dial Transplant. 2011;26(11):3429-36. doi:10.1093/ndt/gfr591.
  • 16. Shen Y, Yu C. The bone-vascular axis: a key player in chronic kidney disease associated vascular calcification. Kidney Dis (Basel). 2024;10(6):545-57. doi:10.1159/000541280.
  • 17. Lee WT, Fang YW, Chen M. Serum intact fibroblast growth factor 23 levels are negatively associated with bone mineral density in chronic hemodialysis patients. J Clin Med. 2023;12(4):1550. doi:10.3390/jcm12041550.
  • 18. Gutiérrez OM, Mannstadt M, Isakova T, Rauh-Hain JA, Tamez H, Shah A, et al. Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis. N Engl J Med. 2008;359(6):584-92. doi:10.1056/NEJMoa0706130.
  • 19. Li GH, Robinson-Cohen C, Sahni S, Au PC, Tan KC, Kung AW, et al. Association of genetic variants related to serum calcium levels with reduced bone mineral density. J Clin Endocrinol Metab. 2020;105(3):e328-36. doi:10.1210/clinem/dgz088.
  • 20. Eskandari Naji H, Ghorbanihaghjo A, Argani H, Raeisi S, Safa J, Alirezaei AH, et al. Serum sTWEAK and FGF-23 Levels in Hemodialysis and Renal Transplant Patients. Int J Organ Transplant Med. 2017;8(2):110-6.
  • 21. Vogt I, Haffner D, Leifheit-Nestler M. FGF23 and phosphate-cardiovascular toxins in CKD. Toxins (Basel). 2019;11(11):647. doi:10.3390/toxins11110647.
  • 22. Komaba H. Roles of PTH and FGF23 in kidney failure: a focus on nonclassical effects. Clin Exp Nephrol. 2023;27(5):395-401. doi:10.1007/s10157-023-02336-y.
  • 23. Isakova T, Wahl P, Vargas GS, Gutiérrez OM, Scialla J, Xie H, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int. 2011;79(12):1370-8. doi:10.1038/ki.2011.47.
  • 24. Delanaye P, Cavalier E, Bouquegneau A, Khwaja A. Sclerostin levels in CKD patients: an important, but not definitive, step on the way to clinical use. Kidney Int. 2015;88(6):1221-3. doi:10.1038/ki.2015.258.
  • 25. Laster M, Pereira RC, Noche K, Gales B, Salusky IB, Albrecht LV. Sclerostin, Osteocytes, and Wnt Signaling in Pediatric Renal Osteodystrophy. 2023;15(19):4127. doi:10.3390/nu15194127.
  • 26. Gómez-Islas VE, García-Fong KR, Aguilar-Fuentes RE, Hernández-Castellanos S, Pherez-Farah A, Méndez-Bribiesca SA, et al. Evaluation of bone densitometry by dual-energy x-ray absorptiometry as a fracture prediction tool in women with chronic kidney disease. Bone Rep. 2020;13:100298. doi:10.1016/j.bonr.2020.100298.
  • 27. Wu PY, Chen SC, Lin YC, Chen PC, Chung WS, Huang YC, et al. Role of fracture risk assessment tool and bone turnover markers in predicting all-cause and cardiovascular mortality in hemodialysis patients. Front Med (Lausanne). 2022;9:891363. doi:10.3389/fmed.2022.891363.
  • 28. Moysés RM, Schiavi SC. Sclerostin, Osteocytes, and Chronic Kidney Disease - Mineral Bone Disorder. Seminars in dialysis. 2015;28(6):578-86.10.1111/sdi.12415.
There are 27 citations in total.

Details

Primary Language English
Subjects Clinical Sciences (Other)
Journal Section Research Article
Authors

Feyza Bircan 0000-0003-0534-8076

Kursad Onec 0000-0003-3866-2838

Submission Date October 1, 2025
Acceptance Date December 10, 2025
Publication Date January 23, 2026
Published in Issue Year 2026 Volume: 16 Issue: 1

Cite

Vancouver Bircan F, Onec K. Serum FGF-23 and Sclerostin Levels in Hemodialysis Patients: Associations with Bone Mineral Density and Fracture Risk. VHS. 2026;16(1):110-5.