THE RELATIONSHIP BETWEEN ARTERIAL STIFNESS AND 25-(OH) VITAMIN D, FGF 23 IN MAINTENANCE HEMODIALYSIS PATIENTS

Yıl 2020, , 215 - 220, 31.12.2020

Suleyman Karakose , Zeynep Bal , Burak Sayin , Mehtap Erkmen Akdoğan , Dilek Gokustun Emre Tutal , Siren Sezer

https://doi.org/10.20492/aeahtd.703865

Öz

PURPOSE: Vascular calcification (VC) is highly prevalent in maintenance hemodialysis (MHD) population and increasing evidence indicates that abnormalities in mineral metabolism are closely associated with VC and increased mortality in chronic kidney disease (CKD) patients. In our study, we hypothesized that high FGF-23 and low endogeneous vitamin D levels might be a result of high calcium load and aimed to determine the relationship between 25-hydroxy vitamin D levels and arterial stiffness in CKD patients.
MATERIALS AND METHODS: One hundred and seventeen patients who were receiving MHD 3 times a week for at least 24 months were selected and followed up for 12 months.We analysed the influence of one years’ cumulative calcium and theraupetic vitamin D (paricalcitol and calcitriol) intake, and serum FGF-23 level on 25(OH)D3 levels and the impacts of these parameters on the change in annual PWV measurement results in MHD patients.
RESULTS: Elementary calcium dose was significantly higher in vitamin D insufficiency group than compared to control group (p=0.014). Seum level of FGF-23 were positively correlated with duration of HD (p=0.001), mean PTH (p=0.001), mean P (p=0.009) and mean CaxP (p=0.006). Baseline PWV measurement were similar between two groups however patients in insufficiency group had higher 12th month PWV measurements compared to control group (p=0.034).
CONCLUSION: Calcium could increase serum FGF23 levels by indeterminate mechanisms independently of serum phosphate level. Elevated FGF-23 levels was found to be insulting a decline in vitamin D levels which may cause VC and stiffening of the arteries and resulting higher PWV measurements.

Anahtar Kelimeler

Calcium load, , FGF-23, , vascular calcification, , 25-hydroxy vitamin D

Kaynakça

• Referans1 . Sarnak MJ, Levey AS, Schoolwerth AC, Coresh J, Culleton B, Hamm LL, et al. Kidney disease as a risk factor for development of cardiovascular disease: astatement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Circulation 2003;108: 2154–2169. Referans2 . Chronic Kidney Disease Prognosis Consortium1, Matsushita K, van der Velde M, Astor BC, Woodward M, Levey AS, et al. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis. Lancet 2010;375: 2073–2081. Referans3 . Vervloet M, Cozzolino M. Vascular calcification in chronic kidney disease: different bricks in the wall? Kidney Int. 2017;91(4):808-817. Referans4 . Suzuki H, Inoue T, Dogi M, Kikuta T, Takenaka T, Okada H. Role of Pulse Wave Velocity in Patients with Chronic Kidney Disease Stages 3–5 on Long-Term Follow-Up. Pulse (Basel) 2014;2(1-4):1-10. Referans5 . Jean G , Souberbielle JC, Chazot C. Vitamin D in Chronic Kidney Disease and Dialysis Patients. Nutrients. 2017;25;9(4). Referans6 . Molina P, Carrero JJ, Bover J, Chauveau P, Mazzaferro S, Torres PU. Vitamin D, a modulator of musculoskeletal health in chronic kidney disease. J Cachexia Sarcopenia Muscle. 2017;8(5):686-701. Referans7 . Obi Y , Hamano T, Isaka Y. Prevalence and prognostic implications of vitamin D deficiency in chronic kidney disease. Dis Markers. 2015;2015:868961. Referans8 . Olauson H, Larsson TE. FGF23 and Klotho in chronic kidney disease. Curr Opin Nephrol Hypertens. 2013;22(4):397-404 Referans9 . de Borst MH, Vervloet MG, ter Wee PM, Navis G. Cross talk between the renin-angiotensin-aldosterone system and vitamin D-FGF-23-klotho in chronic kidney disease. J Am Soc Nephrol. 2011;22(9):1603-9. Referans10 . Kamr AM, Dembek KA, Hildreth BE, Morresey PR, Rathgeber RA, Burns TA, et al. The FGF-23/klotho axis and its relationship with phosphorus, calcium, vitamin D, PTH, aldosterone, severity of disease, and outcome in hospitalised foals. Equine Vet J. 2018;50(6):739-746. Referans11 . Kidney Disease Improving Global Outcomes (KDIGO) CKD Work Group KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Inter Suppl 2013;3:1–150 Referans12 . Mackenzie IS, Wilkinson IB, Cockcroft JR. Assessment of arterial stiffness in clinical practice. QJM. 2002;95(2):67-74. Referans13 . London GM, Guérin AP, Verbeke FH, Pannier B, Boutouyrie P, Marchais SJ, et al. Mineral metabolism and arterial functions in end-stage renal disease: potential role of 25-hydroxyvitamin D deficiency. J Am Soc Nephrol. 2007;18(2):613-20. Referans14 . Kalaitzidis RG, Elisaf MS. Hyperphosphatemia and phosphate binders: effectiveness and safety. Curr Med Res Opin. 2014;30(1):109-12. Referans15 . Ritz E, Gross ML. Hyperphosphatemia in renal failure. Blood Purif. 2005;23(1):6-9. Referans16 . Yilmaz MI, Sonmez A, Saglam M, Yaman H, Kilic S, Eyileten T, et al. Comparison of calcium acetate and sevelamer on vascular function and fibroblast growth factor 23 in CKD patients: a randomized clinical trial. Am J Kidney Dis. 2012;59(2):177-85. Referans17 . Oliveira RB, Cancela AL, Graciolli FG, Dos Reis LM, Draibe SA, Cuppari L, et al. Early control of PTH and FGF23 in normophosphatemic CKD patients: a new target in CKD-MBD therapy? Clin J Am Soc Nephrol. 2010;5(2):286-91.