Progression of arterial stiffness is associated with changes in bone mineral markers in advanced CKD

BMC Nephrology

Research Article

Rathika Krishnasamy¹  Sven-Jean Tan²  Nigel D. Toussaint²  Kevin Lee³  Grahame J. Elder⁴  Tony Stanton⁵  Scott Campbell⁶  David W. Mudge⁶  Nicole M. Isbel⁶  Carmel M. Hawley⁷  David W. Johnson⁷ 

[1] Department of Nephrology, Sunshine Coast University Hospital, PO Box 5340, Sunshine Coast, 4560, Birtinya, MC QLD, Australia;Faculty of Medicine, The University of Queensland, Brisbane, Australia;Department of Nephrology, The Royal Melbourne Hospital (RMH), Melbourne, VIC, Australia;Department of Medicine (RMH), The University of Melbourne, Parkville, VIC, Australia;Department of Radiology, Princess Alexandra Hospital, Brisbane, Australia;Department of Renal Medicine, Westmead Hospital, Sydney, Australia;Osteoporosis and Bone Biology Division, Garvan Institute of Medical Research, Sydney, Australia;Faculty of Medicine, The University of Queensland, Brisbane, Australia;Department of Cardiology, Sunshine Coast University Hospital, Birtinya, Australia;Faculty of Medicine, The University of Queensland, Brisbane, Australia;Department of Nephrology, Princess Alexandra Hospital, Brisbane, Australia;Faculty of Medicine, The University of Queensland, Brisbane, Australia;Translational Research Institute, Brisbane, Australia;Department of Nephrology, Princess Alexandra Hospital, Brisbane, Australia;

关键词: Aortic calcification;    Arterial stiffness;    Chronic kidney disease;    Fibroblast growth factor 23;    Soluble klotho;   

DOI  :  10.1186/s12882-017-0705-4

 received in 2017-03-22, accepted in 2017-08-22,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundArterial stiffness is an independent predictor of all-cause and cardiovascular mortality in patients with chronic kidney disease (CKD). There are limited prospective data however on progression of arterial stiffness in CKD, including evaluating associations with bone mineral markers such as fibroblast growth factor 23 (FGF23) and soluble α-klotho (sKl).MethodsIn this prospective, single-center, observational study, arterial stiffness [measured by pulse wave velocity (PWV)] and hormones influencing mineral homeostasis, including serum FGF23 and sKl, were compared between non-dialysis CKD stages 4/5 and healthy controls at baseline and 12 months (12 m). Abdominal aortic calcification (AAC) was quantitated using lateral lumbar radiography at baseline.ResultsForty patients with CKD [mean estimated glomerular filtration rate (eGFR) 19.5 ± 6.7 mL/min/1.73m2] and 42 controls (mean eGFR 88.6 ± 12.9 mL/min/1.73m2) completed follow-up. There were no differences in age, gender and body mass index between groups. A significant increase in FGF23 [240.6 (141.9–1129.8) to 396.8 (160.3–997.7) pg/mL, p = 0.001] was observed in the CKD group but serum phosphate, corrected calcium, parathyroid hormone and sKl did not change significantly over 12 m. At baseline, CKD subjects had higher AAC prevalence [83.8% versus (vs.) 43.6%, p = 0.002] and higher aortic PWV [9.7(7.6–11.7) vs. 8.1 (7.2–9.7) m/s, p = 0.047] compared to controls. At 12 m, aortic PWV increased by 1.3 m/s (95% confidence interval, 0.56 to 2.08, p < 0.001) in the CKD cohort, with 30% of subjects showing progression from normal aortic elasticity to stiffening (PWV > 10 m/s). Serum FGF23 was associated with AAC, abnormal PWV and progression of PWV at 12 m.ConclusionsArterial stiffness and serum FGF23, both of which are associated with increased cardiovascular risk, increased over one year in individuals with CKD. Additionally, a significant association was found between serum FGF23 and arterial calcification and stiffness. Larger clinical studies and further experimental work are warranted to delineate the temporal relationship as well as the pathological mechanisms linking FGF23 and vascular disease.

【 授权许可】

CC BY   
© The Author(s). 2017