Association of Changes in Bone Remodeling and Coronary Calcification in Hemodialysis Patients: A Prospective Study

Association of Changes in Bone Remodeling and Coronary Calcification in Hemodialysis Patients: A Prospective Study

Author Barreto, Daniela Veit Autor UNIFESP Google Scholar
Barreto, Fellype de Carvalho Autor UNIFESP Google Scholar
Carvalho, Aluizio Barbosa de Autor UNIFESP Google Scholar
Cuppari, Lilian Autor UNIFESP Google Scholar
Draibe, Sergio Antonio Autor UNIFESP Google Scholar
Dalboni, Maria Aparecida Autor UNIFESP Google Scholar
Affonso Moyses, Rosa Maria Autor UNIFESP Google Scholar
Neves, Katia Rodrigues Autor UNIFESP Google Scholar
Jorgetti, Vanda Autor UNIFESP Google Scholar
Miname, Marcio Google Scholar
Santos, Raul D. Google Scholar
Canziani, Maria Eugenia F. Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Abstract Background: Vascular calcification is common and constitutes a prognostic marker of mortality in the hemodialysis population. Derangements of mineral metabolism may influence its development. the aim of this study is to prospectively evaluate the association between bone remodeling disorders and progression of coronary artery calcification (CAC) in hemodialysis patients.Study Design: Cohort study nested within a randomized controlled trial.Setting & Participants: 64 stable hemodialysis patients.Predictor: Bone-related laboratory parameters and bone histomorphometric characteristics at baseline and after 1 year of follow-up.Outcomes: Progression of CAC assessed by means of coronary multislice tomography at baseline and after 1 year of follow-up. Baseline calcification score of 30 Agatston units or greater was defined as calcification. Change in calcification score of 15% or greater was defined as progression.Results: of 64 patients, 26 (40%) had CAC at baseline and 38 (60%) did not. Participants without CAC at baseline were younger (P < 0.001), mainly men (P = 0.03) and nonwhite (P = 0.003), and had lower serum osteoprotegerin levels (P = 0.003) and higher trabecular bone volume (P = 0.001). Age (P 0.003; beta coefficient = 1.107; 95% confidence interval [Cl], 1.036 to 1.183) and trabecular bone volume (P = 0.006; beta coefficient = 0.828; 95% Cl, 0.723 to 0.948) were predictors for CAC development. of 38 participants who had calcification at baseline, 26 (68%) had CAC progression in 1 year. Progressors had lower bone-specific alkaline phosphatase (P = 0.03) and deoxypyridinoline levels (P = 0.02) on follow-up, and low turnover was mainly diagnosed at the 12-month bone biopsy (P = 0.04). Low-turnover bone status at the 12-month bone biopsy was the only independent predictor for CAC progression (P = 0.04; beta coefficient = 4.5; 95% Cl, 1.04 to 19.39). According to bone histological examination, nonprogressors with initially high turnover (n = 5) subsequently had decreased bone formation rate (P = 0.03), and those initially with low turnover (n = 7) subsequently had increased bone formation rate (P = 0.003) and osteoid volume (P = 0.001).Limitations: Relatively small population, absence of patients with severe hyperparathyroidism, short observational period.Conclusions: Lower trabecular bone volume was associated with CAC development, whereas improvement in bone turnover was associated with lower CAC progression in patients with high- and low-turnover bone disorders. Because CAC is implicated in cardiovascular mortality, bone derangements may constitute a modifiable mortality risk factor in hemodialysis patients.
Keywords Hemodialysis
renal osteodystrophy
vascular calcification
cardiovascular disease
Language English
Sponsor Genzyme Corp
Date 2008-12-01
Published in American Journal of Kidney Diseases. Philadelphia: W B Saunders Co-Elsevier Inc, v. 52, n. 6, p. 1139-1150, 2008.
ISSN 0272-6386 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 1139-1150
Origin http://dx.doi.org/10.1053/j.ajkd.2008.06.024
Access rights Closed access
Type Article
Web of Science ID WOS:000261489800015
URI http://repositorio.unifesp.br/handle/11600/31085

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