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Open Access Publications from the University of California

Prevalence and correlates of mitral annular calcification in adults with chronic kidney disease: Results from CRIC study

  • Author(s): Abd alamir, M
  • Radulescu, V
  • Goyfman, M
  • Mohler, ER
  • Gao, YL
  • Budoff, MJ
  • Appel, LJ
  • Feldman, HI
  • Go, AS
  • He, J
  • Kusek, JW
  • Lash, JP
  • Ojo, A
  • Rahman, M
  • Townsend, RR
  • et al.

© 2015 Elsevier Ireland Ltd. Background: Risk factors for mitral annular calcification (MAC) and cardiovascular disease (CVD) demonstrate significant overlap in the general population. The aim of this paper is to determine whether there are independent relationships between MAC and demographics, traditional and novel CVD risk factors using cardiac CT in the Chronic Renal Insufficiency Cohort (CRIC) in a cross-sectional study. Methods: A sample of 2070 subjects underwent coronary calcium scanning during the CRIC study. Data were obtained for each participant at time of scan. Subjects: were dichotomized into the presence and absence of MAC. Differences in baseline demographic and transitional risk factor data were evaluated across groups. Covariates used in multivariable adjustment were age, gender, BMI, HDL, LDL, lipid lowering medications, smoking status, family history of heart attack, hypertension, diabetes mellitus, phosphate, PTH, albuminuria, and calcium. Results: Our study consisted of 2070 subjects, of which 331 had MAC (prevalence of 16.0%). The mean MAC score was 511.98 (SD 1368.76). Age and white race remained independently associated with presence of MAC. Decreased GFR was also a risk factor. African American and Hispanic race, as well as former smoking status were protective against MAC. In multivariable adjusted analyses, the remaining covariates were not significantly associated with MAC. Among renal covariates, elevated phosphate was significant. Conclusion: In the CRIC population, presence of MAC was independently associated with age, Caucasian race, decreased GFR, and elevated phosphate. These results are suggested by mechanisms of dysregulation of inflammation, hormones, and electrolytes in subjects with renal disease.

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