Article

Differences in associated factors between aortic and mitral valve calcification in hemodialysis.

Department of Nephrology and Kidney and Dialysis Center, Shonan Kamakura General Hospital, Kamakura, Kanagawa, Japan.
Hypertension Research (Impact Factor: 2.79). 04/2010; 33(6):622-6. DOI: 10.1038/hr.2010.44
Source: PubMed

ABSTRACT Increased prevalence of aortic and mitral valve calcification has been reported in patients on hemodialysis, but it remains unknown whether aortic and mitral valve calcification arise from similar pathogenesis. We detected heart valve calcification using two-dimensional echocardiography, and we related valve calcification to various clinical parameters in patients treated with hemodialysis three times a week for more than 1 year. In 112 patients (77 men and 35 women, age 67+/-10 years, duration on hemodialysis 95+/-67 months), aortic and mitral valve calcification were observed in 84 (75.0%) and 58 (51.7%) patients, respectively. Aortic valve calcification was associated with increased age, higher serum calcium, lower serum albumin, lower total cholesterol and higher high-sensitivity C-reactive protein. Multivariate analysis showed that increased age and higher serum calcium were independently associated with aortic valve calcification. Conversely, mitral valve calcification was associated with increased age, higher high-sensitivity C-reactive protein and higher serum beta(2)-microglobulin, but not with higher serum calcium. In multivariate analysis, increased age and higher serum beta(2)-microglobulin were independently associated with mitral valve calcification. Serum beta(2)-microglobulin was associated with longer duration on hemodialysis, malnutrition inflammation (lower serum albumin and higher high-sensitivity C-reactive protein) and dyslipidemia. Considering the results in previous studies showing that the distribution of beta(2)-microglobulin amyloid deposition was consistent with that of tissue calcification in patients on hemodialysis, beta(2)-microglobulin may have pathogenic roles in valve calcification.

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