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Clinical Journal of the American Society of Nephrology
Year: 2009  |  Volume: 4  |  Issue: 10  |  Page No.: 1629 - 1636

Is Valvular Calcification a Part of the Missing Link between Residual Kidney Function and Cardiac Hypertrophy in Peritoneal Dialysis Patients?

A. Y. M Wang, C. W. K Lam, M Wang, I. H. S Chan, S. F Lui and J. E. Sanderson    

Abstract:

Background and objectives: Residual renal function (RRF) predicts survival and shows an important inverse relation with cardiac hypertrophy in peritoneal dialysis (PD) patients. We hypothesized that valvular calcification and the calcification milieu may be part of the process linking loss of RRF and cardiac hypertrophy.

Design, setting, participants, & measurements: A cross-sectional study was conducted by performing two-dimensional echocardiography on 230 PD patients to assess valvular calcification and left ventricular (LV) mass and collecting 24-h urine for estimation of RRF.

Results: Patients having valvular calcification had lower RRF than those without. Patients with no RRF showed higher calcium-phosphorus product (Ca x P) and C-reactive protein (CRP). Using multiple logistic regression analysis, every 1-ml/min per 1.73 m2 increase in residual GFR was associated with a 28% reduction in the risk for valvular calcification. The association was lost after additional adjustment for Ca x P and CRP. Using multiple linear regression analysis, loss of RRF showed significant association with increased LV mass index, but this association was lost after additional adjustment for CRP, Ca x P, and valvular calcification. Patients with all three calcification risk factors, namely inflammation, high CaxP, and no RRF, showed the highest prevalence of valvular calcification and had the most severe cardiac hypertrophy.

Conclusions: The association among loss of RRF, valvular calcification, and cardiac hypertrophy was closely linked to increased inflammation and high Ca x P in PD patients. These data suggest that valvular calcification and the calcification milieu are part of the processes linking loss of RRF and worsening cardiac hypertrophy in PD.

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