Revised: May 1, 2013
Accepted: May 4, 2013
Published online: May 6, 2013
Processing time: 89 Days and 23.9 Hours
AIM: To assess the correlation between the serum hepcidin-25 level and left ventricular mass index.
METHODS: This study was a cross-sectional study conducted between March 2009 and April 2010. Demographic and biochemical data, including the serum hepcidin-25 level, were collected for chronic kidney disease (CKD) patients. Two-dimensional echocardiography was performed to determine the left ventricle mass (LVM), left ventricular mass index (LVMI), interventricular septum thickness (IVSd), left ventricle posterior wall thickness (LVPW), right ventricular dimension (RVD), left atrium (LA) and ejection fraction (EF).
RESULTS: A total of 146 patients with stage 1 to 5 CKD were enrolled. Serum hepcidin-25 levels were 16.51 ± 5.2, 17.59 ± 5.32, 17.38 ± 6.47, 19.98 ± 4.98 and 22.03 ± 4.8 ng/mL for stage 1 to 5 CKD patients, respectively. Hepcidin-25 level was independently predicted by the serum ferritin level (β = 0.6, P = 0.002) and the estimated glomerular filtration rate (β = -0.48, P = 0.04). There were negative correlations between the serum hepcidin level and the LVM and LVMI (P = 0.04 and P = 0.005, respectively). Systolic blood pressure (BP) was positively correlated with the LVMI (P = 0.005). In the multivariate analysis, a decreased serum hepcidin-25 level was independently associated with a higher LVMI (β = -0.28, 95%CI: -0.48 - -0.02, P = 0.006) after adjusting for body mass index, age and systolic BP.
CONCLUSION: A lower serum hepcidin level is associated with a higher LVMI in CKD patients. Low hepcidin levels may be independently correlated with unfavorable cardiovascular outcomes in this population.
Core tip: Cardiovascular disease is the primary cause of death among chronic kidney disease (CKD) patients, and left ventricular hypertrophy is a powerful independent predictor of mortality for end-stage renal disease patients. Low left ventricular performance is associated with iron deficiency anemia in rats with CKD. Hepcidin-25, a recently discovered biologically active 25-amino acid peptide, plays a key role in the iron homeostasis. Chronic iron deficiency may, by itself, reduce exercise capacity and cause ultrastructural alterations in cardiomyocytes. In the study, we showed that patients in higher grade of CKD stage had the higher serum hepcidin levels, and that there was negative correlation between serum hepcidin level and LVMI.