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논문분류	춘계학술대회 초록집
제목	Hepcidin is associated with Left ventricular hypertrophy in patient with nondialysis chronic kidney disease.
저자	Hyang ki MIN1, Sung woo LEE2, *Su ah SUNG1
출판정보	2017; 2017(1):
키워드	hepcidin, left ventricular hypertrophy, chronic kidney disease
초록	Objectives : In patient with chronic kidney disease (CKD), cardiovascular disease is the main cause of death. Left ventricular hypertrophy (LVH) is a wellknown biomarker for cardiovascular events and mortality in patient with CKD. Anemia can initiate or accelerate LVH in patients with CKD. Anemia in patient with CKD is associated with abnormal iron metabolism. Hepcidin regulates body iron metabolism by limiting iron efflux from iron storage site. Methods : We used baseline data of the adult division of the KNOW-CKD, a multicenter, prospective cohort study of non-dialysis patient with CKD stages 1-5. CKD and its stage were defined by using the Kidney Disease Improving Global Outcomes 2012 guidelines. A total of 2238 adult non-dialysis patients with CKD stages 1-5 were enrolled from February 2011 to January 2016. Among these patients 1973 were included in this analysis after excluding 265 patients who did not have serum hepcidin levels or echocardiographic parameters measured at base line. Clinical data, including demographic information and baseline laboratory results were extracted from the electronic data management system. Serum hepcidin levels were measured by enzyme linked imunosorbent assay at a single central laboratory. Two-dimensional echocardiograms were performed by experienced cardiologist. LVH was defined as the sex-specific highest quartile of LVMI in the studied patients (≥ 110 g/m2 in men and (≥ 101 g/m2 in women). Results : Patient with LVH had a higher rate of anemia than did those without LVH and also showed more comorbidity than those without LVH: older age, lower income, more smoking, higher hypertension and diabetes rate, more obese, lower levels of eGFR and albumin, and higher CRP levels and UPCR(Table 1). We examined echocardiographic parameters in detail according to serum hepcidin quartiles(Table 2). Thickness parameteres and overall chamber size showed a tendency to increase with progression of serum hepcidin quartiles. We found a positive linear association between serum hepcidin levels and the LVMI(Fig 1 and Table 3). Conclusions : Hepcidin limits the main inflow of iron into plasma from enterocyte during dietary iron absorption, from macrophages during iron recycling, and from hepatocyte involved in iron storage. There have been few studies on the effect of hepcidine on LVH in patients with CKD. So, we performed the current study to identify the association between hepcidin and LVH in non-dialysis patients with CKD. We found that cardiac thickness and diameters were increased with progression of serum hepcidin quartiles, and we concluded that a hepcidin-related increase in the LVMI is in accordance with characteristic changes in the heart in CKD. We propose the following new hypothesis: hepcidin is an undetermined factor for LVH, which is independent from eccentric and concentric stress and dysregulated iron metabolism. A casual relationship need to be evaluated in a future study .
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