Abstract
Background: Hepcidin, a recently discovered 25-amino acid peptide, is mainly synthesized, processed and secreted by hepatocytes. It is the key regulator in iron homeostasis. Renal clearance may be an important way for its excretion, but the influence of estimated glomerular filtration rate (eGFR) on serum level of hepcidin-25 is inconsistent among different reports. Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Iron plays a key role in cardiac diseases, such as iron-overload cardiomyopathy, myocardial ischemia-reperfusion injury, and atherosclerosis. Cardiac expression of hepcidin was demonstrated on mRNA and protein level in vivo in a rat model. Ghrelin is a 28-amino-acid pepetide mainly secreted by gastric fundus and it can stimulate secretion of growth hormone, increase food intake and produce weight gain. In animal models, ghrelin decreased blood pressure, increased stroke volume and inhibited apoptosis of myocardiocyte and endothelium, thus protecting heart. Thus, we aim to investigate the relationship of serum hepcidin and ghrelin level to renal function and left ventricular function in patients with CKD. Methods: We enrolled a cohort of 146 CKD patients, ranging from CKD stage 1 to CKD stage 5, not requiring dialysis. After an overnight fasting for at least 8 hours, a one-time blood sample was collected for measurement biochemical data. Plasma bioactive hepcidin-25 and total ghrelin ( acylated and des-acylated forms) were measured in duplicate by competitive ELISA. Echocardiography was performed by a qualified cardiologist. Results: There was a significant difference in serum hepcidin levels between each CKD stage patients by Kruskal Wallis test ( p = 0.039). In addition, serum hepcidin levels in each CKD stage patients were lower significantly, compared with those in higher CKD stage patients by Jonckheere Terpstra test ( p=0.002). The Pearson correlation analysis demonstrated that serum hepcidin level was significantly and positively correlated with serum BUN, creatinine, phosphate, HDL cholesterol and LDL cholesterol, but negatively correlated with eGFR, serum hemoglobin, albumin and fasting blood sugar. There was no correlation between serum hepcidin and IL-6 or CRP( r = 0.183, p = 0.425; r = 0.19, p = 0.514, respectively ). In multivariate analysis, hepcidin was positively associated with ferritin and inversely correlated with eGFR. Hepcidin was also closely with left ventricle mass index (LVMI).( r = -0.014, p = 0.006). Serum ghrelin levels were not correlated with eGFR or CKD stages but positively with LVMI (r = 0.652，P= 0.003). Conclusion: The serum hepcidin level was closely associated with renal function in CKD patients. Hepcidin was also correlated inversely with LVMI and ghrelin was positively correlated with LVMI. Ghrelin and hepcidin may be crucial for cardiovascular morbidity and mortality in CKD patients.
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