Like total ghrelin, acylated ghrelin is also lower in HD patients with cardiovascular disease

actions. 2 We assessed acylated ghrelin (A-Ghr) in 20 healthy volunteers (57.00±8.62 years) and 68 HD patients (61.24±12.51 years, 22 diabetics). Samples were drawn before 2 years, and at the end of this period 22 HD patients suffered from coronary heart disease (CHD). Plasma A-Ghr was measured using enzyme-linked immunosorbent assay (SPI Bio, Montigny, France). White blood cell count (WBC), C-reactive protein (CRP), and albumin were also assessed. A-Ghr did not differ between HD patients and healthy volunteers (106.40±27.53 versus 120.50±45.04 pg/ml, P ¼ 0.424, Mann–Whitney unpaired test). A-Ghr was lower in HD patients suffering from CHD (95.00±22.04 versus 111.85±28.42 pg/ml, P ¼ 0.023) and was positively correlated with WBC (Spearman’s r ¼ 0.426, Po0.001), CRP (r ¼ 0.261, P ¼ 0.023), that is, with inflammation, and age (r ¼ 0.323, P ¼ 0.007). A-Ghr was negatively correlated with the marker of nutrition albumin (r ¼� 0.368, P ¼ 0.002). Thus, similar to total ghrelin, A-Ghr is also lower in HD patients with cardiovascular disease. This could be simply an epiphenomenon, as in the case of cachexia that accompanies inflammation, A-Ghr increases to counteract weight-loss mechanisms, and it is well known that inflammation also induces atherosclerosis. 2,3 Alternatively, higher A-Ghr could offer protection from atherosclerosis through its direct action on the endothelium or indirectly by attenuating inflammation. 2,4 The second case, if proved true, is promising for pharmaceutical intervention in the near future.