Abstract
Vascular calcification (VC) is a risk factor for cardiovascular events and mortality in chronic kidney disease (CKD). Several components influence the occurrence of VC, among which inflammation. A novel uremic toxin, lanthionine, was shown to increase intracellular calcium in endothelial cells and may have a role in VC. A group of CKD patients was selected and divided into patients with a glomerular filtration rate (GFR) of <45 mL/min/1.73 m2 and ≥45 mL/min/1.73 m2. Total Calcium Score (TCS), based on the Agatston score, was assessed as circulating lanthionine and a panel of different cytokines. A hemodialysis patient group was also considered. Lanthionine was elevated in CKD patients, and levels increased significantly in hemodialysis patients with respect to the two CKD groups; in addition, lanthionine increased along with the increase in TCS, starting from one up to three. Interleukin IL-6, IL-8, and Eotaxin were significantly increased in patients with GFR < 45 mL/min/1.73 m2 with respect to those with GFR ≥ 45 mL/min/1.73 m2. IL-1b, IL-7, IL-8, IL-12, Eotaxin, and VEGF increased in calcified patients with respect to the non-calcified. IL-8 and Eotaxin were elevated both in the low GFR group and in the calcified group. We propose that lanthionine, but also IL-8 and Eotaxin, in particular, are a key feature of VC of CKD, with possible marker significance.
Highlights
Cardiovascular disease is the most common cause of death in patients with chronic kidney disease (CKD) at all stages of the disease
Most factors are linked to calcium-phosphate balance; it can be argued that vascular calcification (VC) is present from the initial stages of CKD when mineral metabolism compensation mechanisms are still preserved; other factors may be at play
Lanthionine Concentration Is Increased in CKD and Hemodialysis Patients and in Higher
Summary
Cardiovascular disease is the most common cause of death in patients with chronic kidney disease (CKD) at all stages of the disease. Cellular microvesicles released from macrophages or apoptotic macrophages form a nidus for calcification, and macrophage-derived inflammatory regulators contribute to the disintegration of elastic fibers and matrix components in the vessel wall, all of which may promote VC It is still not clear if the osteogenic transformation of vascular smooth muscle cells and mineralization are causes or effects of local inflammation. Chemokines, and growth factors, which monitor a state of inflammation, are present in circulation, and an extended set of them can be detected and quantitated in a single measurement and relevant data mining system In this context, we, assessed the potential role of lanthionine, a sulfur-containing uremic toxin, and a panel of several different cytokines in VC of CKD patients
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