MICS, an easily ignored contributor to arterial calcification in CKD patients

Abstract

In chronic kidney disease (CKD), simultaneous mineral and skeleton changes are prevalent, known as CKD-mineral bone disorder (CKD-MBD). Arterial calcification (AC) is a clinically important complication of CKD-MBD. It can increase arterial stiffness, which leads to severe cardiovascular events. However, current treatments have little effect on regression of AC, as its mechanisms are still unclear. There are multiple risk factors of AC, among which Malnutrition-Inflammation Complex Syndrome (MICS) is a new and crucial one. MICS, a combined syndrome of malnutrition and inflammation, generally begins at the early stage of CKD and becomes obvious in end-stage renal disease (ESRD). It was linked to reverse epidemiology and associated with increased cardiovascular mortality in ESRD patients. Recent data suggest that MICS can trigger CKD-MBD and accelerate the course of AC. In this present review, we summarize the recent understanding about the aggravating effects of MICS on AC and discuss the possible underlying mechanisms. A series of findings indicate that targeting MICS will provide a potential strategy for treating AC in CKD.

Roles of High Mobility Group Box 1 in Cardiovascular Calcification

“…Indeed, Abdelbaky et al showed focal aortic inflammation, as detected by 18F-deoxyglucose positron emission tomographic scanning in the aortic valve and atherosclerotic plaque to be significantly higher among patients who exhibited subsequent calcification progression [94]. Although cardiovascular calcification in the medial layer in association with CKD appears to link to long-term elevation of serum phosphate levels, apoptosis and uremic derangements [56], inflammation also acts in this process [95]. By releasing extracellular vesicles containing a phosphatidylserine-annexinV-S100A9 complex that facilitates mineral nucleation, macrophages are involved in the early, pro-inflammatory phase of calcification in atherosclerotic plaques [96].…”

A novel role of cellular interactions in vascular calcification

“…Far from a passive process, VC is widely accepted as an active and regulatory process, which shares many similarities with the process of bone formation. Recent clinical data also indicate a close relationship between osteoporosis and VC, suggesting a crosstalk between bones and vascular systems [2]. There are a variety of osteoblast-like cells and mediators involved in this process, termed as “bone-vascular axis” [2, 3].…”

“…Recent clinical data also indicate a close relationship between osteoporosis and VC, suggesting a crosstalk between bones and vascular systems [2]. There are a variety of osteoblast-like cells and mediators involved in this process, termed as “bone-vascular axis” [2, 3]. However, the underlying molecular mechanisms are largely unknown.…”

The Association Between Self-Management Ability and Malnutrition-Inflammation-Atherosclerosis Syndrome in Peritoneal Dialysis Patients: A Cross-Sectional Study

“…This study also found that 41.9% of the patients had atherosclerosis, which is worthy of considering to avoid further deterioration and improve prognosis. Currently, a targeted treatment is lacking, and screening for malnutrition and in ammation in an early stage and then adopting some effective steps to intervene immediately are critical [7,19]. The present study demonstrated that a close relationship exists between the Dialysis Effect Evaluation and Monitoring dimension and MIAS; meanwhile, the higher the score, the lower the chance of having a component of MIAS.…”

“…MIAS is a complex involving malnutrition, in ammation, and atherosclerosis, and MIAS is divided into MIAS0, MIAS1, MIAS2, and MIAS3 based on the presence of zero, one, two, and three components, respectively [7,10]. We used the MIS to evaluate malnutrition.…”