Malnutrition–inflammation complex syndrome: link between end-stage renal disease, atherosclerosis and valvular calcification

Zapolski, Tomasz

doi:10.1038/hr.2010.50

Cited by 15 publications

(14 citation statements)

References 11 publications

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“…Multiple studies have shown that PD patients have a high incidence of coexistence of inflammation and malnutrition, known as the inflammation-dystrophy syndrome [2,20,21]. This syndrome is a strong predictor of cardiovascular disease and death in dialysis patients [20]; however, the underlying mechanism is not fully understood.…”

Section: Discussionmentioning

confidence: 99%

“…However, ideal control and regular follow-up monitoring are still difficult, leading to an increase in the risk of ectopic calcification in CKD patients. Additionally, CVC is considered a strong predictor of morbidity and mortality due to atherosclerosis, arterial calcification, left ventricular hypertrophy and cardiovascular disease [2,3,8]. Given its increased incidence in end-stage renal disease patients and the associated high risk, it is critical to clarify the mechanism underlying the development and progression of CVC.…”

Section: Introductionmentioning

confidence: 99%

“…Previous research has shown that increased calcium (Ca), phosphorus (P), blood lipids, parathyroid hormone (PTH) and chronic inflammatory mediator release result in an increased incidence of CVC in patients with CKD [2,3,4,5,6]. The Kidney Disease: Improving Global Outcomes (KDIGO) Guidelines for Chronic Kidney Disease-Mineral and Bone Disorder proposed target values of serum P, Ca and PTH in these patients [7].…”

Section: Introductionmentioning

confidence: 99%

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Risk Factors for New-Onset Cardiac Valve Calcification in Patients on Maintenance Peritoneal Dialysis

et al. 2016

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Objective: Patients with end-stage renal disease are susceptible to cardiac valve calcification (CVC) due to mineral metabolism disorders and other factors. The purpose of this study was to investigate the risk factors for new-onset CVC in patients on maintenance peritoneal dialysis (PD). Methods: This study included patients who underwent PD catheter insertion from January 2006 to June 2013 in our Peritoneal Dialysis Center. Clinical data were collected on CVC status during echocardiography evaluations (twice) at an interval of >6 months. The data collected included intact parathyroid hormone, C-reactive protein (CRP), serum phosphorus (P), serum calcium (Ca), albumin (Alb), prealbumin and the use of five types of antihypertensive drugs, statins, active vitamin D₃ and Ca tablets. Results: In total, 194 patients - 105 (54.1%) men, average age 60.5 ± 13.0 years - were included. CVC was present in 50 (25.8%) patients during PD catheter placement. After an average PD duration of 20.9 ± 10.4 months, CVC was detected in 97 patients (50.0%). New-onset CVC was found in 62 patients (32.0%). Multivariate logistic regression analysis revealed that only serum P levels (p = 0.01, OR = 2.569), Alb levels (p = 0.04, OR = 0.935), dialysis duration (p = 0.03, OR = 1.039) and CRP levels (p = 0.02, OR = 1.031) were associated with CVC. Conclusion: Serum P, Alb and CRP levels as well as dialysis duration are independent risk factors for CVC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Risk Factors for New-Onset Cardiac Valve Calcification in Patients on Maintenance Peritoneal Dialysis

et al. 2016

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“…1,2 Vascular calcification, which results in increased vascular stiffness, is a common pathological feature of hemodialysis patients 1,3 and is accompanied by left ventricular hypertrophy (LVH) and diastolic dysfunction. 4,5 Vascular calcification is an active process controlled by a balance of serum calcification inhibitors and enhancers.…”

Section: Introductionmentioning

confidence: 99%

The balance of fetuin-A and osteoprotegerin is independently associated with diastolic dysfunction in hemodialysis patients

et al. 2011

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Fetuin-A and osteoprotegerin (OPG) are arterial calcification regulators, which are related to cardiovascular survival in hemodialysis patients. We hypothesized that a balance of these calcification regulators might mediate the progression of left ventricular (LV) diastolic dysfunction in hemodialysis patients. We recruited 63 hemodialysis patients and measured their serum fetuin-A, OPG, arterial stiffness, aortic calcification and echocardiographic parameters, including the transmitral early diastolic velocity/tissue Doppler mitral annular early diastolic velocity ratio (E/E¢), and analyzed the relationships between these variables. Fetuin-A levels were significantly and negatively correlated with the ankle-brachial pulse wave velocity (baPWV), aortic calcification score (AOCS), left atrial volume index (LAVI), LV mass index (LVMI) and E/E¢. OPG levels and the ratio of OPG to fetuin-A levels were significantly and positively correlated with the baPWV, AOCS, LAVI and E/E¢. A stepwise multiple regression analysis revealed that E/E¢ was independently correlated with fetuin-A levels (b¼À0.334, P¼0.02), OPG levels (b¼0.367, P¼0.01) and the ratio of OPG to fetuin-A (b¼0.295, P¼0.04). Categorizing the patients according to their serum fetuin-A and OPG levels revealed that patients with low fetuin-A and high OPG levels had the highest LAVI, LVMI and E/E¢ values after adjusting for potential confounders. Serum fetuin-A levels negatively reflected, whereas OPG levels and the ratio of OPG to fetuin-A positively reflected an increase in vascular and ventricular stiffness, leading to the aggravation of diastolic dysfunction. Therefore, based on our results, the balance of the tissue calcification regulators fetuin-A and OPG could mediate the progression of LV diastolic dysfunction in hemodialysis patients.

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“…The association between undernutrition and adverse outcomes in ESRD patients has been referred to as reverse epidemiology (36,38). Recently, our and others' findings show that MICS is associated with AC (109,110), which may serve as an explanation for the bad consequences of reverse epidemiology in ESRD patients. In this review, in order to give clinicians in-depth insights into MICS for AC in CKD, we evaluated the roles of MICS in AC and explored the possible mechanisms for MICS-induced AC.…”

mentioning

confidence: 97%

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

Zhang

Gao

Chen

et al. 2016

American Journal of Physiology-Renal Physiology

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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.

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Malnutrition–inflammation complex syndrome: link between end-stage renal disease, atherosclerosis and valvular calcification

Cited by 15 publications

References 11 publications

Risk Factors for New-Onset Cardiac Valve Calcification in Patients on Maintenance Peritoneal Dialysis

Risk Factors for New-Onset Cardiac Valve Calcification in Patients on Maintenance Peritoneal Dialysis

The balance of fetuin-A and osteoprotegerin is independently associated with diastolic dysfunction in hemodialysis patients

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

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