Coronary calcification in patients with end-stage renal disease: a novel endocrine disorder?

Efstratiadis, Georgios; Koskinas, Konstantinos C.; Pagourelias, Efstathios D

doi:10.14310/horm.2002.111108

Cited by 9 publications

(4 citation statements)

References 93 publications

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“…Cardiovascular diseases account for 50% of mortality in patients with end-stage kidney disease (ESKD) [1]. The prevalence of these diseases among hemodialysis patients is about 10-30 times higher than that among general population of the same age and sex [2]. The high prevalence of cardiovascular events in ESKD patients is associated with traditional risk factors including hypertension, dyslipidemia, diabetes mellitus, and smoking.…”

Section: Introductionmentioning

confidence: 99%

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Relationship between Fetuin-A and vascular or valvular calcification in hemodialysis patients

Ossareh¹,

Marghoob²,

Bayat³

2019

J Clini Nephrol

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Purpose: Defi ciency of Fetuin A, as a calcifi cation inhibitor, is assumed to be involved in vascular calcifi cation in patients on maintenance hemodialysis (MHD). This study examined the relationship between serum Fetuin-A and vascular and valvular calcifi cation in a cohort of MHD patients. Methods: The study was conducted on 122 MHD patients. Serum levels of calcium, phosphorus, parathormone, and Fetuin-A were tested. Intima-media thickness (IMT) ≥0.8 mm and the presence of stenosis>50% or plaques in carotid doppler sonography were considered as vascular calcifi cation. Calcifi cation of cardiac valves or mitral annular calcifi cation in twodimensional echocardiography, were considered as cardiac valvular calcifi cation. The presence of any or both of the two conditions was defi ned as cardiovascular calcifi cation (CVC). Results: Fetuin-A was lower than normal in 37% of 122. Totally 106 patients (87%) had CVC, who were older (61±14 vs. 38±14 years, P<0.001), more affected by diabetes (54% vs. 13%, P=0.007), had a longer dialysis vintage (median 5 vs. 2 years, P=0.006), lower levels of creatinine (8.9±2.8 vs. 11.9±3.1 mg/dL, P<0.001) and higher levels of calcium (8.7±0.7 vs. 8.4±0.5 mg/dL, P=0.026). There was no signifi cant difference in mean Fetuin-A level between the two groups (P=0.101). In logistic regression increased age (OR=1.1, CI 95%=1.1-1.2) and serum calcium (OR=2.8, CI 95%=1.1-7.6), and diabetes mellitus (OR=7.4, CI 95%=1.1-47.4) were risk factors. Conclusion: This study showed that 87% of our patients had vascular and/or valvular calcifi cation. Increased age and calcium level and diabetes were the predictors of CVC, whereas Fetuin-A was not.

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Section: Introductionmentioning

confidence: 99%

“…Vascular and valvular calci ications are the most common forms of extra-osseous calci ication in ESKD patients [2]. CVC is associated not only with the traditional risk factors, but also with factors such as abnormalities in the levels of calcium, phosphorus, PTH, and vitamin D [5].…”

Section: Introductionmentioning

confidence: 99%

Relationship between Fetuin-A and vascular or valvular calcification in hemodialysis patients

Ossareh¹,

Marghoob²,

Bayat³

2019

J Clini Nephrol

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“…[ 40 54 ] MHD is the preferred treatment for patients with ESRD, but the degree of CAC in MHD patients is 2–5-fold higher than that of patients with angiographic evidence of coronary artery disease. [ 41 55 ] In one study, 79% of CRD patients had vascular calcification before they received MHD and, afterward, the proportion was close to 100%,[ 56 ] suggesting that, besides the factors mentioned above, other factors that affect calcification might be involved.…”

Section: O Ther F Actorsmentioning

confidence: 99%

Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure

Lai

Gael

et al. 2018

Chinese Medical Journal

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Objective:Coronary artery calcification (CAC) is thought to be a controlled metabolic process that is very similar to the formation of new bone. In patients with chronic renal failure (CRF), CAC is very common, and CAC severity correlates with the deterioration of renal function. We summarized the current understanding and emerging findings of the relationship between CAC and CRF.Data Sources:All studies were identified by systematically searching PubMed, Embase, and CNKI databases for the terms “coronary calcification”, “chronic renal failure”, “vascular smooth muscle cell”, and their synonyms until September 2017.Study Selection:We examined the titles and abstracts of all studies that met our search strategy thoroughly. The full text of relevant studies was evaluated. Reference lists of retrieved articles were also scrutinized for the additional relevant studies.Results:CRF can accelerate CAC progression. CRF increases the expression of pro-inflammatory factors, electrolyte imbalance (e.g., of calcium, phosphorus), parathyroid hormone, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transform into osteoblast-like cells while inhibiting the reduction of vascular calcification factors, thus inducing further CAC.Conclusions:Coronary heart disease in patients with CRF is due to multiple factors. Understanding the mechanism of CAC can help interventionists to protect the myocardium and reduce the prevalence of coronary heart disease and mortality.

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“…With regard to diagnosis of CAC, spiral computer tomography evidenced the relationship between serum fetuin-A levels and degree of coronary calcifications [26]. Concerning this, Efstratiadis and coworkers demonstrated that electron beam computer tomography and multi-detector computer tomography represent the most commonly used non-invasive modalities for the assessment of coronary calcifications [27].…”

Section: Fetuin-a In Esrd Patientsmentioning

confidence: 99%

Fetuin-A: A Novel Cardiovascular Risk Factor

Cacciapuoti

2010

Kidney

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Fetuin-A, or α 2 -Heremans-Schimd glycoprotein, is a potent inhibitor of calcium-phosphate precipitation. In end-stage renal disease (ESRD) patients, its serum levels are significantly reduced favouring ectopic calcifications, such as vascular and valvular calcifications for hyperphosphatemia and increased Ca×P product. Numerous evidences indicate that in low fetuin-A levels patients, mitral and/or aortic calcifications are often present. Coronary, carotid calcifications and/or other vascular phatological findings connected with increased calcium deposition in the lamina media of the arterial wall (Monkeberg's calcinosis or arteriosclerosis), acute inflammation and/or endothelial dysfunction can be also found. Thus, low levels of fetuin-A in ESRD act as "non-traditional" risk factor for cardiovascular disease. Other "non-traditional" cardiovascular risk factors in dialyzed patients are: extracellular volume overload; insulin resistance; anaemia, and oxidative stress, many cross-sectional studies showed a direct associations of high fetuin-A levels with impaired glucose and lipid metabolism inducing metabolic syndrome in non-dialyzed patients. In these, high fetuin-A levels induce atherosclerotic lesions by insulin resistance. In conclusion, fetuin-A is able to induce both arteriosclerosis and atherosclerosis. Its serum levels seems to act (both in dialyzed and non-dialyzed patients) such as "non-traditional" cardiovascular risk factor, even if its action mechanism was not completely elucidated and further studies performed in wide range are requested.Therapeutically, some compounds such as Sevelamer, etidronate, calcium channel blockers and others interventions, are promising in to reduce calcium deposition in the vessel walls and acute inflammation induced by the low α 2 -Heremans-Schmid glycoprotein serum levels in dialyzed patients. On the contrary, extended-release niacin seems to be able to reduce cardiovascular, metabolic and inflammatory complicances dependent on high fetuin-A serum levels.

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Coronary calcification in patients with end-stage renal disease: a novel endocrine disorder?

Cited by 9 publications

References 93 publications

Relationship between Fetuin-A and vascular or valvular calcification in hemodialysis patients

Relationship between Fetuin-A and vascular or valvular calcification in hemodialysis patients

Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure

Fetuin-A: A Novel Cardiovascular Risk Factor

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