Impact of BMI on Cardiovascular Events, Renal Function, and Coronary Artery Calcification

Russo, Domenico; Morrone, L F; Errichiello, Carmela; Gregorio, Maria Grazia De; Imbriaco, Massimo; Battaglia, Yuri; Russo, Luigi; Andreucci, Michele; Iorio, Biagio Raffaele Di

doi:10.1159/000362862

Cited by 22 publications

(26 citation statements)

References 32 publications

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“…Two recent meta-analyses showed that obesity and not only hypertension, but also pre-hypertension, were significant predictors of new onset CKD (Garofalo et al, 2016(Garofalo et al, , 2017. Further analyses showed that high BMI increases also the risk for dialysis initiation but not for CV events (Russo et al, 2014). These important findings confirm that epidemiologic analyses may provide different results, given the different populations examined.…”

Section: Introductionmentioning

confidence: 73%

Unraveling Cardiovascular Risk in Renal Patients: A New Take on Old Tale

Provenzano

Coppolino

Nicola

et al. 2019

Front. Cell Dev. Biol.

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Chronic kidney disease (CKD), defined by an estimated glomerular filtration rate <60 ml/min/1.73 m 2 and/or an increase in urine protein excretion (i.e., albuminuria), is an important public health problem. Prevalence and incidence of CKD have risen by 87 and 89%, worldwide, over the last three decades. The onset of either albuminuria and eGFR reduction has found to predict higher cardiovascular (CV) risk, being this association strong, independent from traditional CV risk factors and reproducible across different setting of patients. Indeed, this relationship is present not only in high risk cohorts of CKD patients under regular nephrology care and in those with hypertension or type 2 diabetes, but also in general, otherwise healthy population. As underlying mechanisms of damage, it has hypothesized and partially proved that eGFR reduction and albuminuria can directly promote endothelial dysfunction, accelerate atherosclerosis and the deleterious effects of hypertension. Moreover, the predictive accuracy of risk prediction models was consistently improved when eGFR and albuminuria have been added to the traditional CV risk factors (i.e., Framingham risk score). These important findings led to consider CKD as an equivalent CV risk. Although it is hard to accept this definition in absence of additional reports from scientific Literature, a great effort has been done to reduce the CV risk in CKD patients. A large number of clinical trials have tested the effect of drugs on CV risk reduction. The targets used in these trials were different, including blood pressure, lipids, albuminuria, inflammation, and glucose. All these trials have determined an overall better control of CV risk, performed by clinicians. However, a non-negligible residual risk is still present and has been attributed to: (1) missed response to study treatment in a consistent portion of patients, (2) role of many CV risk factors in CKD patients not yet completely investigated. These combined observations provide a strong argument that kidney measures should be regularly included in individual prediction models for improving CV risk stratification. Further studies are needed to identify high risk patients and novel therapeutic targets to improve CV protection in CKD patients.

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Section: Introductionmentioning

confidence: 73%

Unraveling Cardiovascular Risk in Renal Patients: A New Take on Old Tale

Provenzano

Coppolino

Nicola

et al. 2019

Front. Cell Dev. Biol.

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“…Such a measure may improve physicians' abilities to identify patients with poor prognoses [109]. One approach involves the discovery of novel biomarkers that may add proper prognostic information on top of already known risk factors [46,107,[110][111][112][113]. Investigators from the Steno Diabetes Center, a prospective cohort that contributed to the comprehension of prognosis of diabetic patients with or without CKD, showed that MMP-1 and MMP-2 are associated with an increased risk of CV events and CV mortality, regardless of age, gender, eGFR, and albuminuria [114].…”

Section: Discussionmentioning

confidence: 99%

The Association of Matrix Metalloproteinases with Chronic Kidney Disease and Peripheral Vascular Disease: A Light at the End of the Tunnel?

et al. 2020

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Chronic Kidney Disease (CKD) represents a risk factor for fatal and nonfatal cardiovascular (CV) events, including peripheral vascular disease (PVD). This occurs because CKD encompasses several factors that lead to poor prognoses, mainly due to a reduction of the estimated glomerular filtration rate (eGFR), the presence of proteinuria, and the uremic inflammatory milieu. The matrix metalloproteinases (MMPs) are a group of zinc-containing endopeptidases implicated in extracellular matrix (ECM) remodeling, a systemic process in tissue homeostasis. MMPs play an important role in cell differentiation, angiogenesis, inflammation, and vascular damage. Our aim was to review the published evidence regarding the association between MMPs, PVD, and CKD to find possible common pathophysiological mechanisms. MMPs favor ECM deposition through the glomeruli, and start the shedding of cellular junctions and epithelial-mesenchymal transition in the renal tubules. MMP-2 and -9 have also been associated with the presence of systemic vascular damage, since they exert a pro-inflammatory and proatherosclerotic actions. An imbalance of MMPs was found in the context of PVD, where MMPs are predictors of poor prognoses in patients who underwent lower extremity revascularization. MMP circulating levels are increased in both conditions, i.e., that of CKD and PVD. A possible pathogenic link between these conditions is represented by the enhanced production of transforming growth factor-β that worsens vascular calcifications and atherosclerosis and the development of proteinuria in patients with increased levels of MMPs. Proteinuria has been recognized as a marker of systemic vascular damage, and this may explain in part the increase in CV risk that is manifest in patients with CKD and PVD. In conclusion, MMPs can be considered a useful tool by which to stratify CV risk in patients with CKD and PVD. Further studies are needed to investigate the causal-relationships between MMPs, CKD, and PVD, and to optimize their prognostic and predictive (in response to treatments) roles.

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“…Several investigators found a graded relationship between severity of CKD and CAC score independent of conventional risk factors for atherosclerosis. 12 , 13 Further, diabetic patients with coexistent CKD had a higher prevalence, greater extent, and more rapid progression of CAC. 14 …”

Section: Introductionmentioning

confidence: 95%

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

Durham

Speer

Scatena

et al. 2018

Cardiovascular Research

768

662

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Vascular calcification is associated with a significant increase in all-cause mortality and atherosclerotic plaque rupture. Calcification has been determined to be an active process driven in part by vascular smooth muscle cell (VSMC) transdifferentiation within the vascular wall. Historically, VSMC phenotype switching has been viewed as binary, with the cells able to adopt a physiological contractile phenotype or an alternate ‘synthetic’ phenotype in response to injury. More recent work, including lineage tracing has however revealed that VSMCs are able to adopt a number of phenotypes, including calcific (osteogenic, chondrocytic, and osteoclastic), adipogenic, and macrophagic phenotypes. Whilst the mechanisms that drive VSMC differentiation are still being elucidated it is becoming clear that medial calcification may differ in several ways from the intimal calcification seen in atherosclerotic lesions, including risk factors and specific drivers for VSMC phenotype changes and calcification. This article aims to compare and contrast the role of VSMCs in driving calcification in both atherosclerosis and in the vessel media focusing on the major drivers of calcification, including aging, uraemia, mechanical stress, oxidative stress, and inflammation. The review also discusses novel findings that have also brought attention to specific pro- and anti-calcifying proteins, extracellular vesicles, mitochondrial dysfunction, and a uraemic milieu as major determinants of vascular calcification.

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Impact of BMI on Cardiovascular Events, Renal Function, and Coronary Artery Calcification

Cited by 22 publications

References 32 publications

Unraveling Cardiovascular Risk in Renal Patients: A New Take on Old Tale

Unraveling Cardiovascular Risk in Renal Patients: A New Take on Old Tale

The Association of Matrix Metalloproteinases with Chronic Kidney Disease and Peripheral Vascular Disease: A Light at the End of the Tunnel?

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

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