Vascular health, systemic inflammation and progressive reduction in kidney function; clinical determinants and impact on cardiovascular outcomes

Yılmaz, Mahmut İlker; Stenvinkel, Peter; Sönmez, Alper; Sağlam, Mutlu; Yaman, Halıl; Kılıç, Selim; Eyıleten, Tayfun; Çağlar, Kayser; Oğuz, Yusuf; Vural, Abdülgaffar; Çakar, Mustafa; Altun, Battal; Yenicesu, Müjdat; Carrero, Juan Jesús

doi:10.1093/ndt/gfr081

Cited by 107 publications

(85 citation statements)

References 41 publications

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“…All patients were diagnosed as having CKD according to their estimated GFR (eGFR) (25) and the presence of kidney injury as defined by National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines. The protocol for this patient material was described in more detail elsewhere (26), and was approved by the local ethical committee. This cohort was designed to study determinants of endothelial function on nondialyzed CKD patients; therefore, a priori exclusion criteria included use of angiotensin converting enzyme inhibitors, angiotensin receptor blockers, statins, erythropoietin, or supplemental vitamin pills.…”

Section: Patientsmentioning

confidence: 99%

“…For nondialyzed patients, routine biochemical measurements included serum albumin, hemoglobin, parathyroid hormone (PTH), calcium, phosphate, and total cholesterol. High-sensitivity C-reactive protein (CRP) was measured by a photometric method (26). Serum prolactin levels were quantified by the Modular Analytics E 170 Module (Roche Diagnostics, Indianapolis, IN).…”

Section: Laboratory Measurementsmentioning

confidence: 99%

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Prolactin Levels, Endothelial Dysfunction, and the Risk of Cardiovascular Events and Mortality in Patients with CKD

Carrero

Kyriazis

Sönmez

et al. 2012

Clinical Journal of the American Society of Nephrology

110

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SummaryBackground and objectives Both prolactin clearance and production are altered in CKD. In nonrenal populations, emerging evidence suggests that prolactin participates in the atherosclerotic process. Given the elevated cardiovascular risk of CKD, this study examined links between prolactinemia, vascular derangements, and outcomes.Design, setting, participants, & measurements This observational study was conducted in two cohorts: one with 457 nondialyzed CKD patients (mean age 52612 years; 229 men) with measurements of flow-mediated dilation (FMD) and carotid intima-media thickness and one with 173 hemodialysis patients (65612 years; 111 men) with measurements of pulse wave velocity (PWV). Patients were followed for cardiovascular events (n=146, nondialyzed cohort) or death (n=79, hemodialysis cohort).Results Prolactin levels increased along with reduced kidney function. Prolactin significantly and independently contributed to explain the variance of both FMD (in nondialyzed patients) and PWV (in hemodialysis patients), but not intima-media thickness. In Cox analyses, the risk of cardiovascular events in nondialyzed patients increased by 27% (hazard ratio [HR], 1.27; 95% confidence interval [95% CI], 1.17-1.38) for each 10 ng/ml increment of prolactin. Similarly, the risk for all-cause and cardiovascular mortality in hemodialysis patients increased by 12% (HR, 1.12; 95% CI, 1.06-1.17) and 15% (HR, 1.15; 95% CI, 1.08-1.21), respectively. This was true after multivariate adjustment for confounders and after adjustment within the purported causal pathway (FMD or PWV).Conclusions Prolactin levels directly associated with endothelial dysfunction/stiffness and with increased risk of cardiovascular events and mortality in two independent cohorts of CKD patients.

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Section: Patientsmentioning

confidence: 99%

Section: Laboratory Measurementsmentioning

confidence: 99%

Prolactin Levels, Endothelial Dysfunction, and the Risk of Cardiovascular Events and Mortality in Patients with CKD

Carrero

Kyriazis

Sönmez

et al. 2012

Clinical Journal of the American Society of Nephrology

110

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“…Evidence indicates that it can predict the development of CVD in high-risk individuals, such as those with peripheral artery diseases, coronary artery disease, and CKD 1,2,20) . On the other hand, other studies have reported that the evaluation of FMD has limited application in some clinical situations.…”

Section: Relationship Of Fmd/nmd Imt and Stiffness Parameter β Withmentioning

confidence: 99%

Association of Endothelial and Vascular Smooth Muscle Dysfunction with Cardiovascular Risk Factors, Vascular Complications, and Subclinical Carotid Atherosclerosis in Type 2 Diabetic Patients

Kawano

Emoto

Mori

et al. 2012

JAT

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Aim: Atherosclerosis and arteriosclerosis are mainly caused by the dysfunction of arterial components, namely, vascular endothelial cells, smooth muscle cells, and the extracellular matrix. Endothelial dysfunction is well established as a predictive surrogate marker of cardiovascular events; however, little is known regarding the clinical implications of vascular smooth muscle dysfunction for cardiovascular disease and microangiopathy. In the present study, we aimed to clarify the association of arterial dysfunction with micro-/macroangiopathy and conventional cardiovascular risk factors in 181 type 2 diabetic patients (T2DM; age±SD, 64±10 years; duration of diabetes, 12±10 years). Methods: Flow-mediated dilatation (FMD) and nitroglycerin-mediated dilatation (NMD) were assessed to evaluate endothelial dysfunction and vascular smooth muscle dysfunction, respectively, by using a novel ultrasound device, UNEXEF18G (Unex Co. Ltd., Japan). Results: The FMD and NMD were 6.4±3.9% and 13.4±6.6%, respectively. No significant differences in FMD were noted between T2DM with and without micro-or macroangiopathy; however, NMD in T2DM patients with micro-and macroangiopathy was significantly lower than that in T2DM patients without angiopathy. NMD decreased with the progression of chronic kidney disease (CKD) stage (p = 0.005), but not FMD (p = 0.071). On multiple regression analysis, significant independent contributors to FMD were age, smoking, systolic blood pressure, glycosylated hemoglobin, and serum total cholesterol, while those for NMD were age, systolic blood pressure, and waist circumference. Conclusion: The relationship of vascular complications and cardiovascular risk factors with NMD is different from that with FMD in type 2 diabetic patients.

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“…Endothelial dysfunction is common in CKD and has been shown to predict CVD prospectively in several groups, including healthy individuals,32, 33 individuals with peripheral vascular disease,34 and CKD 35. To explore this hypothesis we recruited healthy control subjects and patients with stage III and IV CKD.…”

Section: Introductionmentioning

confidence: 99%

Endothelial Microparticles and Systemic Complement Activation in Patients With Chronic Kidney Disease

Jalal

Renner

Laskowski

et al. 2018

JAHA

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BackgroundEndothelial microparticles are associated with chronic kidney disease (CKD) and complement activation. We hypothesized that the complement pathway is activated in patients with CKD via endothelial microparticles and that complement activation correlates with endothelial dysfunction in CKD.Methods and ResultsWe analyzed complement data of 30 healthy subjects, 30 patients with stage III/IV CKD, and 30 renal transplant recipients with stage III/IV CKD, evaluating the potential correlation of complement fragments with brachial artery flow–mediated dilation, Chronic Kidney Disease Epidemiology Collaboration glomerular filtration rate, and urinary albumin/creatinine ratio. Endothelial microparticles were characterized via proteomic analysis and compared between study groups. Complement fragment Ba was significantly increased in CKD and post–kidney transplant CKD. Plasma Ba levels correlated significantly with lower brachial artery flow–mediated dilation, lower Chronic Kidney Disease Epidemiology Collaboration glomerular filtration rate, and higher urinary albumin/creatinine ratio. Factor D levels were significantly higher in the plasma microparticles of patients with CKD versus healthy controls. Plasma microparticles isolated from patients with CKD and containing factor D activated the alternative pathway in vitro.ConclusionThe alternative complement pathway is activated in CKD and correlates with endothelial dysfunction and markers of CKD. Future studies are needed to evaluate whether endothelial microparticles with increased factor D play a pathologic role in CKD‐associated vascular disease.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT02230202.

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Vascular health, systemic inflammation and progressive reduction in kidney function; clinical determinants and impact on cardiovascular outcomes

Abstract: Endothelial dysfunction, arterial thickening and inflammation occur in parallel with the decline in eGFR, contributing to the increased cardiovascular risk of nondialysed CKD. Our results support the use of FMD over IMT measurements to monitor nondialysed CKD patients at risk.

Cited by 107 publications

References 41 publications

Prolactin Levels, Endothelial Dysfunction, and the Risk of Cardiovascular Events and Mortality in Patients with CKD

Prolactin Levels, Endothelial Dysfunction, and the Risk of Cardiovascular Events and Mortality in Patients with CKD

Association of Endothelial and Vascular Smooth Muscle Dysfunction with Cardiovascular Risk Factors, Vascular Complications, and Subclinical Carotid Atherosclerosis in Type 2 Diabetic Patients

Endothelial Microparticles and Systemic Complement Activation in Patients With Chronic Kidney Disease

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