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SummaryBackground and objectives Chronic kidney disease (CKD) conveys high mortality rates. Soluble TNF-like weak inducer of apoptosis (sTWEAK) and long pentraxin 3 (PTX3) are predictors of mortality in dialysis patients and determinants of endothelial dysfunction. Now, we hypothesize that both sTWEAK and PTX3 act as biomarkers of cardiovascular outcomes in nondialysis CKD patients.Design, setting, participants, & measurements Cross-sectional analysis in which flow-mediated dilation (FMD) and intima-media thickness (IMT) were assessed in 257 nondialysis stage 1 to 5 CKD patients (mean age, 52 Ϯ 12 years; 130 men), together with biochemical measurements and sTWEAK and PTX3 assessments. Patients were followed for cardiovascular outcomes.Results PTX3 and IMT increased, whereas FMD and sTWEAK decreased across CKD stages (P Ͻ 0.001 for all). Both PTX3 and sTWEAK appeared as strong determinants of FMD in multivariate analysis. The univariate associations of sTWEAK and PTX3 with IMT were dependent on estimated GFR. After a median of 39 months (range, 2 to 43 months), 22 fatal and 57 nonfatal cardiovascular events occurred. In a Cox model excluding PTX3, decreasing sTWEAK concentration was associated with increased risk of cardiovascular events independently of basic confounders (age, gender, estimated GFR, C reactive protein, diabetes, and cardiovascular comorbidity) and FMD. In a model excluding sTWEAK, circulating levels of PTX3 were directly associated with cardiovascular outcomes independently of basic confounders, but this association was lost after adjustment for FMD.Conclusions Both PTX3 and sTWEAK levels associated with the endothelial dysfunction observed with progressive kidney failure. Additionally, both biomarkers impacted the predictability of cardiovascular outcomes.

Psoriasis is associated with an increased risk of atherosclerosis. Endothelial dysfunction is the critical early step in the process of atherogenesis, and it is commonly investigated by measuring arterial stiffness. We aimed to investigate the relationship between arterial stiffness and high-sensitivity C-reactive protein (hsCRP) in patients with psoriasis. A total of 32 patients with psoriasis and 35 patients with other skin diseases were included in the study. The hsCRP levels and arterial stiffness measurements were compared. Arterial stiffness was significantly different between the 2 groups (P = .01). Arterial stiffness was not associated with the duration of the disease or the disease activity (P = .34 and .64, respectively). In patients with psoriasis, arterial stiffness correlated positively with age, sex, body mass index, diastolic blood pressure, and hsCRP level (P < .05). These findings provide further evidence of a link between inflammation, premature atherosclerosis, and psoriasis.

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.

Neutrophils and lymphocytes (N/L) ratio and carotid intima-media thickness (C-IMT) value have been studied as new predictors of cardiovascular risk. We aimed to investigate N/L ratio and C-IMT value in patients with cardiac syndrome X (CSX) and compare patients with coronary artery disease (CAD) and normal participants. A total of 288 participants were enrolled in the study. The N/L ratio and C-IMT value were compared among the 3 groups. There were no statistically significant differences in N/L levels between CSX and CAD groups. The N/L ratio was found significantly increased in patients with CSX and CAD, compared to the control group. Patients with CAD and CSX had significantly higher C-IMT value compared to control participants. Significant positive correlation was found between C-IMT value and plasma level of N/L ratio. The relationship among CSX and higher N/L ratio level and C-IMT suggests that endothelial dysfunction may contribute to the etiopathogenesis of the CSX.

High levels of circulating Von Willebrand factor (vWf) and increased neutrophil to lymphocyte (N/L) ratio may reflect vascular inflammation in hypertensive patients. In present study, we aimed to investigate the effects of valsartan as an angiotensin II receptor antagonist and amlodipine as a calcium channel blocker on the vWf levels and N/L ratio in patients with essential hypertension. Patients were randomized to one of the following intervention protocols: calcium channel blocker (amlodipine, 5-10 mg/day) as group A (n = 20 mean age = 51.85 ± 11.32 y) and angiotensine II receptor blocker (valsartan, 80-320 mg/day) as group B (n = 26 mean age = 49.12 ± 14.12 y). Endothelial dysfunction and vascular inflammation were evaluated with vWf levels and N/L ratio in hypertensive patients before treatment and after treatment in the 12th week. No statistically significant differences were found among the groups in terms of age, sex, and body mass index (BMI). There was a significant decrease in vWf levels (P < .001) and N/L ratio after treatment (P = .04, P < .001, respectively) in both the groups. Von Willebrand factor levels and N/L ratio are very important markers having a role in vascular inflammation and antihypertensive treatment with amlodipine and valsartan may improve cardiovascular outcomes by decreasing these biomarkers.

In our study, increased MPV is associated with arterial stiffness in patients with BD without significant cardiovascular involvement. It shows that there is a relationship between thrombosis and chronic inflammation in BD. Furthermore, MPV is also a moderate predictor of cardiovascular disease and represents an increase in platelet activation. These findings provide further evidence of a link between inflammation and thrombosis in patients with BD.

We read with great interest the article ''Correlation of Neutrophil to Lymphocyte Ratio With the Presence and Severity of Metabolic Syndrome'' by Buyukkaya et al. 1 They aimed to investigate the relationship between the criteria comprising metabolic syndrome (MS) and neutrophil-lymphocyte ratio (N/L ratio) as a novel, simple, and reliable indicator of inflammation. They showed that patients with MS had significantly higher N/L ratio compared to those without MS. Furthermore, N/L ratio increased as the severity of MS increased. A strong positive correlation was revealed between the severity of MS and N/L ratio and between the severity of MS and the highsensitivity C-reactive protein (hsCRP). In addition, the correlation analysis revealed a positive correlation between hsCRP and NLR in the patient population. The measurements of white blood cells (WBCs), neutrophils, and lymphocytes in the patients with MS were higher than those without MS. The study is successful in planning and presenting the results. We believe that these findings will enlighten further studies about the association between the severity of MS and the N/L ratio. Thanks to the authors for their contribution.The WBC count is one of the useful inflammatory biomarkers in clinical practice. Leukocyte subtype and N/L ratio are also indicators of systemic inflammation. Although WBCs are in normal range, subtypes of WBCs may predict cardiovascular mortality. The N/L ratio is also an inflammatory marker of major adverse cardiac events.2 Some comments may be of interest. Although the authors have showed patients with MS had significantly higher N/L ratio compared to those without MS, some of the factors affecting these markers such as smoking, alcohol, and malignancy were not mentioned in this study. In addition, the authors could add a MS subgroup analysis. A subgroup analysis of MS according to age, sex, CRP, WBCs, neutrophils, and lymphocytes might affect the results of the study. References