Muzaffer Cakmak

Relationship between late arteriovenous fistula (AVF) stenosis and neutrophil–lymphocyte ratio (NLR) in chronic hemodialysis patients

Abstract Objectives: Primary cause of late arteriovenous fistula (AVF) dysfunction is venous stenosis as result of neointimal hyperplasia. The mechanism of AVF stenosis is not exactly understood. But inflammation is a contributing factor for development of AVF stenosis. Neutrophil–lymphocyte ratio (NLR) reflects systemic inflammation, and it was investigated in many diseases. The aim of this study was to investigate the relationship between NLR and AVF stenosis in chronic hemodialysis patients. Materials and methods: Of 593 patients applied to the department of interventional radiology between January 2011 and November 2012, a total of 108 patients meeting the appropriate criteria were included in this study. All patients were assessed with Color Doppler ultrasonography and then digital subtraction angiography was used for the patients with abnormal results. Sixty-four patients were classified as patients with AVF stenosis (group 1) and 44 patients without AVF stenosis (group 2). Routine biochemical and complete blood count values measured six months ago were recorded for all patients. Results: Mean NLR (3.47 ± 0.46 vs. 2.27 ± 0.22; p < 0.001) was higher in group 1 compared to group 2, whereas high-density lipoprotein (HDL; 31.8 ± 12.6 mg/dL vs. 51.5 ± 11.9 mg/dL; p < 0.001) was lower in group 1. NLR level was correlated with degree of AVF stenosis (r = 0.625; p < 0.01). Receiver operating characteristic curve analysis showed that NLR (optimal-cut-off = 2.70) was a useful parameter in prediction of AVF stenosis (AUC = 0.893, sensitivity = 98.4% and specificity = 75%; p < 0.001). NLR level and HDL < 30 mg/dL in logistic regression analysis are independent predictors of AVF stenosis. Conclusions: For hemodialysis patients with increased level of NLR and decreased level of HDL, regular monitoring with regard to the development of AVF stenosis may be beneficial. Our study suggests that the mechanism of AVF stenosis might have similarities to that of atherosclerosis.

Serum levels of endocan correlate with the presence and severity of pre-eclampsia.

Abstract Background: Endocan, a cysteine-rich dermatan sulfate proteoglycan expressed by endothelial cells, is seemed to be a new biomarker for endothelial dysfunction. Pre-eclampsia (PE) is characterized by the new onset of hypertension, proteinuria after 20 weeks of gestation, placental vascular remodeling, systemic vascular inflammation and endothelial dysfunction. The aim of this study was to investigate the relationship of PE and its severity with serum endocan levels. Methods: A cross-sectional study was performed. Serum was collected from women with PE and normotensive controls. Serum endocan and tumor necrosis factor alpha (TNF-α) concentrations were measured by a specific enzyme linked immunosorbent assay. Results: Patients with PE had significantly higher median (interquartile range) endocan and mean TNF-α concentrations than controls [20.04 (12.26) ng/mL vs 15.55 (6.19) ng/mL, p < 0.001 for endocan; 26.49 ± 12.14 pg/mL vs 14.62 ± 5.61 pg/mL, p < 0.001 for TNF-α; respectively]. Serum endocan concentrations were positively correlated with systolic blood pressure (r = 0.618, p < 0.001), diastolic blood pressure (r = 0.608, p < 0.001), the amount of 24-h proteinuria (r = 0.786, p < 0.001) and TNF-α (r = 0.474, p < 0.001) in women with PE. In subgroup analysis, patients with severe PE had significantly higher endocan concentrations than those with mild PE. Receiver operating characteristic analysis of endocan was used to identify the patients with PE and also discriminating between mild and severe PE. Conclusion: Serum endocan concentrations were significantly elevated in women with PE versus normotensive controls, and concentrations seem to be associated with the severity of the disease.

Association between Platelet-to-Lymphocyte Ratio and Contrast-Induced Nephropathy in Patients Undergoing Percutaneous Coronary Intervention for Acute Coronary Syndrome.

Objective: Contrast-induced nephropathy (CIN) is associated with significantly increased morbidity and mortality after percutaneous coronary intervention (PCI). Patients with acute coronary syndrome (ACS) are at higher risk of CIN. The platelet-to-lymphocyte ratio (PLR) is closely linked to inflammatory conditions. We hypothesized that PLR levels on admission can predict the development of CIN after PCI for ACS. Subjects and Methods: A total of 426 patients (mean age 63.17 ± 13.01 years, 61.2% males) with ACS undergoing PCI were enrolled in this study. Admission PLR levels were measured before PCI. Serum creatinine values were measured before and within 72 h after the administration of contrast agents. Patients were divided into 2 groups: the CIN group and the no-CIN group. CIN was defined as an increase in serum creatinine level of ≥0.5 mg/dl or 25% above baseline within 72 h after contrast administration. Results: CIN developed in 53 patients (15.9%). Baseline PLR was significantly higher in patients who developed CIN compared to those who did not (160.8 ± 29.7 and 135.1 ± 26.1, respectively; p < 0.001). Multivariate analyses found that PLR [odds ratio (OR) 3.453, 95% confidence interval (CI) 1.453-8.543; p = 0.004] and admission creatinine (OR 6.511, 95% CI 1.759-11.095; p = 0.002) were independent predictors of CIN. Conclusions: The admission PLR level is an independent predictor of the development of CIN after PCI in ACS.

Association between Red Blood Cell Distribution Width and Coronary Artery Calcification in Patients Undergoing 64-Multidetector Computed Tomography

Background and Objectives The red blood cell distribution width (RDW) has been found to be associated with cardiovascular morbidity and mortality. The objective of this study was to determine whether the RDW measures are associated with the coronary artery calcification score (CACS) in patients who did not present with obvious coronary heart disease (CHD). Subjects and Methods A total of 527 consecutive patients with a low to intermediate risk for CHD but without obvious disease were enrolled in this study. The study subjects underwent coronary computerized tomography angiography and CACS was calculated. The patients were divided into two groups based on CACS: Group I (CACS≤100) and Group II (CACS>100). The two groups were compared in terms of classic CHD risk factors and haematological parameters, particularly the RDW. Results Group I patients were younger than Group II patients. The Framingham risk score (FRS) in patients of Group II was significantly higher than that in patients of Group I. Group II patients had significantly elevated levels of haemoglobin, RDW, neutrophil count, and neutrophil/lymphocyte ratio compared with Group I patients. CACS was correlated with age, RDW, and ejection fraction. In the multivariate analysis, age, RDW, and FRS were independent predictors of CACS. Using the receiver-operating characteristic curve analysis, a RDW value of 13.05% was identified as the best cut-off for predicting the severity of CACS (>100) (area under the curve=0.706). Conclusion We found that the RDW is an independent predictor of the CACS, suggesting that it might be a useful marker for predicting CAD.

Melatonin protects kidney against apoptosis induced by acute unilateral ureteral obstruction in rats.

Introduction To investigate whether there was a protective effect of melatonin on apoptotic mechanisms after an acute unilateral obstruction of the kidney. Material and methods A total of 25 rats consisting of five groups were used in the study, designated as follows: Group 1: control, Group 2: sham, Group 3: unilateral ureteral obstruction treated with only saline, Group 4: unilateral ureteral obstruction treated with melatonin immediately, and Group 5: unilateral obstruction treated with melatonin one day after obstruction. Melatonin was administered as a 10 mg/kg dose intraperitoneally. The kidneys were evaluated according to the apoptotic index and Ki-67 scores. Results Comparison of all obstruction groups (Group 3, 4, and 5), revealed that the apoptotic index was significantly higher in Groups 1 and 2. Despite melatonin reduced apoptotic mechanisms in Groups 4 and 5, there was no significant difference between Groups 4 and 5 in terms of the reduction of apoptosis. However, the reduction of apoptosis in the melatonin treated group did not decrease to the level of Groups 1 and 2. Conclusions Despite melatonin administration, which significantly reduces the apoptotic index occurring after acute unilateral ureteral obstruction, the present study did not observe a return to normal renal histology in the obstruction groups.

Effects of multimedia nursing education on disease-related depression and anxiety in patients staying in a coronary intensive care unit

AIM We evaluated the effectiveness of an accessibility-enhanced multimedia informational educational program in reducing depression and anxiety increasing satisfaction with the information and materials received by patients in coronary care unit. METHODS We selected 100 patients from among the patients who stayed at or who underwent surgery at one of two ICUs for any reason who satisfied the eligibility criteria, and agreed to participate in the research. The participants were included in the control or experimental group by random selection. The patients completed the Hospital Anxiety Depression Scale during ICU admission and 1week after hospital discharge. RESULTS The difference in HADSA score was significantly greater in patients who received education than in patients who did not receive multimedia nursing education (4.2±0.58 vs. 0.6±0.42; p<.01). Additionally, the difference in HADSD score was significantly greater in patients who received multimedia nursing education (2.2±0.53 vs. 0.64±0.46; p<.01). CONCLUSION This study showed that anxiety and depression associated with hospital can be reduced with multimedia nursing education.

Role of interlekin-35 as a biomarker in patients with newly diagnosed Hashimoto's thyroiditis.

Abstract Objective. Interleukin-35 (IL-35), an interleukin-12 (IL-12) cytokine family member, is shown to be a potent immunosuppressive and anti-inflammatory cytokine. Inducible regulatory T cells (Tregs) produce IL-35 that mediates the immune inhibitory function of Tregs. Growing evidence revealed that upregulation of IL-35 expression may play a critical role in the prevention of autoimmune diseases in various experimental autoimmunity models and vice versa. Hashimoto’s thyroiditis (HT) is considered to be a Treg cell-related autoimmune disease with loss of self-tolerance. Methods. One hundred-twenty eight subjects, newly diagnosed hypothyroid HT patients [56 overt (Group 1), 72 subclinical hypothyroid (Group 2)] and 38 healthy controls (Group 3) were enrolled in the study. The levels of serum IL-35 were determined by enzyme-linked immunosorbent assay (ELISA). Results. Serum IL-35 levels were lower in the HT group when compared with subclinical HT group [304.5 (834.6) pg/ml vs. 636.1 (1542.0) pg/ml, p=0.004] and control cases [304.5 (834.6) pg/ml vs. 1064.7 (2526.8) pg/ml, p<0.001]. Serum IL-35 levels were inversely associated with thyroid stimulating hormone (TSH; rs=-0.396, p<0.001) and anti-thyroid peroxidase antibodies (TPOAb; rs=-0.571, p<0.001) in whole group. Serum IL-35 were negatively associated with TSH (rs=-0.264, p=0.003) and TPOAb (rs=-0.735, p<0.001) in patients with Hashimoto’s thyroiditis (Group 1 + Group 2). Conclusion. The results suggest that IL-35 may play a role in the pathogenesis of HT.

Circulating irisin levels reflect visceral adiposity in non-diabetic patients undergoing hemodialysis

Abstract Background: Recent evidence suggests that increased visceral adiposity is a strong independent risk factor for cardiovascular death and all-cause mortality in hemodialysis (HD) patients. Irisin, which is a novel myokine, can play critical roles in diabetes and adiposity. The purpose of our study was to investigate whether serum irisin levels are associated with body mass index, waist circumference (WC), and total fat mass in non-diabetic patients undergoing maintenance HD. Methods: This cross-sectional study included 108 non-diabetic HD patients and 40 age- and sex-matched apparently healthy subjects. Serum irisin concentrations were determined using an enzyme-linked immunosorbent assay. Body fat composition (TBF-410 Tanita Body Composition Analyzer) was measured and calculated. Results: Serum irisin levels did not differ between HD patients and the healthy controls (523.50 ± 229.32 vs. 511.28 ± 259.74, p = 0.782). Serum irisin levels were associated with age (r = 0.314; p =0.006), HOMA-IR (r = 0.472; p = 0.003), WC (r = 0.862; p < 0.001), and total fat mass (r = 0.614; p < 0.001). In multivariate regression analysis, WC (β = 1.240, p < 0.001) and total fat mass (β = 0.792, p = 0.015) were the variables that were significantly associated with irisin concentrations (R2 = 0.684, p < 0.001) after adjusting for confounding factors (age and HOMA-IR). Conclusions: These results suggest that serum irisin levels are related to visceral adiposity in non-diabetic HD patients.

Association of ambulatory arterial stiffness index with sEPCR in newly diagnosed hypertensive patients

Abstract Aim: Increased arterial stiffness is strongly associated with cardiovascular diseases, while thrombotic events are more common than hemorrhagic events in hypertensive patients. Markers of a hypercoagulable state may also predict future cardiovascular events in hypertensive patients. Here, we speculated that increased arterial stiffness might lead to the development of a hypercoagulable state that can play a role in the thrombotic complications of hypertension. Soluble endothelial protein C receptor (sEPCR) is one such marker of hypercoagulation. The ambulatory arterial stiffness index (AASI) could be accepted as a non-invasive measure of arterial stiffness. The aim of this study was to investigate association of AASI with levels of sEPCR in newly diagnosed hypertensive patients. Materials and methods: The study included 263 newly diagnosed essential hypertensive patients and 55 healthy normotensive controls. All subjects underwent 24 h ambulatory blood pressure monitoring (ABPM); the AASI was derived from ABPM tracings. Plasma sEPCR was measured by ELISA. Results: Hypertensive patients (n = 263) had higher AASI, C-reactive protein (CRP) and sEPCR versus the normotensive healthy group (n = 55). Univariate analysis showed that AASI was positively associated with age (r = 0.212, p <  0.001) body mass index (r = 0.412, p < 0.001), pulse pressure (r = 0.350, p < 0.001), plasma sEPCR (r = 0.894, p < 0.001), 24-h heart rate (r = 0.176, p = 0.001) and inversely related to high-density lipoprotein (HDL) (r = −0.293, p < 0.001). Multivariate analyses revealed that sEPCR and HDL are independently correlated to AASI. Conclusion: We suggest that increased AASI is associated with elevated sEPCR. It might be responsible for subsequent thrombotic events in newly diagnosed hypertensive patients.

Antiplatelet Effect of Sequential Administration of Cilostazol in Patients with Acetylsalycilic Acid Resistance.

BACKGROUND Acetylsalicylic acid (ASA) resistance in patients with coronary artery disease is an important medical problem that can affect treatment decision-making and outcomes. Cilostazol has been investigated to determine its effectiveness in patients with acetylsalicylic acid resistance. The aim of this study was to evaluate the antiplatelet efficacy of sequential administration of CLZ in patients with ASA resistance. METHODS A total of 180 patients were enrolled in our study. Patients with stable coronary artery disease were first given orally ASA 100 for 10 days, followed by collagen/epinephrine induced closure time (CTCEPI) measurements. Those who were found to be resistant to orally 100 mg of ASA were given orally 300 mg of ASA for an additional 10 days after which we repeated CTCEPI measurements. Those patients with resistance to orally 300 mg ASA were then given CLZ at a daily dose of orally 200 mg for 10 days followed by a final CTCEPI measurement. RESULTS The rate of resistance to 100 mg ASA was 81/180 (45%) compared to a rate of 35/81 (43.2%) with 300 mg ASA. Of the 35 patients found to be resistant to 300 mg ASA, 22 (62.9%) also failed to respond to CLZ treatment. Overall, sequential administration of 300 mg ASA and 200 mg CLZ resulted in a reduction in the number of non-responders from 45% to 12.2%. CONCLUSIONS Initiation of CLZ could be of benefit in some patients with ASA-resistance for whom an effective anti-aggregant effect is of clinical importance.