The Relationship of Visfatin Levels to Inflammatory Cytokines and Left Ventricular Hypertrophy in Hemodialysis and Continuous Ambulatory Peritoneal Dialysis Patients

Visfatin was recently defined as an adipocytokine; however, the pathophysiological role of visfatin is not completely understood. A few studies suggest that visfatin may be a new proinflammatory adipocytokine. The aim of the present study was to compare serum visfatin levels between hemodialysis and continuous ambulatory peritoneal dialysis (CAPD) patients and evaluate the relationship between visfatin levels to IL-6, TNF-α, and left ventricular hypertrophy. Serum visfatin, IL-6, and TNF-α levels were measured by using the ELISA method, and echocardiographic evaluations were performed in 31 hemodialysis patients, 30 CAPD patients, and 21 healthy volunteers. Serum visfatin levels were higher in the CAPD group (265.27 ± 387.86 ng/mL) than hemodialysis (97.68 ± 244.96 ng/mL,) and control (41.33 ± 48.87 ng/mL) groups (p = 0.04, p = 0.01, respectively). No significant difference was observed between the hemodialysis and control groups. In univariate analysis, visfatin levels were positively correlated with IL-6 (r = 0.24, p = 0.03), TNF-α (r = 0.34, p = 0.002), and BMI (r = 0.26, p = 0.03) and negatively correlated with some left ventricular diastolic parameters [Em and Em/Am (r = ?0.305, p = 0.01), (r = ?0.251, p = 0.03), respectively]. No relationship was found between visfatin and left ventricular mass index. In the linear regression analysis, visfatin levels independently related with TNF-( (β = 0.369, p = 0.001) and IL-6 (β = 0.284, p = 0.015). This study has found significantly higher levels of serum visfatin in CAPD patients when compared to healthy individuals. Increased visfatin levels seem to associate with proinflammatory cytokines such as IL-6 or TNF-α. As for the effects of on left ventricular structure and functions, visfatin might have negative effects on left ventricular diastolic function parameters but have no effects on left ventricular mass index.     

Solutes Transport Characteristics in Peritoneal Dialysis: Variations in Glucose and Insulin Serum Levels

Background. Differences in small solutes transport rate (SSTR) during peritoneal dialysis (PD) may affect water and solutes removal. Patients with high SSTR must rely on shorter dwell times and increased dialysate glucose concentrations to keep fluid balance. Glucose absorption during peritoneal dialysis (PD), besides affecting glucose and insulin metabolism, may induce weight gain. The study aimed at examining acute glucose and insulin serum level changes and other potential relationships in PD patients with diverse SSTR. Methods. This cross-sectional study used a modified peritoneal equilibration test (PET) that enrolled 34 prevalent PD patients. Zero, 15, 30, 60, 120, 180, and 240-minute glucose and insulin serum levels were measured. Insulin resistance index was assessed by the homeostasis model assessment (HOMA-IR) formula. SSTR categories were classified by quartiles of the four-hour dialysate/serum creatinine ratio (D₄/P_Cr). Demographic and clinical variables were evaluated, and the body mass index (BMI) was estimated. Correlations among variables of interest and categories of SSTR were explored. Results. Glucose serum levels were significantly different at 15, 30, and 60 minutes between high and low SSTR categories (p?=?0.014, 0.009, and 0.022). Increased BMI (25.5 ± 5.1) and insulin resistance [HOMA-IR?=?2.60 (1.40–4.23)] were evidenced overall. Very strong to moderate correlations between insulin levels along the PET and HOMA-IR (r?=?0.973, 0.834, 0.766, 0.728, 0.843, 0.857, 0.882) and BMI (r?=?0.562, 0.459, 0.417, 0.370, 0.508, 0.514, 0.483) were disclosed. Conclusions. Early glucose serum levels were associated with SSTR during a PET. Overweight or obesity and insulin resistance were prevalent. An association between insulin serum levels and BMI was demonstrated.     

The relationship between atherogenic index of plasma and epicardial adipose tissue in hemodialysis and peritoneal dialysis patients

Abstract

Introduction: Epicardial adipose tissue (EAT) is the true visceral fat depot of the heart. The relationship between coronary artery disease and EAT was shown in end-stage renal disease (ESRD) patients. One of the established risk factor in this population is dyslipidemia. We aimed to determine the relationship between atherogenic index of plasma (AIP) and EAT in ESRD patients. Methods: This was a cross-sectional study involving 76 ESRD patients receiving PD or HD for ≥6 months and 42 healthy subjects. EAT was measured by using an electrocardiogram-gated 64-multidetector computed tomography (MDCT). Atherogenic index of plasma was calculated as the logarithmically transformed ratio of the serum trigliseride to HDL-cholesterol. Results: The etiology of ESRD patients was diabetic nephropathy (n?=?16), chronic glomerulonephritis (n?=?10), hypertensive nephropathy (n?=?23), polycystic kidney disease (n?=?7), nephrolithiasis (n?=?5) and unknown (n?=?15). There were no differences with respect to the following variables between ESRD patients and healthy subjects: age; sex; BMI; predialysis levels of DBP; serum levels of albumin, HDL-cholesterol and hemoglobin. However, ESRD patients had higher serum levels of trigliseride, hs-CRP and AIP when compared to healthy subjects. There was a statistically significant relationship between EAT, BMI and AIP in ESRD patients (r?=?0.42, p?<?0.001 and r?=?0.25, p?=?0.028, respectively). The stepwise linear regression analysis revealed that age, as well as BMI were independent predictors of EAT. Conclusion: We found a relationship between EAT as defined by MDCT and AIP in ESRD patients. Further clinical and experimental studies are needed.     

The relationship of visfatin levels to inflammatory cytokines and left ventricular hypertrophy in hemodialysis and continuous ambulatory peritoneal dialysis patients

Visfatin was recently defined as an adipocytokine; however, the pathophysiological role of visfatin is not completely understood. A few studies suggest that visfatin may be a new proinflammatory adipocytokine. The aim of the present study was to compare serum visfatin levels between hemodialysis and continuous ambulatory peritoneal dialysis (CAPD) patients and evaluate the relationship between visfatin levels to IL-6, TNF-alpha, and left ventricular hypertrophy. Serum visfatin, IL-6, and TNF-alpha levels were measured by using the ELISA method, and echocardiographic evaluations were performed in 31 hemodialysis patients, 30 CAPD patients, and 21 healthy volunteers. Serum visfatin levels were higher in the CAPD group (265.27 +/- 387.86 ng/mL) than hemodialysis (97.68 +/- 244.96 ng/mL,) and control (41.33 +/- 48.87 ng/mL) groups (p = 0.04, p = 0.01, respectively). No significant difference was observed between the hemodialysis and control groups. In univariate analysis, visfatin levels were positively correlated with IL-6 (r = 0.24, p = 0.03), TNF-alpha (r = 0.34, p = 0.002), and BMI (r = 0.26, p = 0.03) and negatively correlated with some left ventricular diastolic parameters [Em and Em/Am (r = -0.305, p = 0.01), (r = -0.251, p = 0.03), respectively]. No relationship was found between visfatin and left ventricular mass index. In the linear regression analysis, visfatin levels independently related with TNF-( (beta = 0.369, p = 0.001) and IL-6 (beta = 0.284, p = 0.015). This study has found significantly higher levels of serum visfatin in CAPD patients when compared to healthy individuals. Increased visfatin levels seem to associate with proinflammatory cytokines such as IL-6 or TNF-alpha. As for the effects of on left ventricular structure and functions, visfatin might have negative effects on left ventricular diastolic function parameters but have no effects on left ventricular mass index.     

Relationship between aortic valve sclerosis and left ventricular hypertrophy in chronic haemodialysis patients

Background Cardiac valve calcification is a frequent finding in chronic haemodialysis patients. Left ventricular hypertrophy (LVH) is a significant predictor of cardiovascular mortality in patients with end-stage renal disease. We evaluated the influence of aortic valve sclerosis (AVS) on the development of LVH in chronic haemodialysis patients. Methods A total of 82 consecutive patients (52 male, mean age 48 ± 12 years) undergoing chronic haemodialysis treatment for >1 year were subjected to echocardiography for the screening of AVS and the assessment of transaortic flow velocity and the left ventricular mass index (LVMI). The absence (group 1, n = 42) and presence of AVS (group 2, n = 40) was established. The average values of systolic, diastolic and pulse pressure were obtained. Plasma calcium, phosphorus, intact parathyroid hormone, C-reactive protein, haemoglobin and lipid levels were also measured. Results LVH was detected in 59 (72%) of the study patients. The LVMI was higher in the AVS group (171 ± 39 vs. 132 ± 41 g/m², p < 0.001). Patients with AVS also had higher transaortic flow velocities (1.64 ± 0.36 vs. 1.21 ± 0.21 m/s, p < 0.01) and maximal pressure gradients (10.8 ± 7.1 vs. 5.9 ± 3.4 mmHg, p < 0.01). The LVMI showed a direct correlation with transaortic flow velocity in the AVS group (r = 0.60, p < 0.01). Stepwise linear regression analysis revealed transaortic flow velocity (p = 0.02), pulse pressure (p = 0.01) and haemoglobin levels (inverse relationship) (p = 0.02) to be independent predictors of the LVMI. Conclusion These data suggest that AVS is strongly and independently interrelated with LVH in chronic haemodialysis patients. The underlying mechanism might be the valve resistance to left ventricular outflow, as shown by increased transaortic flow velocities and maximal pressure gradients in AVS patients.     

Serum visfatin increases with progressive beta-cell deterioration

Visfatin has shown to be increased in type 2 diabetes but to be unrelated to insulin sensitivity. We hypothesized that visfatin is associated with insulin secretion in humans. To this aim, a cross-sectional study was conducted in 118 nondiabetic men and 64 (35 men and 29 women) type 2 diabetic patients. Type 1 diabetic patients with long-standing disease (n = 58; 31 men and 27 women) were also studied. In nondiabetic subjects, circulating visfatin (enzyme immunoassay) was independently associated with insulin secretion (acute insulin response to glucose [AIRg] from intravenous glucose tolerance tests) but not with insulin sensitivity (Si) or other metabolic or anthropometric parameters, and AIRg alone explained 8% of visfatin variance (beta = -0.29, P = 0.001). Circulating visfatin was increased in type 2 diabetes (mean 18 [95% CI 16-21] vs. 15 ng/ml [13-17] for type 2 diabetic and nondiabetic subjects, respectively; P = 0.017, adjusted for sex, age, and BMI), although this association was largely attenuated after accounting for HbA1c (A1C). Finally, circulating visfatin was found to be increased in patients with long-standing type 1 diabetes, even after adjusting for A1C values (37 ng/ml [34-40]; P < 0.0001, adjusted for sex, age, BMI, and A1C compared with either type 2 diabetic or nondiabetic subjects). In summary, circulating visfatin is increased with progressive beta-cell deterioration. The study of the regulation and role of visfatin in diabetes merits further consideration.     

Importance of Albumin, 25(OH)-Vitamin D and IGFBP-3 as Risk Factors in Elderly Women and Men with Hip Fracture

The relative importance of vitamin D deficiency, secondary hyperparathyroidism, nutritional deficiency and low bone mineral density (BMD) as risk factors for hip fracture is not definitely established. In the framework of a case-control study of risk factors for hip fractured, biochemical markers of bone metabolism and nutrition and femoral BMD data were compared in 136 female and 43 male hip fracture patients, 126 female and 44 male age-matched hospitalized controls, and 47 healthy elderly women (8 men). Patients with hip fracture had lower albumin (−10%9 and 25(OH)-vitamin D (25(OH)D; −19%) compared with hospitalized controls, and lower albumin (−28%) and 25(OH)D levels (−52%) compared with the elderly controls. Serum values of IGFBP-3 were also significantly lower (−33%) in hip fracture patients than in community controls. BMD of femoral neck was lower (p < 0.001) in patients than in hospitalized and community controls. In hip fracture patients, parathyroid hormone (PTH) correlated weakly with BMD (neck: r = −0.19, trochanter: r = −0.17; both p < 0.05). When all women were pooled (n = 233), albumin correlated significantly (age-adjusted) with BMD at all sites (neck: r = 0.27, trochanter: r = 0.25; all p < 0.001). Albumin, but not 25(OH)D, also correlated with skinfold thickness (r = 0.19, p < 0.0025) and with body mass index (BMI) (r = 0.14, p < 0.05). Male patients with hip fracture had lower BMD and albumin (both p < 0.001), 25(OH)D (p = 0.02) and IGFBP-3 levels (p <: 0.005) compared with the controls. When male patients and controls were pooled together, albumin, skinfold thickness and BMI were significantly correlated with each other, but not with BMD. IGFBP-3 was highly correlated with albumin (p < 0.0001), 25(OH)D (p < 0.005) and, less significantly, with PTH (p < 0.05), but not with BMI or skinfold thickness. IGFBP-3 was significantly correlated with BMD at all sites (neck: r = 0.27, p < 0.05); trochanter: r = 0.40, p < 0.0005). In conclusion, low albumin and low BMD were both important risk factors for hip fracture. Low serum albumin was the strongest independent variable correlated with hip fractures. In men, IGFBP-3 was correlated with BMD. The femoral BMD depended only weakly on PTH and 25(OH)D, but was correlated at all sites with albumin, a non-specific parameter of nutrition and general health.     

Plasma Osteocalcin Is Inversely Related to Fat Mass and Plasma Glucose in Elderly Swedish Men

The osteoblast‐derived protein osteocalcin has recently been shown to affect adiposity and glucose homeostasis in mice, suggesting that the skeleton influences energy metabolism through an endocrine mechanism. The aim of this study was to investigate the relationship between plasma osteocalcin and parameters reflecting fat mass and glucose homeostasis in humans. Fasting levels of plasma osteocalcin, plasma glucose, serum insulin, and lipids were analyzed in elderly men (75.3 ± 3.2 yr of age) in the Gothenburg part (all subjects, n = 1010; nondiabetic, n = 857; diabetic, n = 153) of the MrOS Sweden study. Fat mass and lean mass were analyzed using DXA. Diabetic subjects had lower plasma osteocalcin (?21.7%, p < 0.001) than nondiabetic subjects. For both all subjects and nondiabetic subjects, plasma osteocalcin was clearly inversely related to body mass index (BMI), fat mass, and plasma glucose (p < 0.001), whereas it was not associated with height or lean mass. Plasma osteocalcin explained a substantial part (6.3%) of the variance in plasma glucose, whereas it associated moderately with serum insulin. Multiple linear regression models adjusting for serum insulin and fat mass showed that plasma osteocalcin was an independent negative predictor of plasma glucose (p < 0.001). We herein, for the first time in humans, show that plasma osteocalcin is inversely related to fat mass and plasma glucose. Although one should be cautious with mechanistic interpretations of cross‐sectional association studies, our human data support recently published experimental studies, showing endocrine functions of osteoblast‐derived osteocalcin on glucose and fat homeostasis.     

Obesity impairs wound closure through a vasculogenic mechanism

Since obesity impairs wound healing and bone marrow (BM)‐derived vasculogenic progenitor cells (PCs) are important for tissue repair, we hypothesize that obesity‐impaired wound healing is due, in part, to impaired PC mobilization, trafficking, and function. Peripheral blood was obtained from nondiabetic, obese (BMI > 30, n = 25), and nonobese (BMI < 30, n = 17) subjects. Peripheral blood human (h)PCs were isolated, quantified, and functionally assessed. To corroborate the human experiments, 6‐mm stented wounds were created on nondiabetic obese mice (TALLYHO/JngJ, n = 15) and nonobese mice (SWR/J, n = 15). Peripheral blood mouse (m)PCs were quantified and wounds were analyzed. There was no difference in the number of baseline circulating hPCs in nondiabetic, obese (hPC‐ob), and nonobese (hPC‐nl) subjects, but hPC‐ob had impaired adhesion (p < 0.05), migration (p < 0.01), and proliferation (p < 0.001). Nondiabetic obese mice had a significant decrease in the number of circulating PCs (mPC‐ob) at 7 (p = 0.008) and 14 days (p = 0.003) after wounding. The impaired circulating mPC‐ob response correlated with significantly impaired wound closure at days 14 (p < 0.001) and 21 (p < 0.001) as well as significantly fewer new blood vessels in the wounds (p < 0.001). Our results suggest that obesity impairs the BM‐derived vasculogenic PC response to peripheral injury and this, in turn, impairs wound closure.     

Increased visfatin in hemodialysis patients is associated with decreased demands for recombinant human erythropoietin

Abstract

Background: Studies detected an association between visfatin and markers of iron metabolism in patients with insulin resistance. In this study, such a relation was evaluated in hemodialysis (HD) patients. Also relations between visfatin and hepcidin, demands for recombinant human erythropoietin (rHuEpo), inflammation, and situations characterized by insulin resistance were evaluated. Methods: After a four-week washout period from iron treatment, 33 HD patients and 20 healthy volunteers enrolled in the study. Serum visfatin, hepcidin, and interleukin-6 (IL-6) were assessed by means of enzyme-linked immunosorbent assay. Hemoglobin, serum iron, ferritin, and transferrin saturation (TSAT) were also measured. Results: Visfatin was markedly increased in HD patients. Visfatin levels did not differ between diabetics and non-diabetics. No relation was detected between visfatin and body mass index or IL-6 in HD patients. From the markers of iron metabolism, the hepcidin included, visfatin was related only to TSAT. A strong positive relation was revealed between visfatin and hemoglobin, whereas visfatin was inversely related to rHuEpo dose. Resistance to rHuEpo index was inversely and independently of TSAT related to visfatin. Conclusion: Visfatin is increased in HD patients and it is associated with decreased demands for rHuEpo.     

Methylation of Bone SOST,Its mRNA,and Serum Sclerostin Levels Correlate Strongly With Fracture Risk in Postmenopausal Women

Inhibition of sclerostin, a glycoprotein secreted by osteocytes, offers a new therapeutic paradigm for treatment of osteoporosis (OP) through its critical role as Wnt/catenin signaling regulator. This study describes the epigenetic regulation of SOST expression in bone biopsies of postmenopausal women. We correlated serum sclerostin to bone mineral density (BMD), fractures, and bone remodeling parameters, and related these findings to epigenetic and genetic disease mechanisms. Serum sclerostin and bone remodeling biomarkers were measured in two postmenopausal groups: healthy (BMD T‐score > –1) and established OP (BMD T‐score < –2.5, with at least one low‐energy fracture). Bone specimens were used to analyze SOST mRNAs, single nucleotide polymorphisms (SNPs), and DNA methylation changes. The SOST gene promoter region showed increased CpG methylation in OP patients (n = 4) compared to age and body mass index (BMI) balanced controls (n = 4) (80.5% versus 63.2%, p = 0.0001) with replication in independent cohorts (n = 27 and n = 36, respectively). Serum sclerostin and bone SOST mRNA expression correlated positively with age‐adjusted and BMI‐adjusted total hip BMD (r = 0.47 and r = 0.43, respectively; both p < 0.0005), and inversely to serum bone turnover markers. Five SNPs, one of which replicates in an independent population‐based genomewide association study (GWAS), showed association with serum sclerostin or SOST mRNA levels under an additive model (p = 0.0016 to 0.0079). Genetic and epigenetic changes in SOST influence its bone mRNA expression and serum sclerostin levels in postmenopausal women. The observations suggest that increased SOST promoter methylation seen in OP is a compensatory counteracting mechanism, which lowers serum sclerostin concentrations and reduces inhibition of Wnt signaling in an attempt to promote bone formation. © 2014 American Society for Bone and Mineral Research.     

Plasma Ghrelin Levels Are Associated with Coronary Microvascular and Endothelial Dysfunction in Peritoneal Dialysis Patients

Cardiovascular (CV) disease is the main cause of death in peritoneal dialysis (PD) patients, and endothelial dysfunction (ED) is an early sign of vascular pathology. Ghrelin, a gastric peptide with CV actions, has been shown to inhibit proatherogenic changes in experimental models. However, another peptide hormone, leptin, may mediate deleterious effects on the CV system. The aim of this study is to evaluate the relationship between plasma ghrelin and leptin levels, and their association with coronary microvascular and endothelial functions in PD patients. Twenty-four (14 females and 10 males; mean age 44 ± 12 yr) nondiabetic PD patients, between 18 and 70 years of age, were enrolled. In addition to demographic, clinical, and laboratory parameters, plasma concentrations of ghrelin and leptin were evaluated. Endothelial functions of the coronary arteries were determined by coronary flow reserve (CFR) measurement using transthoracic Doppler echocardiography (TTDE). A CFR value of < 2 was used as an evidence for ED. When the study group was divided according to CFR measurements as CFR < 2 and ≥ 2, there were no significant differences considering age, gender, etiology of renal disease, body mass index (BMI), duration of dialysis, PD modality, PD solution type, history of peritonitis, mean arterial pressure, ejection fraction, and biochemical parameters between the two subgroups. Plasma ghrelin levels (129.4 ± 82.1 pg/mL) in patients with CFR ≥ 2 were significantly higher than those in patients with CFR< 2 (63.3 ± 35.8 pg/mL) (p = 0.03). However, no significant differences in plasma leptin levels were found between these groups [31.39 ± 37.81 ng/mL vs. 63.95 ± 72.83 ng/mL (p = 0.28)]. No correlation existed between plasma ghrelin levels and age, BMI, duration of dialysis, mean arterial pressure, ejection fraction, plasma leptin levels, and biochemical parameters. Decreased plasma ghrelin levels may contribute to the development of atherosclerosis in PD patients by causing ED.     

The Association between Serum Adiponectin Levels and Nutritional Status of Hemodialysis Patients

Adiponectin plays an important role in the regulation of body weight, insulin sensitivity, lipid metabolism, and the inflammatory response. Adiponectin is elevated in hemodialysis patients. We investigated the association between altered serum adiponectin levels and the nutritional–inflammation status of hemodialysis patients. Forty-four hemodialysis patients (21 men and 23 women; mean age 53.9 ± 9.2 years) were enrolled and 32 healthy volunteers were included as the control group. Serum adiponectin was measured using a commercial radioimmunoassay kit. Serum albumin, cholesterol, triglyceride, high-sensitivity C-reactive protein, urea, creatinine, transferrin, lean body mass, fat mass, body mass index (BMI), the subjective global assessment (SGA) score, and the malnutrition–inflammation score (MIS) were measured in all patients. Adiponectin levels were significantly elevated in the hemodialysis patients compared with the healthy subjects (24.8 ± 10.4 μg/mL and 6.8 ± 4.2 μg/mL, respectively, p < 0.0001). Serum adiponectin correlated positively with SGA (r = 0.47) and MIS (r = 0.38), and negatively with BMI (r = ?0.34), triglyceride (r = ?0.53), and glucose levels (r = ?0.42). Serum adiponectin levels were significantly higher in malnourished patients than in well-nourished patients when assessed with SGA (20.5 ± 10.4 μg/mL and 29.0 ± 8.7 μg/mL, respectively, p = 0.005). In conclusion, serum adiponectin levels reflect the nutritional–inflammation status of hemodialysis patients. Adiponectin may also be associated with insulin resistance, dyslipidemia, and the inflammatory response in these patients.     

The Relationship between Oxidative Stress,Inflammation, and Atherosclerosis in Renal Transplant and End-Stage Renal Disease Patients

Objectives: Cardiovascular risk is increased in the early stages of chronic kidney disease (CKD) and is also found to be ongoing in renal transplant (Rtx) patients. As a sign of atherosclerosis, increased carotid intima–media thickness (CIMT) has been widely accepted as a strong predictor of cardiovascular disease (CVD) and mortality in the end-stage renal disease (ESRD) patients. Ischemia-modified albumin (IMA), pentraxin-3 (PTX-3), and neutrophil-to-lymphocyte ratio (NLR) were introduced as oxidative stress and inflammatory biomarkers in ESRD. The role of Rtx in terms of atherogenesis, oxidative stress, and inflammation is still unclear. We aimed to investigate the relationship between IMA, PTX-3, NLR, and CIMT in Rtx patients without overt CVD and to compare these results with those obtained from healthy subjects and ESRD patients receiving hemodialysis (HD) and peritoneal dialysis (PD). Design and methods: Cross-sectional analysis in which CIMT measurements, NLR, and serum PTX-3 and IMA levels were assessed in 18 Rtx patients (10 females; mean age: 40.0 ± 13.3 years), 16 PD patients (7 females; 40.2 ± 12.9 years), 14 HD patients (8 females; 46.6 ± 10.7 years), and 19 healthy subjects (9 females; 36.9 ± 8.9 years). Results: IMA, PTX-3, and high-sensitive C-reactive protein (hs-CRP) levels, NLR, and CIMT of Rtx patients were found to be significantly higher compared with healthy subjects (?p = 0.04, p < 0.0001, p < 0.005, p = 0.005, and p = 0.005, respectively). IMA level was positively correlated with hs-CRP and PTX-3 levels, NLR, and CIMT when all participants were included (r = 0.338, p = 0.005; r = 0.485, p < 0.0001; r = 0.304, p = 0.013; and r = 0.499, p < 0.0001, respectively). Conclusion: There has been ongoing inflammation, oxidative stress, and atherosclerosis in Rtx patients.     

Vitamin D deficiency,insulin resistance,and ventricular hypertrophy in the early stages of chronic kidney disease

Background: Chronic kidney disease (CKD) is associated with markedly increased cardiovascular (CV) risk. This increase is not fully explained by traditional CV risk factors but may in part be mediated by nontraditional risk factors, such as inadequate vitamin D (vit D) levels and insulin resistance (IR). Although IR is shown in nondiabetic CKD, its association with vit D deficiency and vascular disease in this population is unknown and what this study aims to investigate. Materials and methods: The study comprised 67 patients with CKD (eGFR?≥?30?mL/min) and 15 healthy controls matched for age and sex. The phlogosis indexes, vit D levels, IR, carotid intima-media thickness (cIMT), and left ventricular mass index (LVMI) were measured. Results: In our study, the mean value of LVMI and cIMT was significantly higher in patients with eGFR?≥?30?mL/min compared with controls (p?=?0.037 and p?p?=?0.044, p?=?0.012, p?=?0.038). A positive correlation was found between LVMI and IR (r?=?0.704, p?=?0.041) and a negative correlation was found between IR and vit D levels (r?=??0.238, p?=?0.031). Conclusions: In our study, IR and vit D deficiency were found to be independent predictors of left ventricular hypertrophy and atherosclerotic disease. Vitamin D deficiency and IR are thus associated with increased CV risk. More novel approaches to improving IR and vit D supplementation in the CKD population might lead to potential strategies for preventing excess CV mortality.     

Increased serum renalase in hemodialysis patients: is it related to left ventricular hypertrophy?

Introduction: Left ventricular hypertrophy (LVH) is one of the most common cardiac abnormalities in patients with end stage renal disease (ESRD). Hypertension, diabetes, increased body mass index, gender, age, anemia, and hyperparathyroidism have been described as risk factors for LVH in patients on dialysis. However, there may be other risk factors which have not been described yet. Recent studies show that renalase is associated with cardiovascular events. The aim of this study was to reveal the relation between renalase, LVH in patients under hemodialysis (HD) treatment.

Methods: The study included 50?HD patients and 35 healthy controls. Serum renalase levels and left ventricle mass index (LVMI) were measured in all participants and the relation between these variables was examined.

Findings: LVMI was positively correlated with dialysis vintage and C-reactive protein (CRP) (r?=?0.387, p?=?0.005 and r?=?0.597, p?r?=??0.324, p?=?0.022 and r?=??0.499, p?r?=?0.263, p?=?0.065). Serum renalase levels were significantly higher in HD patients (212?±?127?ng/mL) compared to controls (116?±?67?ng/mL) (p?r?=?0.677, p?r?=?0.625, p?Discussion: In our study, LVMI was correlated with dialysis vintage, residual diuresis, CRP, and hemoglobin. LVMI tends to correlate with renalase and this correlation may be significant in studies with more patient numbers. The main parameters affecting renalase levels are dialysis vintage and serum creatinine.     

The importance of ultrasonographic measurement of peritoneal wall thickness in pediatric chronic peritoneal dialysis patients

Abstract

Loss of peritoneal function due to peritoneal fibrosing syndrome (PFS) is a major factor leading to treatment failure in chronic peritoneal dialysis (PD) patients. Although the precise biologic mechanisms responsible for these changes have not been defined, the general assumption is that alterations in peritoneal function are related to structural changes in the peritoneal membrane. Studies of the peritoneal membrane by non-invasive ultrasonography (US) in chronic PD patients are limited. The aim of the present study is to assess the relationship between functional parameters of peritoneum and peritoneal thickness measured by US in children treated by chronic PD. We recruited two groups of patients: 23 subjects (13 females, 10 males) on chronic PD (patient group) and 26 (7 females, 19 males) on predialysis out-patient follow-up (creatinine clearance: 20–60?mL/min/1.73?m²) (control group). Age, sex, weight, height, body mass index (BMI), chronic PD duration, episodes of peritonitis and the results of peritoneal equilibration test (PET) were recorded. Hemoglobin (Hb), blood pressure (BP), left ventricular mass index (LVMI) and renal osteodystrophy (ROD) parameters were also obtained. The thickness of the parietal peritoneum was measured by trans-abdominal US in all children. Statistical analyses were performed by using Student's t and Pearson's correlation tests. Mean peritoneal thickness in chronic PD patients (1028.26?±?157.26?μm) was significantly higher than control patients (786.52?±?132.33). Mean peritoneal thickness was significantly correlated with mean body height (R²?=?0.93, p?<?0.05), BMI (R²?=?0.25, p?<?0.05), chronic PD duration (R²?=?0.64, p?<?0.05), episodes of peritonitis (R²?=?0.93, p?<?0.05), D/P_creatinine (R²?=?0.76, p?<?0.05) and D4/D0_glucose (R²?=?0.81, p?<?0.05). No correlation was found between peritoneal thickness and Hb, BP, LVMI and ROD parameters. In conclusion, ultrasonographic measurement of peritoneal membrane thickness is a simple and non-invasive method in chronic PD children. This diagnostic tool likely enables to assess peritoneal structure and function in these patients.     

apoA- AND apoB-CONTAINING LIPOPROTEINS AND Lp(A) CONCENTRATION IN NON-DIALYZED PATIENTS WITH CHRONIC RENAL FAILURE

Background: End-Stage renal disease is associated with accelerated atherosclerosis and a high incidence of cardiovascular disease. Methods: The serum levels of lipids and apolipoproteins and Lp(a) were determined in 51 patients with chronic renal failure (CRF) with various advancement, without interference of factors which might disturb Lp(a) metabolism and with proteinuria less than 0.5 g/24 h. The patients studied were divided into two groups: patients with moderate renal failure (CRF-M) and creatinine levels of 2–6 mg/dL n = 27; and predialysis patients with end stage renal disease (ESRD) and creatinine levels higher than 8.5 mg/dL n = 24. Results: In both studied groups serum concentrations of triglycerides (TG), total apoCIII, apoCIIInonB, apoB:CIII were statistically increased, (except total cholestrol (TC) and LDL-cholestrol (LDL-C), apoB, total apoE, apoEnonB, apoB:E), while the levels of HDL-cholestrol (HDL-C) and apoAI significantly decreased. Lipid and lipoprotein ratios as risk factors of atherosclerosis were similar in both groups. The TC/HDL-C ratio increased, while that of HDL-C/apoAI and apoAI/apoCIII decreased. Serum Lp(a) concentrations were significantly increased in both studied groups. The medians and ranges of Lp(a) concentration were similar in both groups. Serum Lp(a) levels correlated with total cholesterol (r = 0.295; p < 0.05), LDL-C (r = 0.312; p < 0.05) and apoB (r = 0.215; p < 0.05). In addition, no correlation was found between Lp(a) levels and albumin concentrations (r = 0.126; p = 0.421). Conclusion: Our results may indicate that the reduced levels of apoA-containing lipoproteins and increased TG-rich apoB-containing lipoproteins and Lp(a) indicated a clear atherogenic pattern in early renal disease. Increased Lp(a) concentration may result in nonspecific synthesis or catabolism disturbances. Measurement and monitoring of lipoprotein family profiles offers a new means for selecting appropriate therapies targeted for normalizing dyslipidemia in non-dialyzed patients.     

Relation Between Depression,Some Laboratory Parameters,and Quality of Life in Hemodialysis Patients

Depression is common in patients with end-stage renal disease (ESRD) and is associated with increased mortality and morbidity. Several investigators have estimated that depression occurs in about 20% to 30% of dialysis patients. The aim of this study was to investigate the relationship between depression, some laboratory parameters, and quality of life (QOL) in hemodialysis patients. Forty-three hemodialysis patients (mean age 40.5 ± 15.2; M = 28, F = 15) were included in the study. Hamilton Depression Scale (HAMD), Hamilton Anxiety Scale (HAMA), and short form with 36 (SF-36) were used for evaluation. Subsequently, patients were divided into two groups according to HAMD scores: group 1, those who had a low HAMD score (between 0 and 7), and group 2, those who had a high HAMD score (over 7). The two groups were compared in terms of anxiety scores, QOL scores, and some laboratory parameters. The group 2 patients (n = 21; M = 13, F = 8) had lower levels of hemoglobin than the group 1 patients (9.5 ± 1.7 vs. 10.7 ± 1.4 g/dL, respectively; p< 0.01). Group 2 patients also had lower SF-36 scores than group 1 patients (91.5 ± 21.3 vs. 74.9 ± 13.6, respectively; p = 0.03). On the contrary, the patients of group 2 had higher HAMA scores than group 1 patients (16.6 ± 6.9 vs. 6.3 ± 3.5, respectively; p< 0.01) and CRP level (10.7 ± 4.6 vs. 4.5 ± 3.8, respectively; p< 0.001). A significant correlation was found between depression scores and C-reactive protein (CRP) (r = 0.57, p< 0.001) and HAMA scores (r = ? 0.43, p< 0.05). In contrast, a negative correlation was found between HAMD scores and albumin (r = ? 0.43, p< 0.05), hemoglobin (r = ? 0.38, p =0.015) and SF-36 scores (r = 0.39, p = 0.032). These findings demonstrate that there is a relationship among high depression score, low levels of hemoglobin and albumin, high CRP level, low SF-36 score, and high anxiety score. Evaluation of psychiatric status should be part of the care provided to hemodialysis patients.     

Vitamin D and bone mineral density

Bone mineral density (BMD) at the lumbar spine and the neck of femur and serum concentrations of 25-hydroxyvitamin D (25OHD), intact parathyroid hormone (PTH), alkaline phosphatase, calcium, albumin, creatinine and phosphate were measured in a group of 166 postmenopausal women (30–79 years) attending a bone clinic for bone density measurements. Four subjects with suspected primary hyperparathyroidism were excluded from analysis. BMD at the lumbar spine was correlated with body mass index (BMI) (r=0.278,p=0.0003), age (r=−0.194,p=0.0134) and serum 25OHD (r=0.188,p=0.0167). BMD at the neck of femur correlated with BMI (r=0.391,p<0.0001), age (r=−0.356,p<0.0001), PTH (r=−0.156,p=0.047) and serum 25OHD (r=0.231,p=0.0031). Stepwise multiple regression analysis showed that age, BMI and serum 25OHD contributed to the variation in BMD at lumbar spine. At the neck of femur, PTH was an additional contributor. We conclude that serum 25OHD makes a contribution to BMD a lumbar spine and neck of femur.