p-cresol but not p-cresyl sulfate stimulate MCP-1 production via NF-κB p65 in human vascular smooth muscle cells.

Introduction: p-cresol (PC) and p-cresyl sulfate (PCS) are responsible for many of the uremia clinical consequences, such as atherosclerosis in Chronic Kidney Disease (CKD) patients.

Objectives: We investigate the in vitro impact of PC and PCS on monocyte chemoattractant protein-1 (MCP-1) expression via NF-kappa B (NF-κB) p65 in VSMC.

Methods: PCS was synthesized by PC sulfatation.

Uremic Toxicity of Advanced Glycation End Products in CKD.

Advanced glycation end products (AGEs), a heterogeneous group of compounds formed by nonenzymatic glycation reactions between reducing sugars and amino acids, lipids, or DNA, are formed not only in the presence of hyperglycemia, but also in diseases associated with high levels of oxidative stress, such as CKD. In chronic renal failure, higher circulating AGE levels result from increased formation and decreased renal clearance. Interactions between AGEs and their receptors, including advanced glycation end product-specific receptor (RAGE), trigger various intracellular events, such as oxidative stress and inflammation, leading to cardiovascular complications.

Effect of PKC-β Signaling Pathway on Expression of MCP-1 and VCAM-1 in Different Cell Models in Response to Advanced Glycation End Products (AGEs).

Advanced glycation end products (AGEs) are compounds classified as uremic toxins in patients with chronic kidney disease that have several pro-inflammatory effects and are implicated in the development of cardiovascular diseases. To explore the mechanisms of AGEs-endothelium interactions through the receptor for AGEs (RAGE) in the PKC-β pathway, we evaluated the production of MCP-1 and VCAM-1 in human endothelial cells (HUVECs), monocytes, and a coculture of both. AGEs were prepared by albumin glycation and characterized by absorbance and electrophoresis.

The quest for a better understanding of chronic kidney disease complications: an update on uremic toxins.

Chronic kidney disease is characterized by a progressive reduction of glomerular filtration rate and/or the appearance of proteinuria, and subsequently the progressive retention of organic waste compounds called uremic toxins (UT). Over the last decades, a large number of such compounds have been identified and their effects on organs and tissues, especially the cardiovascular system, has been demonstrated. In this review, we present the current classification of UT, as proposed by the EUTox Group, and the effects of some of the probably most important UTs, such as phosphate, FGF-23, PTH, AGEs, indoxyl sulfate and para-cresyl sulfate.

Uremic serum inhibits in vitro expression of chemokine SDF-1: impact of uremic toxicity on endothelial injury.

Introduction: Endothelial dysfunction is important in the pathogenesis of cardiovascular disease (CVD) related to chronic kidney disease (CKD). Stromal cell-derived factor-1 (SDF-1) is a chemokine which mobilizes endothelial progenitor cells (EPC) and together with interleukin-8 (IL-8) may be used as markers of tissue injury and repair.

Objective: This study investigated in vivo and in vitro the effect of uremic media on SDF-1 and IL-8 expression.

Differential effects of indoxyl sulfate and inorganic phosphate in a murine cerebral endothelial cell line (bEnd.3).

Endothelial dysfunction plays a key role in stroke in chronic kidney disease patients. To explore the underlying mechanisms, we evaluated the effects of two uremic toxins on cerebral endothelium function. bEnd.

Short-term effects of moderate intensity physical activity in patients with metabolic syndrome.

Objectives: To evaluate whether a short-term moderate intensity exercise program could change inflammatory parameters, and improve different components of metabolic syndrome in sedentary patients.

Methods: Sixteen patients completed the 12-week program of supervised exercise, which consisted of a 40 to 50 minutes of walking, 3 times a week, reaching 50 to 60% of the heart rate reserve. The parameters evaluated before and after intervention were waist circumference, systolic and diastolic blood pressure, triglycerides, LDL cholesterol, HDL cholesterol, total cholesterol, C-reactive protein and interleukin 8.

Vascular calcification in chronic kidney disease: a review.

Vascular calcification (VC), an independent and strong predictor of cardiovascular risk, is often found in CKD patients. The degree of VC is providing incremental prognostic value over traditional risk markers. There is interest in improving our understanding of mechanisms, establishing diagnostic methods and effective prevention and treatment modalities.

Vascular damage in kidney disease: beyond hypertension.

Chronic kidney disease (CKD) is highly prevalent and a multiplier of cardiovascular disease (CVD) and cannot be completely explained by traditional Framinghan risk factors. Consequently, greater emphasis has been placed in nontraditional risk factors, such as inflammation, endothelial dysfunction, sympathetic overactivation, protein-energy wasting oxidative stress, vascular calcification, and volume overload. The accumulation of uremic toxins (and the involvement of genetic factors) is responsible for many of the clinical consequences of a condition known as uremia.

Hypovitaminosis D is associated with systemic inflammation and concentric myocardial geometric pattern in hemodialysis patients with low iPTH levels.

Background: Vitamin D [25(OH)D] deficiency is a cardiovascular risk factor in the hemodialysis (HD) population. The aim of this study was to identify hypovitaminosis D in HD patients without signs of hyperparathyroidism and to analyze its association to inflammation and echocardiographic alterations.

Methods: Patients on HD with iPTH <300 pg/ml not receiving vitamin D therapy were recruited.

A gut feeling on endotoxemia: causes and consequences in chronic kidney disease.

Chronic inflammation is closely linked to several complications of chronic kidney disease (CKD), such as vascular calcification, accelerated atherosclerosis, loss of appetite, insulin resistance, increased muscle catabolism and anemia. As a consequence, inflammation is a predictor of mortality in this group of patients. Specific causes of the activation of the immune system in CKD are largely unknown.

Acetylcholinesterase inhibitory activity of uleine from Himatanthus lancifolius.

Application of acetylcholinesterase (AChE) inhibitors is the primary treatment for Alzheimer's disease. Alkaloids, such as physostigmine, galanthamine, and huperzine A, play an important role as AChE inhibitors. The aim of this work was to evaluate Himatanthus lancifolius (Muell.

Immune mechanisms involved in cardiovascular complications of chronic kidney disease.

A sustained status of chronic inflammation is closely linked to several complications of chronic kidney disease (CKD), such as vascular degeneration, myocardial fibrosis, loss of appetite, insulin resistance, increased muscle catabolism and anemia. These consequences of a chronically activated immune system impact on the acceleration of atherosclerosis, vascular calcification and development of heart dysfunction. Recent evidence suggests that these immune-mediated consequences of uremic toxicity are not only important to stratify the risk and understand the mechanisms of disease, but also represent an important area for intervention.

Insulin resistance and glucose homeostasis in peritoneal dialysis.

Cardiovascular disease (CVD) is the main cause of death in peritoneal dialysis (PD) patients, a situation that can be explained by a combination of traditional and nontraditional risk factors for CVD in these patients. Glucose and insulin homeostasis are altered in chronic kidney disease (CKD) patients even in the early stages of CKD, leading to insulin resistance by various pathways. Several factors have been implicated in the pathogenesis of insulin resistance, including anemia, dyslipidemia, uremia, malnutrition, excess of parathyroid hormone, vitamin D deficiency, metabolic acidosis, and increase in plasma free fatty acids and proinflammatory cytokines.

Characteristics and causes of immune dysfunction related to uremia and dialysis.

From the immunologic viewpoint, chronic kidney disease (CKD) is characterized by disorders of both the innate and adaptive systems, generating a complex and still not fully understood immune dysfunction. Markers of a chronically activated immune system are closely linked to several complications of CKD and represent powerful predictors for mortality in the CKD population. On the other hand, CKD patients respond poorly to vaccination and to challenges such as bacterial infection.

Controlling inflammation in peritoneal dialysis: the role of pd-related factors as potential intervention targets.

Cardiovascular (CV) disease is the main cause of death in peritoneal dialysis (PD) patients, but the mechanisms mediating the increased CV risk observed in this group of patients are still largely unknown, which limits the perspective on effective therapeutic strategies. Patients on PD are already exposed to a number of traditional risk factors from the start of their chronic kidney disease (CKD), because many of those risk factors are common to CV disease and CKD alike. As renal dysfunction progresses, CKD-related risk factors are introduced, changing the profile of both the CV disease and the markers of risk.

Factors contributing to the differences in peritonitis rates between centers and regions.

Despite improvements in connectology, peritoneal dialysis (PD)-associated peritonitis contributes significantly to morbidity and modality failure in patients maintained on PD therapy. A broad spectrum of organisms-gram-positive, gram-negative, fungal, anaerobic-are involved in this complication. In addition, a significant percentage of episodes involve polymicrobial and culture-negative infection.

The malnutrition and inflammation axis in pediatric patients with chronic kidney disease.

Malnutrition and inflammation are closely linked in adult chronic kidney disease (CKD) patients and are both related to poor outcome, but data on pediatric patients are lacking. To describe the prevalence of inflammation, evaluate nutritional status, their correlation to each other, and their possible determinants in pediatric patients with CKD in predialysis, on hemodialysis (HD), and peritoneal dialysis (PD) who were submitted to demographic, nutritional, and inflammatory evaluations. Patients' nutritional status was evaluated according to anthropometric parameters and body composition assessed by measurements of skinfold thickness and bioelectrical impedance.

Associations between renal function, volume status and endotoxaemia in chronic kidney disease patients.

Inflammation is an important predictor of increased cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD), but the mechanisms behind the chronic activation of the immune system are not clearly understood. CKD patients develop fluid overload, which has been proposed to be a stimulus for inflammatory activation due to the translocation of macromolecules from the gut. We hypothesize that fluid overload is associated with signs of systemic inflammation and endotoxaemia in stages 1-5 CKD patients.

The recommendations from the International Society for Peritoneal Dialysis for Peritonitis Treatment: a single-center historical comparison.

The antibiotic treatment currently recommended by the International Society for Peritoneal Dialysis (ISPD) for peritonitis consists of a combination of a first- and a third-generation cephalosporin. The schedule formerly recommended combined a first-generation cephalosporin and an aminoglycoside. No comparison between the treatment schedules has been performed until now.