Search

Chronic kidney disease (CKD) is a worldwide public health problem related to adverse results of end-stage renal disease (ESRD), kidney failure, cardiovascular disease (CVD), and premature death. The study is aimed to investigate the knowledge, attitude, and practice toward the prevention and early detection of chronic kidney disease. Two ordinal variables and one nominal response variable with 20 predictor variables were independently fitted. Ordinal multicategories , such as proportional odds, continuation ratio, and partial proportional models for attitude and practice, whereas the baseline multicategory logit model for knowledge was fitted. The findings implied that some predictors have a significant effect on attitude, whereas other covariates have a significant effect on practice. Moreover, as there are two independent logit models for the nominal response, in the first logit model Monthly income and Diabetes2, whereas in the second logit model, Smo_R_CKD3 and Diabetes2 have a significant effect on knowledge. In conclusion, more educated ones have more knowledge and attitude toward the prevention and early detection of chronic kidney disease, also more likely to perform preventive and early detecting practices. People are inadequately informed on the prevention and early detection of CKD, especially those who are with low income, are at risk of developing CKD and its complications. [ABSTRACT FROM AUTHOR]

Polycystic kidney disease (PKD) is one of the most common hereditary kidney diseases, which is characterized by progressive cyst growth and secondary hypertension. In addition to cystogenesis and renal abnormalities, patients with PKD can develop vascular abnormalities and cardiovascular complications. Progressive cyst growth substantially alters renal structure and culminates into end-stage renal disease. There remains no cure beyond renal transplantation, and treatment options remain largely limited to chronic renal replacement therapy. In addition to end-stage renal disease, patients with PKD also present with hypertension and cardiovascular disease, yet the timing and interactions between the cardiovascular and renal effects of PKD progression are understudied. Here, we review the vascular dysfunction found in clinical and preclinical models of PKD, including the clinical manifestations and relationship to hypertension, stroke, and related cardiovascular diseases. Finally, our discussion also highlights the critical questions and emerging areas in vascular research in PKD. [ABSTRACT FROM AUTHOR]

Introduction: Chronic Kidney Disease (CKD) has been recognised as a worldwide health threat and understanding its complex patho-physiological mechanisms could go a long way in taking care of patients with CKD. One of the most important causes for mortality in End Stage Renal Disease (ESRD) patients is Cardiovascular Disease (CVD). ESRD is a low grade chronic inflammatory state, suspected to promote atherosclerosis. Aim: To determine if there is any association between elevated High-sensitivity C-Reactive Protein (hs-CRP) and development of future cardiovascular events in stage-5 CKD patients. Materials and Methods: Forty-five CKD stage-5 patients were included in the study, after ruling out patients with established CVD. According to categorisation proposed by the American Heart Association for the cut-off value of hs-CRP-value (3 mg/L), patients were divided into two groups. Those who had hs-CRP more than 3 mg/L were considered to have 'elevated hs-CRP' and those who had a value 3 mg/L and below were considered to have 'normal hs-CRP' levels. These patients were followedup monthly, for a period of one year, to record any occurrence of cardiovascular events (coronary events/cerebrovascular accidents/peripheral occlusive vascular disease). Statistical Package for the Social Sciences (SPSS) 16.0 was used for analysis. Chi-square test and Mann-Whitney U-test were used for statistical comparison between the groups and a p-value of 0.05 or less was considered to be statistically significant. Receiver Operating Characteristic (ROC) curve was also plotted to determine the cut-off value for hs-CRP based on the occurrence of any cardiovascular event. Results: Baseline hs-CRP level was more than 3 mg/L in 42% of patients. Among those who had elevated hs-CRP, 78.9% of patients developed cardiovascular events during the follow-up period. This signifies a strong association between elevated hs- CRP and CVD in ESRD patients. The hs-CRP cut-off point of 3 mg/L was obtained from ROC curve. Conclusion: There was a significant association between elevated hs-CRP and development of cardiovascular events in ESRD patients. Hence, hs-CRP can be used as a marker of future cardiovascular events in CKD stage-5 patients. [ABSTRACT FROM AUTHOR]

Cardiovascular disease is the main cause of morbidity and mortality in end-stage renal disease (ESRD) patients. Recent population based epidemiological studies demonstrated a correlation between reduced renal function and risk for all causes and cardiovascular mortality, 50% of patients dying before the commencement of renal replacement therapy. Vascular calcifications (VC) and arterial stiffness are major contributors to cardiovascular disease and are independent predictors of cardiovascular mortality in ESRD patients. Scarce information is available on the risk factors and prognosis of predialysis patients with VC. The aim of this study was to evaluate the contribution of traditional and uremia related risk factors to abdominal aortic calcification in predialysis patients. A single center, retrospective study was performed on 305 adult patients monitored at the Bucharest University Emergency Hospital for at least 6 months. Our study reports an increased incidence of VC in predialysis chronic kidney disease (CKD) patients, higher in those with advanced age, history of cardiovascular disease, osteoporosis, and declining renal function. [ABSTRACT FROM AUTHOR]

Introduction: Clinical parameters especially co-morbidities among end stage renal disease (ESRD) patients are associated with mortality. This study aims to determine the risk factors that are associated with mortality within three years among prevalent patients with ESRD. Methods: This is a cohort study where prevalent ESRD patients' details were recorded between May 2012 and October 2012. Their records were matched with national death record at the end of year 2015 to identify the deceased patients within three years. Four models were formulated with two models were based on logistic regression models but with different number of predictors and two models were developed based on risk scoring technique. The preferred models were validated by using sensitivity and specificity analysis. Results: A total of 1332 patients were included in the study. Majority succumbed due to cardiovascular disease (48.3%) and sepsis (41.3%). The identified risk factors were mode of dialysis (P < 0.001), diabetes mellitus (P < 0.001), chronic heart disease (P < 0.001) and leg amputation (P = 0.016). The accuracy of four models was almost similar with AUC between 0.680 and 0.711. The predictive models from logistic regression model and risk scoring model were selected as the preferred models based on both accuracy and simplicity. Besides the mode of dialysis, diabetes mellitus and its complications are the important predictors for early mortality among prevalent ESRD patients. Conclusions: The models either based on logistic regression or risk scoring model can be used to screen high risk prevalent ESRD patients. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease (CVD) is the most important cause of morbidity and mortality in patients with end stage renal disease (ESRD). Apelin expressed in endothelial and other tissues including brain and kidney is an adipocytokine defined recently and is emerging an important mediator of cardiovascular homeostasis. The aim of this study was to test whether apelin levels might be associated with carotid artery atherosclerosis and left ventricular mass index (LVMI) in peritoneal dialysis patients. Patients and methods: Fifty peritoneal dialysis patients (25 female, mean age 41.4 ± 11.9 years, mean dialysis vintage 65.0 ± 35.4 months) and 18 healthy individuals (9 female, mean age 41.7 ± 6.8 years) were included in this cross-sectional study. Serum apelin 12 levels, echocardiographic findings and carotid intima media thickness (CIMT) were recorded as well as clinical and laboratory data. Results: There were no differences between the patient and the control groups with regard to demographic characteristics. In patient group, LVMI, CIMT, CRP and apelin levels were elevated compared to control group. However there was no association between apelin, LVMI and CIMT. There was a positive correlation between apelin and CRP, which was not statistically significant. When patients were divided into two groups according to the mean serum apelin levels, LVMI, CIMT and CRP were higher in the high apelin group but this difference did not reach statistical significance. Conclusion: We observed an increased inflammation and CVD risk in peritoneal dialysis patients. However, serum apelin levels seem not to be associated with cardiovascular risk in this group of patients. [ABSTRACT FROM AUTHOR]

Background The cardiovascular safety and efficacy of sitagliptin, a dipeptidyl peptidase 4 (DPP-4) inhibitor, in type 2 diabetic patients with chronic kidney disease (CKD) after acute myocardial infarction (AMI) are unclear. Methods We analyzed data from the Taiwan National Health Insurance Research Database between March 1st, 2009 and December 31st, 2011. A total of 1025 AMI patients with diabetes with chronic kidney disease were selected as the study cohort. The study evaluated the cardiovascular safety and efficacy of sitagliptin by comparing 205 subjects (20%) who use sitagliptin to 820 matched subjects (80%) who do not. The primary outcomes included myocardial infarction, ischemic stroke or cardiovascular death. Results Primary composite outcomes occurred in 54 patients in the sitagliptin group (26.3%) and in 164 patients in the comparison group (20.0%) (HR, 1.32; 95% CI, 0.97-1.79; P = 0.079) during the mean follow-up of 1.02 years (SD = 0.71 years). The sitagliptin group had similar risks of ischemic stroke, all-cause mortality or hospitalization for heart failure (HF) compared to the non-sitagliptin group (P = 0.938, 0.523 and 0.795 respectively). However, sitagliptin use was associated with increased risks of recurrent myocardial infarction (HR, 1.73; 95% CI, 1.15-2.58; P = 0.008) and percutaneous coronary revascularization (HR, 1.43; 95% CI, 1.04-1.95; P = 0.026). Conclusions Among type 2 diabetic patients with CKD after AMI, the use of sitagliptin was not associated with an increased risk of cardiovascular death, ischemic stroke or hospitalization for HF but was associated with increased risks of recurrent MI and percutaneous coronary revascularization. [ABSTRACT FROM AUTHOR]

On comparing the rates of graft failure and death among United States and Spanish kidney transplant recipients…the 10 year graft and patient survival was significantly better in the Spanish population.”Background The long-term outcomes of kidney transplantation are suboptimal because many patients lose their allografts or experience premature death. Cross-country comparisons of long-term outcomes of kidney transplantation may provide insight into factors contributing to premature graft failure and death. We evaluated the rates of late graft failure and death among US and Spanish kidney recipients. Methods This is a cohort study of US (n = 9609) and Spanish (n = 3808) patients who received a deceased donor kidney transplant in 1990, 1994, 1998 or 2002 and had a functioning allograft 1 year after transplantation with follow-up through September 2006. Ten-year overall and death-censored graft survival and 10-year overall recipient survival and death with graft function (DWGF) were estimated with multivariate Cox models. Results Among recipients alive with graft function 1 year after transplant, the 10-year graft survival was 71.3% for Spanish and 53.4% for US recipients (P < 0.001). The 10-year, death-censored graft survival was 75.6 and 76.0% for Spanish and US recipients, respectively (P = 0.73). The 10-year recipient survival was 86.2% for Spanish and 67.4% for US recipients (P < 0.001). In recipients with diabetes as the cause of ESRD, the adjusted DWGF rates at 10 years were 23.9 and 53.8 per 1000 person-years for Spanish and US recipients, respectively (P < 0.001). Among recipients whose cause of ESRD was not diabetes mellitus, the adjusted 10-year DWGF rates were 11.0 and 25.4 per 1000 person-years for Spanish and US recipients, respectively. Conclusions US kidney transplant recipients had more than twice the long-term hazard of DWGF compared with Spanish kidney transplant recipients and similar levels of death-censored graft function. Pre-transplant medical care, comorbidities, such as cardiovascular disease, and their management in each country's health system are possible explanations for the differences between the two countries. [ABSTRACT FROM PUBLISHER]

The importance of cardiovascular disease in adults with chronic kidney disease is now well recognized. For children who develop chronic kidney disease, cardiovascular disease is also a leading cause of eventual morbidity and mortality. Although the clinical manifestations of cardiovascular disease may not be apparent until later, early subclinical findings can be observed even during childhood. This review updates the reader on the epidemiology of cardiovascular disease in pediatric chronic kidney disease, discusses risk factors and potential mechanisms of accelerated cardiovascular disease, reviews evidence of early manifestations of cardiovascular disease in pediatric chronic kidney disease, and briefly discusses prevention and treatment strategies. [ABSTRACT FROM AUTHOR]

Abstract: Nitric oxide (NO) is important in the maintenance of vascular tone and regulation of blood pressure. NO may also play a role in the development of both nephropathy and cardiovascular disease (CVD) in patients with diabetes. The susceptibility to nephropathy and CVD depends to some extent on genetic factors, therefore polymorphisms in the gene coding for endothelial NO-synthase, NOS3, can affect the risk of developing these diseases. Type 1 diabetes patients attending the Steno Diabetes Center, Denmark, between 1993 and 2001 were enrolled in this study. A total of 458 cases with diabetic nephropathy (albumin excretion >300mg/24h) and 319 controls with persistent normoalbuminuria (<30mg/24h), despite ⩾20years of diabetes duration at follow-up were identified. Patients were followed until death or end of the study. Associations between seven NOS3-gene polymorphisms and nephropathy, progression of nephropathy and CVD were studied. There was significant association between the rs743507 TT-genotype and diabetic nephropathy. When including age at diabetes onset, diabetes duration at follow-up, baseline HbA1c, sex and ever smoking in the analysis the OR was 1.43 (95% CI=1.03–2.00), P =0.035. In analyses of CVD development using Cox-regression the rs1799983 GG-genotype was a significant protective factor in normoalbuminuric patients, HR=0.32 (0.12–0.82), P =0.018, but not in patients with macroalbuminuria (covariates were; age at follow-up, baseline HbA1c, baseline systolic blood pressure, baseline cholesterol, sex and ever smoking). Our conclusion is that the NOS3-gene may be involved in the development of diabetic nephropathy in patients with type 1 diabetes and can be predictive of CVD during follow-up. [Copyright &y& Elsevier]

Cardiovascular disease (CVD) is highly prevalent among end-stage renal disease (ESRD) patients and is the main reason for their high mortality and morbidity rates. The large proportion of patients starting renal replacement therapy who also have CVD, suggests that pathogenetic factors leading to cardiac dysfunction begin in the early stages of chronic kidney disease (CKD). Anaemia may be an important pathogenetic factor responsible for cardiovascular abnormalities, in particular left ventricular hypertrophy (LVH), which significantly worsens the prognosis of CKD patients. This would account for the association between anaemia and both hospitalisation and mortality rates in such patients and leads to the expectation that correction of anaemia will improve cardiovascular status and long-term prognosis. A partial regression of LVH after a partial correction of anaemia has been observed in several studies, but it is still unclear whether normalizing haemoglobin concentrations produces additional cardiac advantages. Indeed, no significant differences between partial and complete correction of anaemia in inducing regression of established LVH have been demonstrated so far, but further investigation is needed. Furthermore, normalization of anaemia improves quality of life and physical function of selected categories of patients. Also keeping in mind the potential risks of haemoglobin normalization in haemodialysis patients with severe heart disease and grafts, individualising the target haemoglobin concentration to the characteristics of the patients is probably one of the winning strategies in the modern management of renal anaemia. [Copyright &y& Elsevier]

Urea at post-dialysis levels induces increased ROS in a number of cell types. The aim of this study was to determine whether urea-induced production of ROS remains elevated after urea is no longer present, and, if it does, to characterize its origin and effects. Human arterial endothelial cells were incubated with 20 mM urea for two days, and then cells were incubated for an additional two days in medium alone. Maximal ROS levels induced by initial urea continued at the same level despite urea being absent. These effects were prevented by either MnSOD expression or by Nox1/4 inhibition with GKT13781. Sustained urea-induced ROS caused a persistent reduction in mtDNA copy number and electron transport chain transcripts, a reduction in transcription of mitochondrial fusion proteins, an increase in mitochondrial fission proteins, and persistent expression of endothelial inflammatory markers. The SOD-catalase mimetic MnTBAP reversed each of these. These results suggest that persistent increases in ROS after cells are no long exposed to urea may play a major role in continued kidney damage and functional decline despite reduction of urea levels after dialysis. [ABSTRACT FROM AUTHOR]