Risk Of Chronic Kidney Disease In Patients Research Articles

The vulnerable patient with chronic kidney disease.

Patients with chronic kidney disease (CKD) exhibit an increased cardiovascular risk. The high susceptibility to cardiovascular disease renders CKD patients 'vulnerable patients'. The overall cardiovascular risk of a vulnerable patient with CKD is determined by the components of the vulnerable myocardium, the vulnerable vessel and the vulnerable blood which in sum contribute to the increased morbidity and mortality risk in CKD patients. Future therapeutic strategies to reduce cardiovascular morbidity and mortality in this high-risk population should address all three aspects of vulnerability in CKD patients.

Hypomagnesemia and atherogenic dyslipidemia in chronic kidney disease: surrogate markers for increased cardiovascular risk.

Recent reports suggest that 40-70% chronic kidney disease (CKD) patients receiving dialysis have significant coronary artery disease. Magnesium depletion is being considered as the missing link between the cardiovascular risk factors and atherosclerosis in CKD. The present work aimed to study the association between magnesium status and lipid alterations in pre-dialysis CKD patients attending the Nephrology Clinic in a tertiary care hospital in South India. 90 cases of CKD and 90 age and gender matched healthy controls were included in the study. Framingham risk scoring was done and presence of metabolic syndrome was assessed. Lipid profile, serum and urine magnesium, blood glucose, calcium, phosphorus, urea and creatinine levels were assayed in all study subjects. In this study we observed a significantly lower serum magnesium levels and dyslipidemic alterations, a significantly raised total cholesterol and low-density lipoprotein and non-HDL in patients with CKD. We also observed a significant correlation between the lowered serum magnesium concentrations and atherogenic dyslipidemia, suggesting a link to increased cardiovascular risk in CKD patients. CKD patients had higher risk of cardiovascular disease (according to their Framingham risk score), which also showed significant correlation with the hypomagnesaemia. Our results suggest a strong association of hypomagnesemia and atherogenic dyslipidemia in patients with CKD. This gains particular importance in the high cardiovascular risk-borne CKD patients, as supplementing magnesium would go a long way in reducing the risk of cardiovascular morbidity and mortality in CKD.

Is schizophrenia associated with an increased risk of chronic kidney disease? A nationwide matched-cohort study

ObjectiveThe impact of schizophrenia on vital diseases, such as chronic kidney disease (CKD), has not as yet been verified. This study aims to establish whether there is an association between...

Low Magnesium Levels and FGF-23 Dysregulation Predict Mitral Valve Calcification as well as Intima Media Thickness in Predialysis Diabetic Patients.

Background. Mitral valve calcification and intima media thickness (IMT) are common complications of chronic kidney disease (CKD) implicated with high cardiovascular mortality. Objective. To investigate the implication of magnesium and fibroblast growth factor-23 (FGF-23) levels with mitral valve calcification and IMT in CKD diabetic patients. Methods. Observational, prospective study involving 150 diabetic patients with mild to moderate CKD, divided according to Wilkins Score. Carotid-echodoppler and transthoracic echocardiography were used to assess calcification. Statistical tests used to establish comparisons between groups, to identify risk factors, and to establish cut-off points for prediction of mitral valve calcification. Results. FGF-23 values continually increased with higher values for both IMT and calcification whereas the opposite trend was observed for magnesium. FGF-23 and magnesium were found to independently predict mitral valve calcification and IMT (P < 0.05). Using Kaplan-Meier analysis, the number of deaths was higher in patients with lower magnesium levels and poorer Wilkins score. The mean cut-off value for FGF-23 was 117 RU/mL and for magnesium 1.7 mg/dL. Conclusions. Hypomagnesemia and high FGF-23 levels are independent predictors of mitral valve calcification and IMT and are risk factors for cardiovascular mortality in this population. They might be used as diagnostic/therapeutic targets in order to better manage the high cardiovascular risk in CKD patients.

Associations of sugar-sweetened and artificially sweetened soda with chronic kidney disease: a systematic review and meta-analysis.

The risk of chronic kidney disease (CKD) in patients who regularly drink soda is controversial. The objective of this meta-analysis was to evaluate the associations between consumption of sugar-sweetened and artificially sweetened soda and CKD. A literature search was performed using MEDLINE, EMBASE and the Cochrane Database of Systematic Reviews from inception until 30 June 2014. Studies that reported odds ratios or hazard ratios comparing the risk of CKD in patients consuming significant amounts of either sugar-sweetened or artificially sweetened soda versus those who did not consume soda were included. Pooled risk ratios (RR) and 95% confidence intervals (CI) were calculated using a random-effects, generic inverse variance method. Five studies were included in our analysis of the association between consumption of sugar-sweetened soda and CKD. The pooled RR of CKD in patients consuming sugar-sweetened soda was 1.58 (95% CI 1.00-2.49). Four studies were selected to assess the association between consumption of artificially sweetened soda and CKD. The pooled RR of CKD in patients consuming artificially sweetened soda was 1.33 (95% CI 0.82-2.15). Our study demonstrates statistically significant increased risks of CKD in patients consuming sugar-sweetened soda, but not in patients consuming artificially sweetened soda. This finding suggests that sugar-sweetened soda consumption is associated with CKD and may impact clinical management and primary prevention of CKD in high-risk patients.

Sonographic Evaluation of the Carotid Intima-media Complex Thickness in Nigerian Chronic Kidney Disease Patients

Atherosclerotic cardiovascular disease is the leading cause of mortality in patients with chronic kidney disease (CKD). Measurement of the carotid artery intima-media thickness (CIMT) is being used by many investigators to detect an increased risk of coronary artery atherosclerotic disease and document treatment effects. This study compares CIMT measurements in 75 patients with chronic kidney disease to a matched cohort of 75 subjects with normal kidney function. In plaque-free arterial segments, the CIMT was measured manually in the longitudinal plane from the far walls of a segment of the common carotid artery 3 cm in length adjacent to the carotid bifurcation. Patients with CKD had a significantly higher mean CIMT compared to those with normal renal function (0.86 ± 0.42 mm vs 0.69 ± 0.21 mm; P &lt; .01). Mean CIMT values did not differ significantly between patients with different stages of CKD (stage 3: 0.88 ± 0.14 mm; stage 4: 0.89 ± 0.18 mm; and stage 5: 0.87 ± 0.14 mm, P = .94). These data indicate that CIMT is significantly higher in patients with CKD compared with controls, regardless of the stage of their disease, and may be a readily available noninvasive means of further assessing cardiovascular risk in CKD patients.

Fluctuation between fasting and 2-H postload glucose state is associated with chronic kidney disease in previously diagnosed type 2 diabetes patients with HbA1c ≥ 7%.

ObjectiveTo investigate how the glucose variability between fasting and a 2-h postload glucose state (2-h postload plasma glucose [2hPG]-fasting plasma glucose [FPG]) is associated with chronic kidney disease (CKD) in middle-aged and elderly Chinese patients previously diagnosed with type 2 diabetes.Design and MethodsThis cross-sectional study included 1054 previously diagnosed type 2 diabetes patients who were 40 years of age and older. First, the subjects were divided into two groups based on a glycated hemoglobin (HbA1c) value of 7%. Each group was divided into two subgroups, with or without CKD. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation was used to estimate the glomerular filtration rate (GFR). CKD was defined as eGFR<60 mL/min/1.73 m2. Multiple linear regression analysis was used to estimate the association between the 2hPG-FPG and eGFR. The 2hPG-FPG value was divided into four groups increasing in increments of 36 mg/dl (2.0 mmol/L): 0–72, 72–108, 108–144 and ≥144 mg/dl, based on the quartiles of patients with HbA1c levels ≥7%; then, binary logistic regression analysis was used to investigate the association between 2hPG-FPG and the risk of CKD.ResultsIn the patients with HbA1c levels ≥7%, the 2hPG-FPG was significantly associated with decreased eGFR and an increased risk of CKD independent of age, gender, body mass index (BMI), systolic blood pressure (BP), diastolic BP, smoking, and drinking, as well as fasting insulin, cholesterol, triglyceride, and HbA1c levels. The patients with 2hPG-FPG values ≥144 mg/dl showed an increased odds ratio (OR) of 2.640 (P = 0.033). Additionally, HbA1c was associated with an increased risk of CKD in patients with HbA1c values ≥7%.ConclusionsThe short-term glucose variability expressed by 2hPG-FPG is closely associated with decreased eGFR and an increased risk of CKD in patients with poor glycemic control (HbA1c≥7%).

AB0331 Chronic Kidney Disease in Patients with Rheumatoid Arthritis

BackgroundThe prevalence of chronic kidney disease (CKD) in general population is about 10%.ObjectivesThe aim of this study was to determine the prevalence of CKD in patients with rheumatoid arthritis (RA)...

Extracellular hydration, cardiovascular risk, and the interstitium: a three-dimensional view

Volume expansion is a major contributor to poor cardiovascular outcomes in kidney disease. The relationship of extracellular volume (ECV) overload to cardiovascular changes in chronic kidney disease (CKD) remains speculative. Recent studies are challenging traditional concepts and providing new insight into mechanisms and the relationship of ECV to cardiovascular health. A dynamic role of the extracellular interstitium in inducing cardiovascular risk is emerging in CKD.

It’s time for a practical method quantifying vascular calcification

It’s time for a practical method quantifying vascular calcification

Hypertriglyceridemic Waist is Associated with Increased Carotid Atherosclerosis in Chronic Kidney Disease Patients

Background: Patients with chronic kidney disease (CKD) have an unacceptably high risk of death, primarily as a result of cardiovascular disease (CVD). The ‘hypertriglyceridemic waist' phenotype has been proposed as a simple and strong predictor of CVD risk. Therefore, we investigated the relationship between the hypertriglyceridemic waist phenotype and carotid atherosclerosis in CKD patients. Methods: In a cross-sectional study, we enrolled 785 prevalent CKD patients [416 males, aged 44.6 years (21.7-69.4), glomerular filtration rate 52.5 ml/min/1.73 m² (5.3-119.4)]. We divided the patients into three groups: group 1: waist circumference >90 cm in men or >85 cm in women and triglycerides ≥2 mmol/l (n = 109); group 3: waist circumference ≤90 cm in men or ≤85 cm in women and triglycerides <2 mmol/l (n = 379), and group 2: the remaining patients (n = 297). Routine biochemical parameters and carotid artery intima-media thickness (IMT) were measured. Results: The prevalence of the hypertriglyceridemic waist phenotypes was 13.8% in the CKD patients. Triglyceride, total cholesterol, HDL-cholesterol and LDL-cholesterol concentrations in group 1 were significantly higher than those in group 3. Carotid artery IMT of the hypertriglyceridemic waist group was the highest. Conclusion: The hypertriglyceridemic waist phenotype was associated with worse carotid atherosclerosis in CKD patients. This suggests that the hypertriglyceridemic waist phenotype may be useful for predicting CVD risk in CKD patients.

Does Brachial Blood Pressure Need to Predict Cardiovascular Outcomes in End Stage Renal Disease? An Update

Hypertension is responsible for a significantly increased burden of cardiovascular events and it is cause and a consequence of Chronic Kidney Disease (CKD) and a determinant factor in its progression to End Stage Kidney Disease (ESKD). Therefore, nephrologists have been focusing their attention on hypertension control to prevent CKD progression, delaying it but with poor results on cardiovascular mortality reduction. An important effect is the difficulty to adequately reduce BP levels in CKD patients and especially in dialysis patients despite the polipharmacological therapy. We have to take into account other aspects influencing mortality risk in CKD patients .The first aspect to consider is whether brachial blood pressure (BP) measurement is sufficient to describe the complex relationship between the alteration of BP and outcomes in renal subjects. The second aspect to consider is the variability of BP (BPV). We think that BP measurement cannot only take into account brachial BP, because it represents a limited measure of a complex clinical condition in CKD or ESRD patients. The inability to evaluate hypertension in its complexity explains why several aspects are still unrecognized.

Vitamin D: something new under the sun.

Vitamin D: something new under the sun.

Ongoing gaps in CKD and CVD care: re-evaluating strategies for knowledge dissemination

Over the last decade, the nephrology community has come to recognize the importance of chronic kidney disease (CKD) as an important modifier of outcomes and of cardiovascular risk. We have attempted to categorize and quantify the risks of dying, having a cardiovascular event and going on to dialysis, and we have published extensively in both nephrology and non-nephrology journals about the importance of CKD in general populations [1–7]. Some jurisdictions have embarked on formal and well-organized education campaigns for general practitioners (GPs) and patients (UK, Canada, Australia, USA) with professional messaging and public campaigns. Guidelines have been written and disseminated [8, 9]. Despite these efforts and the quantity of publications regarding CKD, we have not systematically evaluated the impact of these efforts on quality of care for those persons with CKD. The paper in the current edition of Nephrology Dialysis Transplantation (27/4) by Razavian et al. describes GP awareness of CKD, gaps in treatment and gaps in prescribing in Australia in 2008, after the implementation of estimated glomerular filtration rate (eGFR) reporting by laboratories and 6 years after the publication of the Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines for CKD definition, evaluation and classification. The study leveraged the infrastructure of the Australian Hypertension and Absolute Risk Study (AusHEART) and describes cardiovascular risk management in CKD in Australian primary care using a nationally representative, cluster stratified, cross-sectional survey among 322 GPs. Each GP was asked to provide data for 15–20 patients over the age of 55 who presented between April and June 2008. Within the study framework, records on 4966 patients were collected, in whom 37% had abnormal kidney function. The study describes the under-recognition of CKD by GPs (only 18% of the overall CKD cohort were correctly identified, with 67% of those being in Stages 4 and 5 and 28% being Stage 3), under-estimation of cardiovascular disease (CVD) risk in CKD patients and, paradoxically, the overestimation of CVD risk in non-CKD patients. Furthermore, the study identified gaps in achievement of targets for hypertension, use of renin-angiotensin system (RAS) blockade and lipid-lowering agents in CKD patients. The study is meritorious on a number of levels. Firstly, the robust methodology for random sampling of GP practices participating in the AusHEART study, stratified by state and urban/rural locations to reflect the distribution of the Australian adult population, ensures a representative sample of practices. While one may argue that those who volunteered to participate might be the ‘best’ practices, this would only lead to a conservative estimate of the ‘gap’ in knowledge and practice identified in the study. Within that sample, the ability to determine ‘prevalence’ of CKD (albeit using single time point values for eGFR and uACR measurements) adds another important quantitative dimension to the study. Simple one-page questionnaires were given to GPs, which included estimates of CVD risk in each of the patients without specifying how to determine this risk. The authors then compared these GP-generated risks to risk scores generated centrally from Framingham risk equa

Impact of chronic kidney disease on carotid plaque vulnerability

Little is known about the effect of chronic kidney disease (CKD) on plaque morphology in cerebral vessels. We therefore analyzed plaque composition and metabolic and chemical parameters with regard to clinical outcome in patients with advanced carotid artery stenosis (>70%) and normal or impaired renal function. Carotid endarterectomy plaques were collected from 114 patients, 51 with CKD and 63 without CKD (mean estimated glomerular filtration rate, 49 ± 9 vs 88 ± 14 mL/min), and analyzed by histology and immunohistochemistry. Serum levels of matrix metalloproteinases (MMP-1, -2, -3, -7, -8, and -9), calcium, phosphate, parathyroid hormone, fetuin-A, osteoprotegerin, and inflammatory factors, including fibrinogen, and high-sensitive C-reactive protein (hsCRP) were measured by appropriate enzyme-linked immunosorbent assay. Compared with patients without CKD, patients with CKD had significantly more early-stage (11.2% vs 2.8%, P = .002) and end-stage (7.4% vs 0.2%, P = .036) calcification, unstable (50.8% vs 20.4%, P = .001) and ruptured (53.1% vs 32.8%, P = .035) lesions, and a significantly lower amount of collagenous fibers (39.2% vs 54.6%, P = .001). Serum samples of CKD patients had significantly enhanced levels of fibrinogen (393 ± 88 vs 331 ± 60 mg/dL, P = .018), hsCRP (1.7 ± 2.9 vs 0.8 ± 0.9 mg/dL; P = .042), parathyroid hormone (47.3 ± 24.1 vs 32.8 ± 12.2 ng/L, P = .010), fetuin-A (0.21 ± 0.05 vs 0.18 ± 0.04 mg/mL, P = .039), and MMP-7 (13.0 ± 5.3 vs 8.3 ± 3.0 ng/mL; P < 0.001). The incidence of cerebrovascular events >6 months before carotid surgery was significantly increased in CKD patients (84.0% vs 26.2% P < .001). In patients with CKD and advanced carotid artery stenosis, morphologic changes in plaque composition may contribute to plaque vulnerability and consequently to the risk of cerebrovascular events. Furthermore, relevant serum markers of inflammation, vascular calcification, and vessel wall degradation might be an indication of stroke risk in CKD patients.

Protein-energy wasting and mortality in chronic kidney disease.

Protein-energy wasting (PEW) is common in patients with chronic kidney disease (CKD) and is associated with an increased death risk from cardiovascular diseases. However, while even minor renal dysfunction is an independent predictor of adverse cardiovascular prognosis, PEW becomes clinically manifest at an advanced stage, early before or during the dialytic stage. Mechanisms causing loss of muscle protein and fat are complex and not always associated with anorexia, but are linked to several abnormalities that stimulate protein degradation and/or decrease protein synthesis. In addition, data from experimental CKD indicate that uremia specifically blunts the regenerative potential in skeletal muscle, by acting on muscle stem cells. In this discussion recent findings regarding the mechanisms responsible for malnutrition and the increase in cardiovascular risk in CKD patients are discussed. During the course of CKD, the loss of kidney excretory and metabolic functions proceed together with the activation of pathways of endothelial damage, inflammation, acidosis, alterations in insulin signaling and anorexia which are likely to orchestrate net protein catabolism and the PEW syndrome.

Cardiovascular Complications in CKD Patients: Role of Oxidative Stress

Starting with the early stages, patients with chronic kidney disease (CKD) experience higher burden of cardiovascular disease (CVD). Moreover, CVD complications are the major cause of mortality in CKD patients as compared with complications from chronic kidney failure. While traditional CVD risk factors, including diabetes, hypertension, hyperlipidemia, obesity, physical inactivity, may be more prevalent among CKD patients, these factors seem to underestimate the accelerated cardiovascular disease in the CKD population. Search for additional biomarkers that could explain the enhanced CVD risk in CKD patients has gained increasing importance. Although it is unlikely that any single nontraditional risk factor would fully account for the increased CVD risk in individuals with CKD, oxidative stress appears to play a central role in the development and progression of CVD and its complications. We will review the data that support the contribution of oxidative stress in the pathogenesis of CVD in patients with chronic kidney failure.

Current problems in hypertension and nephrology

The aim of this issue of Expert Opinion on Pharmacotherapy is to present the most important and controversial problems in hypertension and nephrology. To this end, the most important points of the current (2009) recommendations of the European Society of Hypertension (ESH) are discussed, including aspects related to the treatment of hypertension – the role of beta-blockers, combined therapy with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) the treatment of hypertension in elderly patients, and role of destiffening therapy. The authors also present current recommendations for the management of dyslipidemia in hypertensive and chronic kidney disease (CKD) patients, and new strategies to prevent cardiovascular risk in CKD patients, the optimal level of blood pressure in patients with hypertensive nephropathy and which hypotensive drugs are the most nephroprotective. The Editors are aware that many other important problems have not been addressed in this issue of the journal; however, they hope the readers find it interesting and useful.

Serum visfatin as a non-traditional biomarker of endothelial dysfunction in chronic kidney disease: An Egyptian study

Background Endothelial dysfunction (ED) is closely linked to cardiovascular disease and outcome in patients with chronic kidney disease (CKD). Visfatin is an adipocytokine that recently generated much interest; however, its role in CKD remains to be clarified. This study aimed to assess visfatin in correlation with markers of ED and inflammation in Egyptian patients with CKD. Methods The study included 40 non-diabetic, clinically stable CKD patients and 20 healthy volunteers. Serum levels of visfatin, markers of ED (intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)) and markers of inflammation (interleukin-6 (IL-6), and C-reactive protein (CRP)) were measured. Endothelial function was evaluated using brachial artery flow-mediated dilatation (FMD). Results Serum visfatin, ICAM-1, VCAM-1, CRP, and IL-6 levels were significantly elevated and FMD% was decreased in CKD patients as compared to controls. Visfatin correlated positively with ICAM-1, VCAM-1, CRP, and IL-6 and negatively with FMD% in CKD patients. In a multiple regression model, visfatin was strongly and independently associated with FMD (Beta = −0.02, P < 0.001) in CKD patients. Conclusions Serum visfatin is strongly associated with endothelial adhesion molecules and FMD%, suggesting that visfatin is an important promising biomarker for prediction of ED and future cardiovascular risk in CKD patients. Moreover, the relationship between visfatin and IL-6 indicates that circulating visfatin may reflect the sub-clinical inflammatory status. Thus, visfatin might be involved in the complex interactions between ED, inflammation, and atherosclerosis and their major clinical consequences; however, further prospective studies are required to prove this hypothesis.

Circulating Endotoxemia

Translocated endotoxin derived from intestinal bacteria has a wide range of adverse effects on cardiovascular (CV) structure and function, driving systemic inflammation, atherosclerosis and oxidative stress. This study's aim was to investigate endotoxemia across the spectrum of chronic kidney disease (CKD). Circulating endotoxin was measured in 249 patients comprising CKD stage 3 to 5 and a comparator cohort of hypertensive patients without significant renal impairment. Patients underwent extended CV assessment, including pulse wave velocity and vascular calcification. Hemodialysis (HD) patients also received detailed echocardiographic-based intradialytic assessments. Patients were followed up for 1 year to assess survival. Circulating endotoxemia was most notable in those with the highest CV disease burden (increasing with CKD stage), and a sharp increase was observed after initiation of HD. In HD patients, predialysis endotoxin correlated with dialysis-induced hemodynamic stress (ultrafiltration volume, relative hypotension), myocardial stunning, serum cardiac troponin T, and high-sensitivity C-reactive protein. Endotoxemia was associated with risk of mortality. CKD patients are characteristically exposed to significant endotoxemia. In particular, HD-induced systemic circulatory stress and recurrent regional ischemia may lead to increased endotoxin translocation from the gut. Resultant endotoxemia is associated with systemic inflammation, markers of malnutrition, cardiac injury, and reduced survival. This represents a crucial missing link in understanding the pathophysiology of the grossly elevated CV disease risk in CKD patients, highlighting the potential toxicity of conventional HD and providing a novel set of potential therapeutic strategies to reduce CV mortality in CKD patients.