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Background: Cardiovascular disease (CVD) is the leading cause of death in patients with end-stage renal disease (ESRD). Disregulation of apoptosis within the vessel wall and upregulation of the Fas/Fas-ligand (Fas-L) system contribute to the development of atherosclerosis. Cross-sectional studies have suggested that elevated plasma levels of the soluble form of Fas (sFas) are associated with CVD. However, the role of sFas and sFas-L in predicting future cardiovascular events has yet to be defined. Methods: We evaluated the role of plasma sFas and sFas-L levels as predictors of CVD in a prospective cohort of 107 chronic hemodialysis patients. Results: During the study period (27 months), 53 patients (49.5%) presented with at least one cardiovascular end point. On univariate analysis, baseline sFas levels were significantly associated with the occurrence of cardiovascular end points, whereas sFas-L levels were not. Using Cox proportional hazards, increased sFas levels were associated with a significantly greater risk for cardiovascular end points ( P = 0.03). This effect was independent of baseline CVD history, classic risk factors for atherosclerosis (diabetes, hypercholesterolemia, hypertension, and smoking), and markers of inflammation (C-reactive protein [CRP], soluble intercellular adhesion molecule-1). Increased CRP levels also were associated with cardiovascular end points ( P = 0.04). In addition, increased cardiovascular mortality was found in patients in the highest sFas tertile compared with those in the lowest tertile (27.8% versus 8.6%; P = 0.04). Conclusion: Increased plasma sFas levels are predictive of future CVD. These results suggest that sFas is a novel and independent predictor of active atherosclerotic disease in patients with ESRD.

Growing evidence has been gathered over the last 15 years regarding the role of nontraditional or uremia-related risk factors in the pathogenesis of atherosclerosis in subjects with renal failure. Among those factors, dyslipidemia, inflammation, hyperhomocysteinemia, and oxidant stress have been extensively studied. However, the clinical significance of many of these factors remains controversial in light of reported studies. In this article, the existing evidence regarding the role of uremia-related risk factors in the pathogenesis of atherosclerosis is reviewed, with special emphasis on prevalence, cardiac risk, and management in patients with chronic kidney disease (CKD). Consensus treatment recommendations are provided for risk factors for which there is evidence to support preventive or therapeutic interventions.

Understanding the mechanisms of injury associated with cardiac arrest is essential for defining strategies aimed at improving preservation and function of kidneys harvested in non-heart-beating (NHB) donors.We standardized a model of NHB donors in rats and studied the kinetics and types (apoptosis vs. necrosis) of renal cell death developing during cold storage. Using quantitative polymerase chain reaction, immunoblotting, and caspase inhibition, we also studied the molecular pathways regulating renal cell death in this model.The kinetics and extent of cell death developing in cortical tubules during cold storage were found to be increased in non-heart-beating (NHB) kidneys. Apoptosis of cortical tubules predominated in NHB kidneys exposed to 10 hr of cold storage, whereas necrosis increased after longer periods of cold ischemia. Shortly after cardiac arrest, a rapid up-regulation of Bax and Hsp 70 was found at the protein level in NHB kidneys. After 24 hr of cold storage, induction of Bax was maintained, whereas protein levels of Hsp70 returned to levels comparable to heart-beating (HB) controls. Also, mRNA levels of Bax were found to increase during cold storage in NHB kidneys. Cortical cell death was found to be largely caspase-independent but responsive to hydroxyl-radical scavenging with dimethyl sulfoxide (DMSO).Cardiac arrest promotes activation of death-inducing molecules such as Bax and is associated with increased development of caspase-independent renal cell death during cold storage. Developing strategies, such as free radical scavenging, aimed at inhibiting cell death during cold storage, could prove useful for improving preservation of NHB kidneys.

In summary, use of plasmapheresis has changed in recent years given advances in medical technology that have allowed a wider clinical application in the critical care setting. Membrane filtration technology has provided an alternative to centrifugation that can be easily applied in intensive care units. Use of plasmapheresis has also changed in recent years reflecting the availability of evidence largely obtained from controlled prospective studies. However, the clinical efficacy of plasmapheresis for many acute renal conditions is still controversial. Plasmapheresis appears to be a useful adjunct to conventional therapy in the treatment of anti-GBM nephritis, severe dialysis-dependent forms of pauciimmune RPGN, cryoglobulinemia, and HUS-TTP. Reported data also suggest a possible benefit of plasmapheresis in patients with myeloma cast nephropathy, sepsis, and poisoning/overdose, but the case for plasmapheresis in these disorders is largely unproven and the reported evidence insufficient to recommend its use outside research settings. In contrast, data from controlled trials do not support a role for plasmapheresis in immune complex-mediated RPGN, such as lupus nephritis, and acute allograft rejection. The more widespread application of prospective, randomized, controlled clinical trials should help to better define the value of plasmapheresis for treatment of acute renal diseases.

Background. Peripheral arterial occlusive disease (PAOD) including lower-extremity and cerebrovascular atherosclerosis is a leading cause of morbidity in haemodialysis patients. Recent evidence suggests that the expression of Fas, a molecule implicated in the initiation of apoptosis in various cell types, is increased at sites of atherosclerotic plaques. However, the significance of plasma levels of the soluble form of Fas (sFas) as a marker of peripheral arterial disease has yet to be defined. Methods. The present report is based on a crosssectional analysis of baseline data from an ongoing prospective study designed to evaluate the role of sFas as marker of PAOD in end-stage renal disease (ESRD). We evaluated the association between sFas levels and evidence of PAOD in a cohort of 107 chronic haemodialysis patients. Results. Compared with subjects without evidence of disease (ns56), subjects with PAOD (ns51) had significantly higher plasma levels of sFas (30.0"8.9 vs 26.4"9.5 nguml; Ps 0.04). Using multiple regression, sFas was found to be associated with PAOD independently of classical risk factors for atherosclerosis (hypercholesterolaemia, diabetes, hypertension, and smoking), markers of inflammation (e.g. C-reactive protein, intercellular cell adhesion molecule type 1), and other risk factors (e.g. age, gender). An increase of one quintile in the plasma concentration of sFas was associated with an odds ratio of PAOD of 1.69 (95% CI: 1.09–2.63, Ps 0.01). In addition, models that incorporated sFas were significantly better at predicting PAOD than models limited to classical risk factors for atherosclerosis, alone or in combination with CRP levels (Ps 0.01). Conclusions. Increased plasma levels of sFas are associated with established PAOD. These results suggest that sFas may represent a novel and independent marker of atherosclerosis.

Coronary artery disease (CAD) is the leading cause of death in patients with end-stage renal disease (ESRD). Recent evidence suggests that the expression of Fas, a molecule implicated in the initiation of apoptosis in various cell types, is increased at sites of atherosclerotic plaques. However, the significance of plasma levels of the soluble form of Fas (sFas) and its ligand (sFas-L) as markers of atherosclerosis has yet to be defined. The present report is a cross-sectional analysis of baseline data from an ongoing prospective study designed to evaluate the role of sFas and sFas-L as markers of CAD in ESRD. We evaluated the association between plasma levels of sFas and sFas-L and evidence of CAD in a cohort of 107 chronic hemodialysis patients. Plasma levels of sFas were significantly greater ( P = 0.04) among subjects with (n = 64) than without evidence of CAD (n = 43). Plasma levels of sFas-L were similar in both groups. Using multivariate analysis, sFas level was found to be independently associated with CAD ( P = 0.01) after adjustment for classic risk factors for CAD (hyperlipidemia, diabetes, hypertension, and smoking), markers of inflammation (C-reactive protein [CRP], intercellular adhesion molecule 1), and other confounders. An increase of one quintile in plasma concentration of sFas was associated with an odds ratio for CAD of 1.64 (95% confidence interval, 1.11 to 2.41). Models that incorporated sFas were significantly better at identifying patients with CAD than models limited to classic risk factors for atherosclerosis, alone ( P = 0.008) or in combination with CRP levels ( P = 0.006). In summary, increased plasma levels of sFas are associated with CAD in stable patients with ESRD. These results suggest that sFas may represent a novel and independent marker of CAD. © 2001 by the National Kidney Foundation, Inc.

chronic ambulatory peritoneal dialysis (CAPD) [1,2]. Inappropriate treatment of ESTI may lead to refractBackground. Partial replantation (i.e. replacement of the extraperitoneal portion of the catheter with cre- ory or recurrent peritonitis, cuV infections, and extensive cellulitis of the abdominal wall [3]. In addition, a ation of a new subcutaneous tunnel ) has been suggested to avoid catheter removal in patients with significant proportion of ESTI are unresponsive to treatment or require prolonged courses of antibiotics persistent exit-site/tunnel infection ( ESTI ). However, published experience with this technique is limited. [1‐3]. Catheter removal with or without simultaneous reinsertion of a new catheter is frequently required in Methods. Partial replantation was performed on an outpatient basis under local anesthesia for seven cases of unresponsive ESTI [3,4]. Data from the National CAPD Registry indicate that up to 39% of patients with persistent ESTI of >3 months duration. All patients resumed CAPD immediately following catheter removals are related to persistent ESTI unresponsive to antibiotic therapy [5]. Moreover, intractsurgery. Results. One patient had dialysate leakage less than 1 able ESTI are a major cause of catheter-related complications that are responsible for up to 20% of all week after surgery that required catheter removal. The other patients had no complications and mean catheter permanent transfers from CAPD to haemodialysis

Resume L’infection a Candida est une cause relativement frequente d’infection hematogene nosocomiale chez le patient immunosupprime. Cependant, l’atteinte renale demeure inhabituelle. De plus, l’identification directe de Candida a la biopsie renale est rarement possible. Nous presentons un cas d’insuffisance renale aigue secondaire a une nephrite tubulo-interstitielle a Candida albicans .

A positive association between nephrolithiasis and blood pressure has been suggested in previous studies. However, controversy remains, due to methodological problems in some of the previous studies and absence of prospective data. We evaluated the relationship between nephrolithiasis and the risk of hypertension in a cohort of 51,529 men followed prospectively for 8 years. Information was obtained by biennial mailed questionnaires. At baseline in 1986, 4111 (8.0%) subjects reported a history of nephrolithiasis and 11,623 (22.6%) a diagnosis of hypertension. A positive association was found between the two disorders (age adjusted odds ratio [OR]: 1.31; 95% confidence interval [CI]: 1.30 to 1.32). Among men who reported both disorders, 79.5% reported that the occurrence of nephrolithiasis was prior to or concomitant with the diagnosis of hypertension. Among men without hypertension at baseline, the odds ratio for incident hypertension in men with a history of nephrolithiasis compared with those without was 1.29 (95% CI: 1.12 to 1.41; adjusted for age, body mass index, and intake of calcium, sodium, potassium, magnesium, and alcohol). The occurrence of incident nephrolithiasis during follow-up was similar in men with hypertension at baseline compared with that in men without (adjusted OR: 0.99, 95% CI: 0.82 to 1.21). These data support the hypothesis that prior occurrence of nephrolithiasis increases the risk of subsequent hypertension.

Despite the prevalent use of recombinant human erythropoietin (rhEPO), anemia is a frequent finding in hemodialysis patients. The goal of this study was to evaluate the impact of anemia on patient survival and characterize the determinants of hematopoiesis that may be amenable to therapeutic manipulation to enhance rhEPO responsiveness and reduce death risk. Patient characteristics and laboratory data were collected for 21,899 patients receiving hemodialysis three times per week in dialysis centers throughout the United States in 1993. Hemoglobin concentrations (Hb)or =80 g/L were associated with a twofold increase in the odds of death (odds ratio = 2.01; P = 0.001) when compared with Hb 100 to 110 g/L. No improvement in the odds of death was afforded for Hb110 g/L. Using multiple linear regression, variables of rhEPO administration (rhEPO dose and percentage of treatments that rhEPO was administered), variables of iron status (serum iron, transferrin saturation, and ferritin), variables of nutritional status (serum albumin and creatinine concentration), and the dose of dialysis (urea reduction ratio) were found to be significantly associated with hemoglobin concentration (P0.001). Age, race, and gender were also found to be significantly associated with hemoglobin concentrations (P0.001). From this report, the following conclusions may be made. (1) Anemia may be predictive of an increased risk of mortality in some hemodialysis patients. (2) Hemoglobin concentrations110 g/L are not associated with further improvements in the odds of death. (3) Laboratory surrogates of iron stores, nutritional status, and the delivered dose of dialysis are predictive of hemoglobin concentration. Whether manipulation of the factors that improve anemia will also enhance the survival of patients on hemodialysis is unknown and should be evaluated by prospective, interventional studies.

A positive association between nephrolithiasis and blood pressure has been suggested in previous studies. However, controversy remains, due to methodological problems in some of the previous studies and absence of prospective data. We evaluated the relationship between nephrolithiasis and the risk of hypertension in a cohort of 51,529 men followed prospectively for 8 years. Information was obtained by biennial mailed questionnaires. At baseline in 1986, 4111 (8.0%) subjects reported a history of nephrolithiasis and 11,623 (22.6%) a diagnosis of hypertension. A positive association was found between the two disorders (age adjusted odds ratio [OR]: 1.31; 95% confidence interval [CI]: 1.30 to 1.32). Among men who reported both disorders, 79.5% reported that the occurrence of nephrolithiasis was prior to or concomitant with the diagnosis of hypertension. Among men without hypertension at baseline, the odds ratio for incident hypertension in men with a history of nephrolithiasis compared with those without was 1.29 (95% CI: 1.12 to 1.41; adjusted for age, body mass index, and intake of calcium, sodium, potassium, magnesium, and alcohol). The occurrence of incident nephrolithiasis during follow-up was similar in men with hypertension at baseline compared with that in men without (adjusted OR: 0.99, 95% CI: 0.82 to 1.21). These data support the hypothesis that prior occurrence of nephrolithiasis increases the risk of subsequent hypertension.

Accumulating evidence suggests that periodontal disease is associated with increased risk of cardiovascular disease (CVD). Several mechanisms have been proposed to explain this association. To date, however, a causal relation has not been firmly established. In addition, the extent to which treatment of periodontal disease might result in lower incidence of CVD has not been addressed in any study to date. Further research is needed before recommendations are made regarding monitoring and therapy of periodontal disease.

Les patients souffrant d’insuffisance rénale chronique (IRC) présentent un taux important de maladies cardiovasculaires (MCV). En effet, la prévalence des MCV est 10 à 30 fois plus élevée chez ces patients que dans la population générale. Cet excès est lié en partie à une prévalence accrue de facteurs de risque « classiques » tels que l’hypertension artérielle, le diabète et la dyslipidémie. Cependant, plusieurs autres facteurs de risque « non traditionnels » ont été identifiés au cours des dernières années et contribuent également à la prévalence accrue des MCV dans cette population. Les facteurs les plus étudiés et les plus influents en termes de risque cardiovasculaire sont l’inflammation et le stress oxydatif. Cet article présente, de façon critique, les données concernant l’impact de ces facteurs sur le développement de l’athérosclérose chez les sujets ayant une IRC, en mettant l’accent sur l’aspect épidémiologique et les recommandations thérapeutiques en matière d’insuffisance rénale., Patients with chronic kidney disease (CKD) have a substantially increased risk of cardiovascular disease (CVD) compared with the general population. The high prevalence of established traditional risk factors for atherosclerosis (diabetes, hypertension, dyslipidemia) in these patients undoubtedly contributes to the accelerated rate of vascular disease. In addition, several hypotheses have emerged to explain the high prevalence of CVD in patients with chronic renal failure. Growing evidence has been gathered over the last 15 years regarding the role of uremia-related risk factors such as inflammation and oxidant stress in the pathogenesis of atherosclerosis in subjects with renal failure. This paper will review current knowledge regarding the potential role of these non-traditional or uremia-related risk factors for atherosclerosis with special emphasis on prevalence, cardiac risk, and management in patients with CKD.