Cardiovascular complications are the most important cause of death in patients on dialysis with end-stage renal disease. Antibodies reacting with β-glycoprotein I seem to play a pathogenic role in antiphospholipid syndrome and stroke and are involved in the origin of atherosclerosis. Here we evaluated the presence of anticardiolipin and anti-β-glycoprotein I antibodies together with other vascular risk factors and their relationship with mortality and cardiovascular morbidity in a cohort of 124 hemodialysis patients prospectively followed for 2 years. Of these, 41 patients were significantly positive for IgA anti-β-glycoprotein I, and the remaining had normal values. At 24 months, overall and cardiovascular mortality and thrombotic events were all significantly higher in patients with high anti-β-glycoprotein I antibodies. Multivariate analysis using Cox regression modeling found that age, hypoalbuminemia, use of dialysis catheters, and IgA β-glycoprotein I antibodies were independent risk factors for death. Thus, IgA antibodies to β-glycoprotein I are detrimental to the clinical outcome of hemodialysis patients.
BackgroundAnemia is a common condition in CKD that has been identified as a cardiovascular (CV) risk factor in end-stage renal disease, constituting a predictor of low survival. The aim of this study was to define the onset of anemia of renal origin and its association with the evolution of kidney disease and clinical outcomes in stage 3 CKD (CKD-3).MethodsThis epidemiological, prospective, multicenter, 3-year study included 439 CKD-3 patients. The origin of nephropathy and comorbidity (Charlson score: 3.2) were recorded. The clinical characteristics of patients that developed anemia according to EBPG guidelines were compared with those that did not, followed by multivariate logistic regression, Kaplan-Meier curves and ROC curves to investigate factors associated with the development of renal anemia.ResultsDuring the 36-month follow-up period, 50% reached CKD-4 or 5, and approximately 35% were diagnosed with anemia (85% of renal origin). The probability of developing renal anemia was 0.12, 0.20 and 0.25 at 1, 2 and 3 years, respectively. Patients that developed anemia were mainly men (72% anemic vs. 69% non-anemic). The mean age was 68 vs. 65.5 years and baseline proteinuria was 0.94 vs. 0.62 g/24h (anemic vs. non anemic, respectively). Baseline MDRD values were 36 vs. 40 mL/min and albumin 4.1 vs. 4.3 g/dL; reduction in MDRD was greater in those that developed anemia (6.8 vs. 1.6 mL/min/1.73 m2/3 years). These patients progressed earlier to CKD-4 or 5 (18 vs. 28 months), with a higher proportion of hospitalizations (31 vs. 16%), major CV events (16 vs. 7%), and higher mortality (10 vs. 6.6%) than those without anemia. Multivariate logistic regression indicated a significant association between baseline hemoglobin (OR=0.35; 95% CI: 0.24-0.28), glomerular filtration rate (OR=0.96; 95% CI: 0.93-0.99), female (OR=0.19; 95% CI: 0.10-0.40) and the development of renal anemia.ConclusionsRenal anemia is associated with a more rapid evolution to CKD-4, and a higher risk of CV events and hospitalization in non-dialysis-dependent CKD patients. This suggests that special attention should be paid to anemic CKD-3 patients.
In conclusion, pretransplant IgA-aB2GP1 was the main risk factor for graft thrombosis and early graft loss. Further research should be made on whether anticoagulation in antibody-positive patients could ameliorate this catastrophic complication.
In the current immunosuppressive therapy era, vessel thrombosis is the most common cause of early graft loss after renal transplantation. The prevalence of IgA anti-b 2 -glycoprotein I antibodies (IgA-aB2GPI-ab) in patients on dialysis is elevated (.30%), and these antibodies correlate with mortality and cardiovascular morbidity. To evaluate the effect of IgA-
IgA anti-beta-2-glycoprotein I (aB2GPI) antibodies have been related to vascular pathology in the general population and mainly in hemodialyzed patients (prevalence 33%) in whom an elevated incidence of thrombosis and mortality is found. In this paper we have studied the presence of IgA aB2GPI antibodies at pretransplant and their evolution after transplantation with a cross-sectional-based follow-up study of a cohort of 288 endstage renal disease (ESRD) patients treated with kidney transplantation. Pretransplant IgA aB2GPI levels were elevated 31.7 ± 4.2 U/mL without differences in age or type of dialysis. Patients with different etiologies of ESRD showed higher levels of IgA aB2GPI than blood donors, except the groups of non-IgA glomerular disease and systemic erythematosus lupus, whose nonsignificant differences were observed. IgA aB2GPI antibodies dropped immediately after transplantation (10.7 ± 1.0 U/mL, P < 0.0001), coinciding with a high degree of immunosuppression, and remained significantly lower than that observed in pretransplant status. Prevalence of patients with elevated antibodies was also less in transplanted patients (8.9% versus 30.4%, P < 0.0001). Among, positivity for IgA aB2GPI was higher than in patients who had received their first transplant that those were retransplanted. This finding could have important clinical implications and can suggest new therapeutic strategies in patients with IgA aB2GPI antibodies.
The presence of B2A-CIC is a predictor of acute thrombotic events. Patients who were positive for IgA aB2GP1 only are at risk of experiencing thrombosis if they are B2A-CIC positive. If they are B2A-CIC-negative patients, they have the same risk as the control group. Treatments to prevent acute thrombotic events should focus on B2A-CIC-positive patients.
Executive summary:The objective of this program is to develop phosphor systems and LED light engines that have steady-state LED efficacies (using LEDs with a 60% wall-plug efficiency) of 105-120 lm/W with correlated color temperatures (CCT) ~3000 K, color rendering indices (CRI) >85, <0.003 distance from the blackbody curve (dbb), and <2% loss in phosphor efficiency under high temperature, high humidity conditions. In order to reach these goals, this involves the composition and processing optimization of phosphors previously developed by GE in combination with light engine package modification. To meet these requirements, the accomplishments of this program have been:Optimized Phosphors for Warm White LED Light Engines Contract#DE-EE003251 Final ReportPage 2 of 49Development of optical models for remote phosphor systems with correlation to phosphor scattering and absorption coefficients derived from direct measurement of powder phosphors. Development of fundamental models for the thermal quenching of the green phosphors within this program. These models point to an inherent limit in the activator concentration which leads us to the conclusion that the reduction in scattering losses in these materials will come from particle size/morphology modifications, not compositional changes. Use of the combined optical and thermal model to set guidelines for phosphor properties (particle size distribution, parasitic absorption, etc.) and development paths for the phosphors in this program. Invention and development of particle coating chemistries to coat our (Sr,Ca) 3 (Al,Si)O 4 (F,O):Ce 3+ particles in order to prevent degradation under high temperature, high humidity (HTHH) conditions. Development of elutriation methods to remove fine particles that arise from phosphor milling and that disproportionally contribute to the scattering coefficient of our phosphors. In some cases, these methods can reduce the phosphor scattering coefficient by ~40% with <20% mass loss through the removal of fine particles. Scale-up and optimization at 50 g scale for all green phosphors; the quantum efficiency of our green phosphors ranges from 87-90% with batch-to-batch variability. We have also scaled-up our particle coating methods for moisture protection of our (Sr,Ca) 3 (Al,Si)O 4 (F,O):Ce 3+ green phosphor. Optimization of elutriation/decanting methods to remove fine particles that arise from phosphor milling and that disproportionally contribute to the scattering coefficient of our phosphors. Apart from the reduction in phosphor scattering coefficient, we have also found that the "fine" particles in our samples also have lower quantum efficiency. The removal of these fine particles has led to the high quantum efficiencies for all of our phosphors. Optimization of our K 2 SiF 6 :Mn 4+ (PFS) line-emitting phosphor to have quantum efficiencies of 83-87% while minimizing degradation under high temperature, high humidity (HTHH) conditions. Development of 40-800 lumen (pulsed) light engines that have phosphor/package efficiencies of ~185-225...
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