Predialysis Vitamin D Receptor Activator Treatment and Cardiovascular Events after Dialysis Initiation: A Multicenter Observational Study

&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Vitamin D receptor activator (VDRA) administration has been linked with a reduced incidence of cardiovascular disease (CVD). However, it is unclear whether VDRA administration during the predialysis stage is associated with CVD incidence after dialysis initiation in patients with chronic kidney disease. Therefore, we examined the association between VDRA use and CVD events. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; This multicenter observational study included 1,516 patients; they were divided into 2 groups: those who did and did not receive oral VDRA for at least 3 months before dialysis initiation. The CVD incidence was compared between these groups. Factors that impacted CVD incidence were extracted through a multivariate analysis. Subgroups were created based on prior CVD history and serum CRP levels. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; The incidence of CVD was significantly lower in the VDRA group (log-rank test, p = 0.014). Stepwise multivariate analyses identified age, gender, diabetes, CVD history, calcium-channel blockers, beta-blockers, loop diuretics, anti-platelet agents, phosphate binders, VDRA, erythropoiesis stimulating agents, and cardiothoracic ratio as factors affecting CVD incidence. In the group with no CVD history, VDRA use was associated with a low incidence of CVD (HR 0.35). In the group with serum CRP levels &lt;1.0 mg/dl, VDRA use was associated with a low incidence of CVD (HR 0.47). &lt;b&gt;&lt;i&gt;Conclusion:&lt;/i&gt;&lt;/b&gt; Administration of VDRA during predialysis was associated with a low incidence of CVD onset after dialysis initiation.</jats:p

Presence of Atrial Fibrillation at the Time of Dialysis Initiation Is Associated with Mortality and Cardiovascular Events

&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Death in dialysis patients results mainly from cardiovascular and cerebrovascular diseases. To our knowledge, no prospective study has compared the rates of mortality or cardiovascular events between patients with and without atrial fibrillation (AF) at the time of dialysis initiation. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; This study included 1,516 patients who were initiated into dialysis between October 2011 and August 2013. Rates of mortality and cardiovascular events were compared between patients with and without AF, and between AF patients with and without warfarin (WF) treatment. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; The study comprised 1,025 men and 491 women with a mean age of 67.5 ± 13.1. Of these patients, 93 had AF, while 1,423 did not; 22.6% of the former group and 9.7% of the latter group died by March 2014 (p &lt; 0.01). Cardiovascular events occurred in 34.4% of patients with AF and 15.1% of patients without (p &lt; 0.01). Even after adjustments for various factors, AF remained an independent risk factor for mortality (hazard ratio (HR) 1.873, 95% CI 1.168-3.002, p &lt; 0.01). It was also an independent risk factor for cardiovascular events (HR 1.872, 95% CI 1.262-2.778, p &lt; 0.01). No difference in any parameter was noted between the groups that did and did not receive WF treatment. &lt;b&gt;&lt;i&gt;Conclusion:&lt;/i&gt;&lt;/b&gt; Patients with AF at the time of dialysis initiation show a poor prognosis and are at high risk of cardiovascular events. Therefore, AF should be taken into consideration in dialysis patients.</jats:p

Production and release of polyphosphate by a genetically engineered strain of Escherichia coli

A recombinant strain of Escherichia coli MV1184, which contains plasmid-borne genes encoding the phosphate-specific transport (Pst) system and polyphosphate (polyP) kinase, accumulated high levels of Pi and released polyP into the medium. PolyP could be separated from the culture supernatant by DEAE-Toyopearl 650M chromatography and identified by high-resolution 31P nuclear magnetic resonance spectroscopy. Once E. coli recombinants accumulated high levels of polyP, they released polyP concomitantly with Pi uptake. PolyP release did not accompany the decrease in the cell density, indicating that it is not simply a result of cell lysis. PolyP release ceased when Pi became depleted in the medium and resumed upon addition of Pi to the medium. When Pi uptake was inhibited by 0.1 mM carbonyl cyanide m-chlorophenylhydrazone (CCCP), no polyP release was observed. Furthermore, neither Pi uptake nor polyP release occurred when cells were incubated at 4 degrees C. These findings suggest that the occurrence of polyP release is a possible mechanism that limits a further increase in the cellular polyP concentration in E. coli recombinants. High-resolution 31P nuclear magnetic resonance spectroscopy also detected a surface pool of polyP in intact cells of the E. coli recombinant. The polyP resonance increased when cells were treated with EDTA and broadened upon the addition of a shift reagent, praseodymium. Although the mechanism of surface polyP accumulation is unclear, surface polyP seems to serve as the source for polyP release.</jats:p