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  • Ovid Technologies (Wolters Kluwer Health)  (2)
  • 1
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 80, No. 4 ( 2023-04)
    Abstract: There is paucity of information on the incidence, clinical characteristics, admission trends, and outcomes of hypertensive crisis (HTN-C) in patients with end-stage kidney disease (ESKD) who are on maintenance dialysis. Methods: We conducted a retrospective observational study of HTN-C admissions in patients with end-stage kidney disease using the United States Renal Data System. We identified patients with end-stage kidney disease aged ≥18 years on dialysis and were hospitalized for HTN-C from January 2006 to August 2015. Results: A total of 54 483 patients with end-stage kidney disease were hospitalized for HTN-C during the study period. After study exclusions, 37 214 patients were included in the analysis. A majority of patients were Black, there were more women than men and the South region of the country accounted for a great majority of patients. During the study period, hospitalization rates increased from 1060 per 100 000 beneficiary years to 1821 ( P trend 〈 0.0001). Overall, in-hospital mortality, 30-day, and 1-year mortality were 0.6%, 2.3%, and 21.8%, respectively, and 30-day readmission rate was 31.1%. During the study period, most study outcomes showed a significant decreasing trend (in-hospital mortality 0.6%–0.5%, 30-day mortality 2.4%–1.9%, 1-year mortality 23.9%–19.7%, P trend 〈 0.0001 for all). Conclusions: Hospitalizations for HTN-C have increased consistently during the decade studied. Although temporal trends showed improving mortality and readmission rates, the absolute rates were still high with 1 in 3 patients readmitted within 30 days and 1 in 5 patients dying within 1 year of index hospitalization.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2094210-2
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  • 2
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 87, No. 8 ( 2000-10-13), p. 656-662
    Abstract: Abstract —Electrical uncoupling at gap junctions during acute myocardial ischemia contributes to conduction abnormalities and reentrant arrhythmias. Increased levels of intracellular Ca 2+ and H + and accumulation of amphipathic lipid metabolites during ischemia promote uncoupling, but other mechanisms may play a role. We tested the hypothesis that uncoupling induced by acute ischemia is associated with changes in phosphorylation of the major cardiac gap junction protein, connexin43 (Cx43). Adult rat hearts perfused on a Langendorff apparatus were subjected to ischemia or ischemia/reperfusion. Changes in coupling were monitored by measuring whole-tissue resistance. Changes in the amount and distribution of phosphorylated and nonphosphorylated isoforms of Cx43 were measured by immunoblotting and confocal immunofluorescence microscopy using isoform-specific antibodies. In control hearts, virtually all Cx43 identified immunohistochemically at apparent intercellular junctions was phosphorylated. During ischemia, however, Cx43 underwent progressive dephosphorylation with a time course similar to that of electrical uncoupling. The total amount of Cx43 did not change, but progressive reduction in total Cx43 immunofluorescent signal and concomitant accumulation of nonphosphorylated Cx43 signal occurred at sites of intercellular junctions. Functional recovery during reperfusion was associated with increased levels of phosphorylated Cx43. These observations suggest that uncoupling induced by ischemia is associated with dephosphorylation of Cx43, accumulation of nonphosphorylated Cx43 within gap junctions, and translocation of Cx43 from gap junctions into intracellular pools.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 1467838-X
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