4 research outputs found

    Clinical and patient-reported outcomes of Chinese patients undergoing haemodialysis in hospital or in the community: A 1-year longitudinal study

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    © 2015 The Authors Nephrology published by Wiley Publishing Asia Pty Ltd on behalf of Asian Pacific Society of Nephrology Aim: Little is known about the effect of haemodialysis (HD) setting on outcomes of patients with end stage renal disease (ESRD). The study aimed at comparing clinical outcomes and patient-reported outcomes (PRO) of patients on community-based (CBHD) and hospital-based haemodialysis (HBHD). Methods: A prospective cohort of Chinese ESRD patients receiving HBHD (n = 89) or CBHD (n = 117) in Hong Kong were followed up for 12 months. Subjects were assessed on clinical outcomes of dialysis adequacy (Kt/V) and blood haemoglobin and PRO of health-related quality of life (SF-12v2), general health condition (Global Rating Scale (GRS)) and confidence to cope with their illness (Patient Enablement Instrument (PEI)). Differences between groups were analyzed by independent t-tests for the SF-12v2, GRS and PEI scores. Ï 2 tests were used to analyze the difference in proportion of patients reaching the targets of Kt/V and blood haemoglobin and with GRS > 0 and PEI > 0. Multiple linear and logistic regressions were performed to assess the adjusted difference-in-difference estimation. Results: The mean PEI and GRS scores of CBHD patients at 12 months were significantly higher than those of HBHD patients. CBHD patients had significantly greater improvement in self-efficacy and were more likely to be enabled after 12 months than the HBHD patients. Conclusion: The study showed similar clinical outcomes and PRO between CBHD and HBHD but CBHD was more effective than HBHD in promoting patient enablement over a 12-month period. The results suggest added value for patients receiving CBHD and support the transfer of HD care from the hospital to the community.Link_to_subscribed_fulltex

    Validation of the Disease-Specific Components of the Kidney Disease Quality of Life-36 (KDQOL-36) in Chinese Patients Undergoing Maintenance Dialysis

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    AIM: The aim of this study was to evaluate the validity, reliability and sensitivity of the disease-specific items of the Kidney Disease Quality of Life-36 (KDQOL-36) in Chinese patients undergoing maintenance dialysis. METHODS: The content validity was assessed by content validity index (CVI) in ten subjects. 356 subjects were recruited for pilot psychometric testing. The internal construct validity was assessed by corrected item-subscale total correlation. Confirmatory factor analysis (CFA) was used to confirm the factor structure. The convergent validity was assessed by Pearson's correlation test between the disease specific subscale scores and SF-12 version 2 Health Survey (SF-12 v2) scores. The reliability was assessed by the internal consistency (Cronbach's Alpha coefficient) and 2-week test-retest reliability (intraclass correlation coefficient (ICC)). The sensitivity was determined by performing known group comparisons by independent t-test. RESULTS: The CVI on clarity and relevance was ⥠0.9 for all items. Corrected item- total correlation scores were â¥0.4 for all, except an item related to problems with access site. CFA confirmed the 3-factor structure of the disease-specific component of the KDQOL-36. The correlation coefficients between the disease-specific domain scores and the SF-12 v2 physical and mental component summary scores ranged from 0.328 to 0.492. The reliability was good (Cronbach's alpha coefficients ranged from 0.810 to 0.931, ICC ranged from 0.792 to 0.924). Only the effect subscale was sensitive in detecting differences in HRQOL between haemodialysis and peritoneal dialysis patients, with effect size = 0.68. CONCLUSION: The disease-specific items of the KDQOL-36 are a valid, reliable and sensitive measure to assess the health-related quality of life of Chinese patients on maintenance dialysis.Link_to_subscribed_fulltex

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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