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      Determinants of quality of life as measured with variants of SF-36 in patients with predialysis chronic kidney disease

      review-article
      , MPH, PhD Candidate, , FRCP, CCST, , BSc, PhD, , MSc, PhD, , MHSc, MMedStat, , MPH, PhD
      Saudi Medical Journal
      Saudi Medical Journal

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          Abstract

          Objectives:

          To determine the average health-related quality of life (HRQOL) score levels and their determinants in patients with predialysis chronic kidney disease (CKD).

          Methods:

          A systematic literature search was conducted for relevant observational studies published between April 2007 and April 2017 in MEDLINE, EBSCOhost, and CINAHL databases.

          Results:

          Thirteen observational studies with a total sample of 8635 subjects comprising 53.3% male with an aggregate mean age of 59.5 (SD 14.9) years were included in this review. Of the 8 generic HRQOL domains of the Short-Form Health Surveys, Social Functioning had the highest mean score whereas General Health had the lowest mean score in patients with predialysis CKD. Physical component summary (PCS) was more impaired than mental component summary (MCS). The determinants of poor HRQOL in predialysis CKD patients included both modifiable risk factors such as comorbidities (namely anxiety and depression), low serum hemoglobin level, sedentary lifestyle, unemployment and non-modifiable risk factors such as poor glomerular filtration rate, female gender, and older age. The risk factors impeded PCS more than MCS.

          Conclusion:

          Several risk factors influence HRQOL impairment in patients with predialysis CKD, with PCS being more impacted than MCS. The risk factors for poor HRQOL are important for future research and for improving renal care in patients with predialysis CKD.

          PROSPERO registration number: CRD42018093385

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          Most cited references26

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          Guidance for conducting systematic scoping reviews.

          Reviews of primary research are becoming more common as evidence-based practice gains recognition as the benchmark for care, and the number of, and access to, primary research sources has grown. One of the newer review types is the 'scoping review'. In general, scoping reviews are commonly used for 'reconnaissance' - to clarify working definitions and conceptual boundaries of a topic or field. Scoping reviews are therefore particularly useful when a body of literature has not yet been comprehensively reviewed, or exhibits a complex or heterogeneous nature not amenable to a more precise systematic review of the evidence. While scoping reviews may be conducted to determine the value and probable scope of a full systematic review, they may also be undertaken as exercises in and of themselves to summarize and disseminate research findings, to identify research gaps, and to make recommendations for the future research. This article briefly introduces the reader to scoping reviews, how they are different to systematic reviews, and why they might be conducted. The methodology and guidance for the conduct of systematic scoping reviews outlined below was developed by members of the Joanna Briggs Institute and members of five Joanna Briggs Collaborating Centres.
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            Leptin and renal disease.

            Leptin is a small peptide hormone that is mainly, but not exclusively, produced in adipose tissue. The circulating leptin concentration therefore directly reflects the amount of body fat. Leptin was identified through positional cloning of the obese (ob) gene, which is mutated in the massively obese ob/ob mouse, and it has a pivotal role in regulating food intake and energy expenditure. It binds to the so-called long receptor (Ob-Rb) in the hypothalamus and regulates food intake through the release of other neurotransmitters. Moreover, leptin exerts several other important metabolic effects on peripheral tissue, including modification of insulin action, induction of angiogenesis, and modulation of the immune system. As a small peptide, leptin is cleared principally by the kidney. Not surprisingly, serum leptin concentrations are increased in patients with chronic renal failure and those undergoing maintenance dialysis. Whether the hyperleptinemia of chronic renal failure contributes to some uremic manifestations, such as anorexia and weight loss, requires additional investigation. The kidney expresses abundant concentrations of the truncated isoform of the leptin receptor Ob-Ra, but only a small amount of the full-length receptor Ob-Rb. We recently discovered that leptin has direct effects on renal pathophysiological characteristics. Both cultured glomerular endothelial cells and mesangial cells obtained from the diabetic db/db mouse possess the Ob-Ra receptor, but whether biological effects of leptin are transduced through this receptor remains unknown. In glomerular endothelial cells, leptin stimulates cellular proliferation, transforming growth factor-beta1 (TGF-beta1) synthesis, and type IV collagen production. Conversely, in mesangial cells, leptin upregulates synthesis of the TGF-beta type II receptor, but not TGF-beta1, and stimulates glucose transport and type I collagen production through signal transduction pathways involving phosphatidylinositol-3-kinase. These data suggest that leptin triggers a paracrine interaction in which glomerular endothelial cells secrete TGF-beta, to which sensitized mesangial cells may respond. Both cell types increase their expression of extracellular matrix in response to leptin. Infusion of leptin into normal rats for 3 weeks fosters the development of focal glomerulosclerosis and proteinuria. Additional previously described direct and indirect effects of leptin on the kidney include natriuresis, increased sympathetic nervous activity, and stimulation of reactive oxygen species. These findings collectively suggest that the kidney is not only a site of leptin metabolism, but also a target organ for leptin action in pathophysiological states. Copyright 2002 by the National Kidney Foundation, Inc.
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              Interpreting SF-36 summary health measures: a response.

              In response to questions raised about the "accuracy" of SF-36 physical (PCS) and mental (MCS) component summary scores, particularly extremely high and low scores, we briefly comment on: how they were developed, how they are scored, the factor content of the eight SF-36 subscales, cross-tabulations between item-level responses and extreme summary scores, and published and new tests of their empirical validity. Published cross-tabulations between SF-36 items and PCS and MCS scores, reanalyses of public datasets (N = 5919), and preliminary results from the Medicare Health Outcomes Survey (HOS) (N = 172,314) yielded little or no evidence in support of Taft's hypothesis that extreme scores are an invalid artifact of some negative scoring weights. For example, in the HOS, those (N = 432) with "unexpected" PCS scores worse than 20 (which, according to Taft, indicate better mental health rather than worse physical health) were about 25% more likely to die within two years, in comparison with those scoring in the next highest (21-30) category. In this test and in all other empirical tests, results of predictions supported the validity of extreme PCS and MCS scores. We recommend against the interpretation of average differences smaller than one point in studies that seek to detect "false" measurement and we again repeat our 7-year-old recommendation that results based on summary measures should be thoroughly compared with the SF-36 profile before drawing conclusions. To facilitate such comparisons, scoring utilities and user-friendly graphs for SF-36 profiles and physical and mental summary scores (both orthogonal and oblique scoring algorithms) have been made available on the Internet at www.sf-36.com/test.
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                Author and article information

                Journal
                Saudi Med J
                Saudi Med J
                Saudi Medical Journal
                Saudi Medical Journal (Saudi Arabia )
                0379-5284
                July 2018
                : 39
                : 7
                : 653-661
                Affiliations
                [1] From the PAPRSB Institute of Health Sciences (Alhaji, Hamid, Naing, Tuah), Universiti Brunei Darussalam, from the Nephrology Unit (Tan), RIPAS Hospital, Bandar Seri Begawan, Brunei Darussalam, Brunei, from the Human Anatomy Department (Timbuak), Ahmadu Bello University Zaria, Kaduna, Nigeria, and from the Primary Care & Public Health Department (Tuah), Imperial College London, London, United Kingdom
                Author notes
                Address correspondence and reprint request to: Dr. Mohammed M. Alhaji, PAPRSB Institute of Health Sciences, Universiti Brunei Darussalam, Bandar Seri Begawan, Brunei Darussalam. E-mail: mohalhaj20@ 123456yahoo.com.sg ORCID ID: orcid.org/0000-0002-3383-2917
                Article
                SaudiMedJ-39-653
                10.15537/smj.2018.7.21352
                6146254
                29968886
                2733b248-d3a7-4ec5-8ffe-f9e92e535425
                Copyright: © Saudi Medical Journal

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 23 September 2017
                : 25 April 2018
                Categories
                Systematic Review

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