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      Impact of blood urea nitrogen to creatinine ratio on mortality and morbidity in hemodialysis patients: The Q-Cohort Study

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          Abstract

          The association between blood urea nitrogen to creatinine ratio (UCR) and survival is uncertain in hemodialysis patients. We examined the influence of UCR on mortality and morbidity in hemodialysis patients. A total of 3,401 hemodialysis patients were prospectively followed for 4 years. The association between UCR with overall survival was analyzed using a Cox regression model. During a 4-year follow-up period, 545 patients died from any cause and 582 experienced MACE, 392 with coronary heart disease (CHD), 114 with infection-related death, 77 with hemorrhagic stroke, 141 with ischemic stroke, and 107 with cancer death. Every 1 increase in UCR level was significantly associated with an increased risk for all-cause mortality (hazard ratio [HR] 1.07; 95% confidence interval [CI] 1.03–1.12), CHD (HR 1.08; 95% CI 1.02–1.14), and infection-related death (HR 1.11; 95% CI 1.02–1.21). There was no evidence of a significant association between UCR and death from cancer, and incidence of stroke. A high UCR was significantly associated with an increased risk for all-cause mortality, infection-related death and incidence of CHD in hemodialysis patients.

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          Strong association between malnutrition, inflammation, and atherosclerosis in chronic renal failure.

          P Stenvinkel, O Heimbürger, F Paultre … (1999)
          Atherosclerotic cardiovascular disease and malnutrition are widely recognized as leading causes of the increased morbidity and mortality observed in uremic patients. C-reactive protein (CRP), an acute-phase protein, is a predictor of cardiovascular mortality in nonrenal patient populations. In chronic renal failure (CRF), the prevalence of an acute-phase response has been associated with an increased mortality. One hundred and nine predialysis patients (age 52 +/- 1 years) with terminal CRF (glomerular filtration rate 7 +/- 1 ml/min) were studied. By using noninvasive B-mode ultrasonography, the cross-sectional carotid intima-media area was calculated, and the presence or absence of carotid plaques was determined. Nutritional status was assessed by subjective global assessment (SGA), dual-energy x-ray absorptiometry (DXA), serum albumin, serum creatinine, serum urea, and 24-hour urine urea excretion. The presence of an inflammatory reaction was assessed by CRP, fibrinogen (N = 46), and tumor necrosis factor-alpha (TNF-alpha; N = 87). Lipid parameters, including Lp(a) and apo(a)-isoforms, as well as markers of oxidative stress (autoantibodies against oxidized low-density lipoprotein and vitamin E), were also determined. Compared with healthy controls, CRF patients had an increased mean carotid intima-media area (18.3 +/- 0.6 vs. 13.2 +/- 0.7 mm2, P or = 10 mg/liter). Malnourished patients had higher CRP levels (23 +/- 3 vs. 13 +/- 2 mg/liter, P < 0.01), elevated calculated intima-media area (20.2 +/- 0.8 vs. 16.9 +/- 0.7 mm2, P < 0.01) and a higher prevalence of carotid plaques (90 vs. 60%, P < 0.0001) compared with well-nourished patients. During stepwise multivariate analysis adjusting for age and gender, vitamin E (P < 0.05) and CRP (P < 0.05) remained associated with an increased intima-media area. The presence of carotid plaques was significantly associated with age (P < 0.001), log oxidized low-density lipoprotein (oxLDL; P < 0.01), and small apo(a) isoform size (P < 0.05) in a multivariate logistic regression model. These results indicate that the rapidly developing atherosclerosis in advanced CRF appears to be caused by a synergism of different mechanisms, such as malnutrition, inflammation, oxidative stress, and genetic components. Apart from classic risk factors, low vitamin E levels and elevated CRP levels are associated with an increased intima-media area, whereas small molecular weight apo(a) isoforms and increased levels of oxLDL are associated with the presence of carotid plaques.
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            Hemodynamic shear stress and its role in atherosclerosis.

            Adel Malek (1999)
            Atherosclerosis, the leading cause of death in the developed world and nearly the leading cause in the developing world, is associated with systemic risk factors including hypertension, smoking, hyperlipidemia, and diabetes mellitus, among others. Nonetheless, atherosclerosis remains a geometrically focal disease, preferentially affecting the outer edges of vessel bifurcations. In these predisposed areas, hemodynamic shear stress, the frictional force acting on the endothelial cell surface as a result of blood flow, is weaker than in protected regions. Studies have identified hemodynamic shear stress as an important determinant of endothelial function and phenotype. Arterial-level shear stress (>15 dyne/cm2) induces endothelial quiescence and an atheroprotective gene expression profile, while low shear stress (<4 dyne/cm2), which is prevalent at atherosclerosis-prone sites, stimulates an atherogenic phenotype. The functional regulation of the endothelium by local hemodynamic shear stress provides a model for understanding the focal propensity of atherosclerosis in the setting of systemic factors and may help guide future therapeutic strategies.
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              Malnutrition-inflammation complex syndrome in dialysis patients: causes and consequences.

              Kamyar Kalantar-Zadeh, T.Alp Ikizler, Gladys Block … (2003)
              Protein-energy malnutrition (PEM) and inflammation are common and usually concurrent in maintenance dialysis patients. Many factors that appear to lead to these 2 conditions overlap, as do assessment tools and such criteria for detecting them as hypoalbuminemia. Both these conditions are related to poor dialysis outcome. Low appetite and a hypercatabolic state are among common features. PEM in dialysis patients has been suggested to be secondary to inflammation; however, the evidence is not conclusive, and an equicausal status or even opposite causal direction is possible. Hence, malnutrition-inflammation complex syndrome (MICS) is an appropriate term. Possible causes of MICS include comorbid illnesses, oxidative and carbonyl stress, nutrient loss through dialysis, anorexia and low nutrient intake, uremic toxins, decreased clearance of inflammatory cytokines, volume overload, and dialysis-related factors. MICS is believed to be the main cause of erythropoietin hyporesponsiveness, high rate of cardiovascular atherosclerotic disease, decreased quality of life, and increased mortality and hospitalization in dialysis patients. Because MICS leads to a low body mass index, hypocholesterolemia, hypocreatininemia, and hypohomocysteinemia, a "reverse epidemiology" of cardiovascular risks can occur in dialysis patients. Therefore, obesity, hypercholesterolemia, and increased blood levels of creatinine and homocysteine appear to be protective and paradoxically associated with a better outcome. There is no consensus about how to determine the degree of severity of MICS or how to manage it. Several diagnostic tools and treatment modalities are discussed. Successful management of MICS may ameliorate the cardiovascular epidemic and poor outcome in dialysis patients. Clinical trials focusing on MICS and its possible causes and consequences are urgently required to improve poor clinical outcome in dialysis patients.
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                Author and article information

                Contributors
                Kazuhiko Tsuruya: tsuruya@intmed2.med.kyushu-u.ac.jp
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 2 November 2017
                Publication date PMC-release: 2 November 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 14901
                Affiliations
                [1 ]ISNI 0000 0000 9611 5902, GRID grid.418046.f, Division of Internal Medicine, Fukuoka Dental College, ; Fukuoka, Japan
                [2 ]ISNI 0000 0001 2242 4849, GRID grid.177174.3, Department of Epidemiology and Public Health, , Graduate School of Medical Sciences, Kyushu University, ; Fukuoka, Japan
                [3 ]Fukuoka Renal Clinic, Fukuoka, Japan
                [4 ]ISNI 0000 0001 2242 4849, GRID grid.177174.3, Department of Medicine and Clinical Science, , Graduate School of Medical Sciences, Kyushu University, ; Fukuoka, Japan
                [5 ]ISNI 0000 0001 2242 4849, GRID grid.177174.3, Department of Integrated Therapy for Chronic Kidney Disease, , Graduate School of Medical Sciences, Kyushu University, ; Fukuoka, Japan
                Author information
                http://orcid.org/0000-0002-4808-6689
                Article
                Publisher ID: 14205
                DOI: 10.1038/s41598-017-14205-2
                PMC ID: 5668292
                PubMed ID: 29097750
                SO-VID: 9e8f60a4-a1bf-45b1-91fd-0793a8f5dc01
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 12 June 2017
                Date accepted : 2 October 2017
                Categories
                Subject: Article
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                issue-copyright-statement © The Author(s) 2017

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