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      Alcohol Consumption Can be a “Double-Edged Sword” for Chronic Kidney Disease Patients

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          Abstract

          Excessive drinking of alcohol is becoming a worldwide problem, and people have recognized that there exists a close relationship between chronic kidney disease (CKD) and alcohol consumption. However, there are many inconsistencies between experimental and clinical studies on alcohol consumption and kidney damage. The possible reason for this contradictory conclusion is the complex drinking pattern of humans and some bioactivators in wine. In addition, the design itself of the clinical studies can also produce conflicting interpretations of the results. Considering the benefits of light-to-moderate alcohol consumption, we recommend that CKD patients continue light-to-moderate drinking, which is beneficial to them. Because alcohol consumption can lead to adverse events, we do not advise non-drinkers to start to drink. Although light-to-moderate alcohol consumption may not pose a risk to patients with CKD, the patients’ condition needs to be considered. Consumption of even small amounts of alcohol can be associated with increased death risk. Additional clinical and experimental studies are needed to clarify the effect of alcohol on the kidneys and alcohol consumption on CKD patients.

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          Most cited references115

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          Evidence that chronic alcohol exposure promotes intestinal oxidative stress, intestinal hyperpermeability and endotoxemia prior to development of alcoholic steatohepatitis in rats.

          Not all alcoholics develop liver disease (ALD). Thus, excessive ethanol consumption is necessary, but not sufficient, to induce alcoholic steatohepatitis (ASH) and ALD. Since endotoxemia is present in patients with ALD, it has been proposed that gut-derived, circulating endotoxin is the necessary co-factor for ASH. But, it is not known whether endotoxemia is the consequence or the trigger for ALD. Accordingly, the aim of the current study was to determine whether endotoxemia occurs prior to development of ASH and whether gut leakiness is the primary cause of the endotoxemia in an animal model of ASH. Time courses for development of gut hyperpermeability, nitric oxide production, oxidative injury to the gut, endotoxemia, and liver injury were assessed in rats during 10 weeks of daily alcohol gavage. Liver fat and serum transaminase increased after 2 weeks, but evidence of liver cell injury and inflammation (ASH) occurred after 8 weeks. Gut leakiness, intestinal oxidative injury, and endotoxemia occurred in weeks 2-4 and progressed thereafter. That alcohol-induced gut leakiness and endotoxemia preceded steatohepatitis indicates they are not the consequence of ALD. Our data support the hypothesis that gut leakiness resulting in endotoxemia is a key co-factor (trigger) for ASH.
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            Serum creatinine and renal function.

            Serum creatinine is widely interpreted as a measure only of renal function; however, the serum level reflects not only renal excretion, but also the generation, intake, and metabolism of creatinine. In this review, we demonstrate that serum creatinine does not provide an adequate estimate of glomerular filtration rate (GFR), and contrary to recent teachings, that the slope of the reciprocal of serum creatinine vs time does not permit an accurate assessment of the rate of progression of renal disease. In clinical investigation, it is essential to utilize more accurate and sensitive measures of renal function to estimate GFR and progression. As effective treatments for progressive renal diseases are discovered, it will also be necessary to employ these measurements in clinical practice.
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              Induction of Oxidative Stress in Kidney

              Emin Ozbek (2012)
              Oxidative stress has a critical role in the pathophysiology of several kidney diseases, and many complications of these diseases are mediated by oxidative stress, oxidative stress-related mediators, and inflammation. Several systemic diseases such as hypertension, diabetes mellitus, and hypercholesterolemia; infection; antibiotics, chemotherapeutics, and radiocontrast agents; and environmental toxins, occupational chemicals, radiation, smoking, as well as alcohol consumption induce oxidative stress in kidney. We searched the literature using PubMed, MEDLINE, and Google scholar with “oxidative stress, reactive oxygen species, oxygen free radicals, kidney, renal injury, nephropathy, nephrotoxicity, and induction”. The literature search included only articles written in English language. Letters or case reports were excluded. Scientific relevance, for clinical studies target populations, and study design, for basic science studies full coverage of main topics, are eligibility criteria for articles used in this paper.
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                Author and article information

                Journal
                Med Sci Monit
                Med. Sci. Monit
                Medical Science Monitor
                Medical Science Monitor : International Medical Journal of Experimental and Clinical Research
                International Scientific Literature, Inc.
                1234-1010
                1643-3750
                2019
                20 September 2019
                : 25
                : 7059-7072
                Affiliations
                [1 ]Graduate School of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, P.R. China
                [2 ]First Clinic School of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, P.R. China
                Author notes
                Corresponding Authords: Zhenliang Fan, e-mail: fanmlov@ 123456sina.cn , Liqun Song, e-mail: qunli@ 123456sina.com
                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                Article
                916121
                10.12659/MSM.916121
                6767945
                31538630
                cd2b105d-a677-4d4d-b9a6-1373ed9ea5a7
                © Med Sci Monit, 2019

                This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International ( CC BY-NC-ND 4.0)

                History
                : 09 March 2019
                : 01 June 2019
                Categories
                Review Articles

                alcohol drinking,drinking behavior,polyphenols,reactive oxygen species,renal insufficiency, chronic

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