Zoltan V Varga, Csaba Matyas, Janos Paloczi, Pal Pacher
{"title":"Alcohol Misuse and Kidney Injury: Epidemiological Evidence and Potential Mechanisms.","authors":"Zoltan V Varga, Csaba Matyas, Janos Paloczi, Pal Pacher","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Chronic alcohol consumption is a well-known risk factor for tissue injury. The link between alcohol use disorder (AUD) and kidney injury is intriguing but controversial, and the molecular mechanisms by which alcohol may damage the kidneys are poorly understood. Epidemiological studies attempting to link AUD and kidney disease are, to date, inconclusive, and there is little experimental evidence directly linking alcohol consumption to kidney injury. However, studies conducted primarily in other organs and tissues suggest several possible mechanisms by which alcohol may promote kidney dysfunction. One possible mechanism is oxidative stress resulting from increased production of reactive oxygen species, which leads to an excessive amount of free radicals, which in turn trigger tissue injury and increase inflammation. In addition, AUD's effect on other major organs (liver, heart, intestines, and skeletal muscle) appears to promote unfavorable pathological processes that are harmful to the kidneys. Notably, these mechanisms have not yet been validated experimentally in the kidney. Additional research is needed to clarify if alcohol does indeed promote kidney injury and the mechanisms by which alcohol-induced kidney injury may occur.</p>","PeriodicalId":7736,"journal":{"name":"Alcohol Research : Current Reviews","volume":" ","pages":"283-288"},"PeriodicalIF":9.0000,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513691/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Alcohol Research : Current Reviews","FirstCategoryId":"3","ListUrlMain":"","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"SUBSTANCE ABUSE","Score":null,"Total":0}
引用次数: 0
Abstract
Chronic alcohol consumption is a well-known risk factor for tissue injury. The link between alcohol use disorder (AUD) and kidney injury is intriguing but controversial, and the molecular mechanisms by which alcohol may damage the kidneys are poorly understood. Epidemiological studies attempting to link AUD and kidney disease are, to date, inconclusive, and there is little experimental evidence directly linking alcohol consumption to kidney injury. However, studies conducted primarily in other organs and tissues suggest several possible mechanisms by which alcohol may promote kidney dysfunction. One possible mechanism is oxidative stress resulting from increased production of reactive oxygen species, which leads to an excessive amount of free radicals, which in turn trigger tissue injury and increase inflammation. In addition, AUD's effect on other major organs (liver, heart, intestines, and skeletal muscle) appears to promote unfavorable pathological processes that are harmful to the kidneys. Notably, these mechanisms have not yet been validated experimentally in the kidney. Additional research is needed to clarify if alcohol does indeed promote kidney injury and the mechanisms by which alcohol-induced kidney injury may occur.
期刊介绍:
Alcohol Research: Current Reviews (ARCR) is an open-access, peer-reviewed journal published by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) at the National Institutes of Health. Starting from 2020, ARCR follows a continuous, rolling publication model, releasing one virtual issue per yearly volume. The journal offers free online access to its articles without subscription or pay-per-view fees. Readers can explore the content of the current volume, and past volumes are accessible in the journal's archive. ARCR's content, including previous titles, is indexed in PubMed, PsycINFO, Scopus, and Web of Science.