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Int. J. Mol. Sci. 2016, 17(11), 1826; doi:10.3390/ijms17111826

Role of Oxidative Stress in Drug-Induced Kidney Injury

Education and Reseearch Center for Clinical Pharmacy, Osaka University of Pharmaceutical Sciences, Osaka 569-1094, Japan
Academic Editor: Satohiro Masuda
Received: 1 September 2016 / Revised: 11 October 2016 / Accepted: 18 October 2016 / Published: 1 November 2016
(This article belongs to the Special Issue Biomarkers in Drug-Induced Organ Injury)
View Full-Text   |   Download PDF [715 KB, uploaded 1 November 2016]   |  

Abstract

The kidney plays a primary role in maintaining homeostasis and detoxification of numerous hydrophilic xenobiotics as well as endogenous compounds. Because the kidney is exposed to a larger proportion and higher concentration of drugs and toxins than other organs through the secretion of ionic drugs by tubular organic ion transporters across the luminal membranes of renal tubular epithelial cells, and through the reabsorption of filtered toxins into the lumen of the tubule, these cells are at greater risk for injury. In fact, drug-induced kidney injury is a serious problem in clinical practice and accounts for roughly 20% of cases of acute kidney injury (AKI) among hospitalized patients. Therefore, its early detection is becoming more important. Usually, drug-induced AKI consists of two patterns of renal injury: acute tubular necrosis (ATN) and acute interstitial nephritis (AIN). Whereas AIN develops from medications that incite an allergic reaction, ATN develops from direct toxicity on tubular epithelial cells. Among several cellular mechanisms underlying ATN, oxidative stress plays an important role in progression to ATN by activation of inflammatory response via proinflammatory cytokine release and inflammatory cell accumulation in tissues. This review provides an overview of drugs associated with AKI, the role of oxidative stress in drug-induced AKI, and a biomarker for drug-induced AKI focusing on oxidative stress. View Full-Text
Keywords: acute kidney injury; acute interstitial nephritis; acute tubular necrosis; oxidative stress; early biomaker; vanin-1 acute kidney injury; acute interstitial nephritis; acute tubular necrosis; oxidative stress; early biomaker; vanin-1
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Hosohata, K. Role of Oxidative Stress in Drug-Induced Kidney Injury. Int. J. Mol. Sci. 2016, 17, 1826.

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