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Journal of Diabetes Research
Volume 2016, Article ID 7047238, 7 pages
Review Article

Oxidative Stress in Diabetic Nephropathy with Early Chronic Kidney Disease

1Department of Physiology, University Health Sciences Centre (Centro Universitario de Ciencias de la Salud), University of Guadalajara, 44150 Guadalajara, JAL, Mexico
2Nephrology Service, Civil Hospital of Guadalajara “Dr. Juan I. Menchaca”, Guadalajara, JAL, Mexico

Received 6 April 2016; Accepted 9 May 2016

Academic Editor: Konstantinos Papatheodorou

Copyright © 2016 Alejandra Guillermina Miranda-Díaz et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The increase in the prevalence of diabetes mellitus (DM) and the secondary kidney damage produces diabetic nephropathy (DN). Early nephropathy is defined as the presence of microalbuminuria (30–300 mg/day), including normal glomerular filtration rate (GFR) or a mildly decreased GFR (60–89 mL/min/1.73 m2), with or without overt nephropathy. The earliest change caused by DN is hyperfiltration with proteinuria. The acceptable excretion rate of albumin in urine is <30 mg/day. Albuminuria represents the excretion of >300 mg/day. Chronic kidney disease (CKD) is characterized by abnormalities in renal function that persist for >3 months with health implications. Alterations in the redox state in DN are caused by the persistent state of hyperglycemia and the increase in advanced glycation end products (AGEs) with ability to affect the renin-angiotensin system and the transforming growth factor-beta (TGF-β), producing chronic inflammation and glomerular and tubular hypertrophy and favoring the appearance of oxidative stress. In DN imbalance between prooxidant/antioxidant processes exists with an increase in reactive oxygen species (ROS). The overproduction of ROS diminishes expression of the antioxidant enzymes (manganese superoxide dismutase, glutathione peroxidase, and catalase). The early detection of CKD secondary to DN and the timely identification of patients would permit decreasing its impact on health.