ABC | Volume 112, Nº5, May 2019

Review Article Amorim et al Kidney disease in diabetes Arq Bras Cardiol. 2019; 112(5):577-587 Conclusion Recently, there has been increasing evidence that redox imbalance and inflammation in response to intermittent or chronic exposure to hyperglycemia play an important role in initiation and perpetuation of DMcomplications, including DKD. They are now considered the main contributors to the development of DKD and end-stage kidney disease. Newpathological pathways, associated with renal dysfunction in DM and that particularly exacerbate metabolic pathways, have been identified, such as the association betweenDKD and obesity. Therefore, metabolic, inflammatory and oxidative interference of DM and other risk factors for DKD should be continuously investigated and updated not only to improve the understanding of the mechanisms, but also to determine new therapeutic targets. Acknowledgment The present work was carried out with the support of the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES) - Financing Code 001. Figure 3 – Mediators of kidney injury induced by chronic hyperglycemia via redox imbalance and inflammation in the pathogenesis of diabetic kidney disease. ROS: reactive oxygen species; ERK: extracellular signal-related kinases; TNF- α : tumor necrosis factor alpha; NF- κ B: nuclear factor-kappa B; VEGF: the vascular endothelial growth factor; IL-1: interleukin 1; IL-6: interleukin 6; IL-18: interleukin 18; ECM: extracellular matrix; NOX: NADPH oxidase; - O-GLaNAc: O-glycosylated into N-acetylglucosamine; PAI-1: plasminogen activator inhibitor-1; AGE: advanced glycation end-products; PKC: protein kinase C; MCP-1: monocyte chemotactic protein-1; RPGA: receptor for advanced glycation end products; RAAS: renin-angiotensin aldosterone system; TGF- β : transforming growth factor-beta. EXTRACELLUAR MATRIX INTRACELLULAR GLOMERULAR HYPERTROPHY MESANGIAL EXPANSION RENAL INFLAMMATION DRD GLOMERULOSCLEROSIS RENAL FIBROSIS INFLAMMATION OBESITY DM HYPERGLYCEMIA AGE RAGE NOX PKC O 2 POLYOL HEXOSAMINE AUTO-OXIDATION REDOX IMBALANCE TNF- α IL-1 IL-6 IL-18 MCP-1 NF- κ B AGEs NADPH ROS TGF- β PKC- α and β – O-GLaNAc RAAS TGF- β ENDOTHELINS TGF- β VEGF PAI-1 COLLAGEN INFLAMMATORY METABOLIC HEMODYNAMIC FIBROTIC Author contributions Conception and design of the research: Santos JCF, Amorim RG, Vasconcelos S; Writing of the manuscript and Critical revision of the manuscript for intellectual content: Santos JCF, Amorim RG, Guedes GS, Vasconcelos S. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding There were no external funding sources for this study. Study Association This article is part of the thesis of master submitted by Rayne Gomes Amorim, from Pós-graduação em Nutrição da Universidade Federal de Alagoas. 584