Copyright
©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Jun 15, 2014; 5(3): 393-398
Published online Jun 15, 2014. doi: 10.4239/wjd.v5.i3.393
Published online Jun 15, 2014. doi: 10.4239/wjd.v5.i3.393
Diabetic nephropathy and inflammation
Montserrat B Duran-Salgado, Alberto F Rubio-Guerra, Clinical Research Unit, Hospital General de Ticomán, Col Ticomán, DFCP 07330, México
Montserrat B Duran-Salgado, Alberto F Rubio-Guerra, Mexican Group for Basic and Clinical Research in Internal Medicine, Col Ticomán, DFCP 07330, México
Author contributions: All authors contributed equally to this work.
Correspondence to: Montserrat B Duran-Salgado, MD, Clinical Research Unit, Hospital General de Ticomán, Plan de San Luis S/N Esq Bandera, Col Ticomán, DFCP 07330, México. montserratdus@hotmail.com
Telephone: +52-555-7541390 Fax: +52-555-7541390
Received: December 5, 2013
Revised: February 11, 2014
Accepted: April 17, 2014
Published online: June 15, 2014
Revised: February 11, 2014
Accepted: April 17, 2014
Published online: June 15, 2014
Core Tip
Core tip: In recent years, new pathways involved in the development and progression of diabetic kidney disease have been elucidated; accumulated data have emphasized the critical role of inflammation in its pathogenesis. Expression of cell adhesion molecules, growth factors, chemokines and pro-inflammatory cytokines increased in renal tissues of diabetic patients, and serum and urinary levels of cytokines and cell adhesion molecules, correlated with albuminuria. We review the role of inflammation in the development of diabetic nephropathy, discussing some of the major inflammatory cytokines involved in its pathogenesis, including the role of adipokines, and other mediators of inflammation, as adhesion molecules.