title: [Renal disease in diabetics. Immunological bases of tubule-interstitial fibrosis and glomeruloesclerosis. Current therapeutic approach].
abstract: Susceptibility of kidney to become target of the immunological aggression is easily recognizable when we consider the high number of diseases that, with a pathogenesis explained by autoimmunity mechanisms, have the kidney as a target organ. In diabetes mellitus, hyperglycemic state stimulates different molecular factors conditioning tubule-interstitial fibrosis and glomerulosclerosis, among them the most important are: formation of products of advanced glycation; activation of protein kinase C, activation of the angiotensin II and the activation of the nuclear factor kappaB. These factors are closely related to the production of inflammatory cytokines and to the progression of renal damage. This paper reviews the role of these factors in the renal damage of diabetic patients and the effect of some drugs on the progression of the immunological damage.
authors.affiliation: Facultad de Medicina Dr Ignacio Chavez, Universidad Michoacana San Nicolas de Hidalgo. arorozco@hotmail.com
authors.forename: Alain R Rodríguez
authors.initials: AR
authors.lastname: Orozco
authors.forename: Rafael Leyva
authors.initials: RL
authors.lastname: Jiménez
authors.forename: Alvarez Cleto
authors.initials: AC
authors.lastname: Aguilar
authors.forename: Martha Cortés
authors.initials: MC
authors.lastname: Arredondo
authors.forename: Victor M Farías
authors.initials: VM
authors.lastname: Rodríguez
mesh_terms: D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D000954:Antigens, Surface; D015815:Cell Adhesion Molecules / Q000276:immunology; D003928:Diabetic Nephropathies / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D018450:Disease Progression; D005355:Fibrosis; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D008562:Membrane Glycoproteins / Q000276:immunology; D016328:NF-kappa B / Q000502:physiology; D009395:Nephritis, Interstitial / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D011493:Protein Kinase C / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D000954:Antigens, Surface; D015815:Cell Adhesion Molecules; D017127:Glycation End Products, Advanced; D008562:Membrane Glycoproteins; D016328:NF-kappa B; C085434:TINAG protein, human; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D000804:Angiotensin II; D011493:Protein Kinase C