Renal disease in diabetics. Immunological bases of tubule-interstitial fibrosis and glomeruloesclerosis. Current therapeutic approach

• Published in: Revista alergia Mexico (Tecamachalco, Pueblo, Mexico : 1993) Vol. 51; no. 4; pp. 155 - 161
• Main Authors: Orozco, Alain R Rodríguez, Jiménez, Rafael Leyva, Aguilar, Alvarez Cleto, Arredondo, Martha Cortés, Rodríguez, Victor M Farías
• Format: Journal Article
• Language: Spanish
• Published: Mexico 01-07-2004
• Subjects: Angiotensin II - physiology; Animals; Antigens, Surface; Cell Adhesion Molecules - immunology; Diabetic Nephropathies - immunology; Diabetic Nephropathies - pathology; Diabetic Nephropathies - therapy; Disease Progression; Fibrosis; Glycation End Products, Advanced - metabolism; Humans; Membrane Glycoproteins - immunology; Nephritis, Interstitial - immunology; Nephritis, Interstitial - pathology; Nephritis, Interstitial - therapy; NF-kappa B - physiology; Protein Kinase C - physiology; Transforming Growth Factor beta - physiology; Tumor Necrosis Factor-alpha - physiology
• ISSN: 0002-5151

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.