PHYSIOPATHOLOGY OF DIABETIC KIDNEY DISEASE

• Published in: Revista de la Sociedad Argentina de Diabetes Vol. 51; no. 3; pp. 69 - 76
• Main Author: Fabiana Vázquez
• Format: Journal Article
• Language: Spanish
• Published: Sello Editorial Lugones 01-08-2018
• Subjects: aumento de la presión intraglomerular; enfermedad renal por diabetes; feedback túbulo-glomerular; hiperglucemia, podocitos; sglt-1; sglt-2
• ISSN: 0325-5247; 2346-9420
• DOI: 10.47196/diab.v51i3.101

Kidney disease caused by diabetes is a microvascular compli- cation in which hemodynamic, metabolic changes, oxidative stress and inflammation increase occur in the kidneys. This determines an increase of the mesangial extracellular matrix, basement membrane thickness, loss of podocyte foot and tubu- lar cells disruption with fibrosis and proteinuria. The increase of receptors SGLT-1 and SGLT-2 expression, with the resulting and marked reduction of Na+ offer to the macula densa is wrongly construed as a reduction of plasmatic volume by the yuxta-glo- merular complex through the “tubuloglomerular feedback”, ge- nerating vasodilation of the afferent arterioles and the resulting increase in intraglomerular pressure. This changes the classical glomerular concept, interpreting that there may be an initial le- sion at the tubular level.