Revista de Nefrología, Diálisis y Trasplante (Dec 2014)
Pathophysiology of glomerular hyperfiltration in diabetes. Part II
Abstract
Glomerular hyperfiltration (GH) in diabetic renal disease is a complex hemodynamic phenomenon that occurs early in the course of the disease and most likely has associated with poor prognosis with respect to the development of microalbuminuria and overt diabetic nephropathy. The factors involved in its pathophysiology are multiple and include the diabetic milieu and the effects of several humoral factors such as nitric oxide, prostaglandins, renin angiotensin aldosterone system, atrial natriuretic peptide, reactive oxygen species and other humoral and growth factors that act basically causing or enhancing the afferent arteriole vasodilation (AA) or vasoconstriction over the efferent arteriola, all considered primary vascular factors. However, these factors could not entirely explain other observed abnormalities that include primary tubular abnormalities such as increased reabsorption in the proximal tubule probably influenced by renal growth and cotransporter SGLT2 upregulation. This increased proximal reabsorption elicit a lower solute delivery to the dense macula, which would be incompatible with glomerulotubular balance function, but would with actions mediated by tubuloglomerular feedback (TGF) that would sense low NaCl concentration at the MD, deactivating TGF and producing AA vasodilation, thereby increasing the glomerular filtration rate (GFR) and renal plasma flow (RPF), characteristic of the GH process.
