Interaction of haemodynamic and metabolic pathways in the genesis of diabetic nephropathy.
Clinical diabetic nephropathy is characterized by an earlier functional phase in which hyperglycaemia is accompanied by an increased glomerular filtration rate and microalbuminuria; the persistence of this high-flow and high-pressure state, added to a poor control of hyperglycaemia, fosters renal damage and proteinuria, accompanied by a decline in glomerular filtration rate and progression to end-stage renal disease. In this review, we present glucose transporter 1 (GLUT-1) as a novel link that connects the glomerular hyperfiltration (hypertension) state and the complex cascade of events that leads to nephropathy. The interplay between angiotensin II and nitric oxide, and its interactions with reactive oxygen species, are also discussed, in an attempt to provide an integrated view of the pathophysiology of diabetic nephropathy.
Leon
Carlos A
CA
Division of Nephrology and Hypertension, University of Miami School of Medicine, Nephrology-Hypertension Section, Veterans Affairs Medical Center, FL 33125, USA.
Raij
Leopoldo
L
D003928:Diabetic Nephropathies / Q000378:metabolism* / Q000503:physiopathology* / Q000628:therapy; D051272:Glucose Transporter Type 1 / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000378:metabolism
D051272:Glucose Transporter Type 1; D017382:Reactive Oxygen Species; D016212:Transforming Growth Factor beta; D009569:Nitric Oxide