1,721,279 research outputs found
Pathogenetic mechanisms of diabetic nephropathy
No full textDiabetes is the leading cause of ESRD because diabetic nephropathy develops in 30 to 40% of patients. Diabetic nephropathy
does not develop in the absence of hyperglycemia, even in the presence of a genetic predisposition. Multigenetic predisposition
contributes in the development of diabetic nephropathy, thus supporting that many factors are involved in the
pathogenesis of the disease. Hyperglycemia induces renal damage directly or through hemodynamic modifications. It induces
activation of protein kinase C, increased production of advanced glycosylation end products, and diacylglycerol synthesis. In
addition, it is responsible for hemodynamic alterations such as glomerular hyperfiltration, shear stress, and microalbuminuria.
These alterations contribute to an abnormal stimulation of resident renal cells that produce more TGF-1. This growth factor
upregulates GLUT-1, which induces an increased intracellular glucose transport and D-glucose uptake. TGF-1 causes
augmented extracellular matrix protein deposition (collagen types I, IV, V, and VI; fibronectin, and laminin) at the glomerular
level, thus inducing mesangial expansion and glomerular basement membrane thickening. However, low enzymatic degradation
of extracellular matrix contributes to an excessive accumulation. Because hyperglycemia is the principal factor
responsible for structural alterations at the renal level, glycemic control remains the main target of the therapy, whereas
pancreas transplantation is the best approach for reducing the renal lesions
An "evidence-based" survey of therapeutic options for IgA nephropathy: assessment and criticism
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Il quesito eziologico in nefrologia: modelli di studio ed obiettivi della futura ricerca clinica
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Valutazione critica di una review sistematica nefrologica: concetti teorici ed esempi pratici per la lettura del principale modello di evidenza
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