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Study of markers of nephropathy in adult rats with low weight at birth


Since the beginning of the twentieth century authors such as Barker have proposed explanations for the fetal origin of coronary heart disease in adulthood, which has received support from researchers such as Brenner. He described the association between the systemic hypertension and the reduced number of nephrons caused by low weight at birth or prematurity. These may be responsible for hypertension and for the presence of early markers of vascular injury such as microalbuminuria, resulting from increased clearance per nephron in kidneys with less renal mass. This increase in the clearance maintains renal filtration at normal levels, but with less renal functional reserve which is defined as the increase in glomerular filtration in response to the infusion of amino acids. The evaluation of renal functional reserve indirectly shows the acute and chronic injury as in the case of hypertension, diabetes and obesity. In order to study the influence of low weight at birth in the onset of markers to nephropathy and renal functional reserve, rats will be submitted to the condition of low birth weight induced by maternal malnutrition and analyzed for hypertension, kidney capacity to increase the glomerular filtration rate through stimulation with the infusion of L-Arginine (renal functional reserve), kidney blood flow and microalbuminuria in two stages of adulthood, at 70 and 90 days. The glomerular filtration will be measured by the clearance of inulin. The animals will be submitted to nephrectomy for the counting glomerulii, glomerular volume and histological analysis. The results will be discussed with parameters of literature and we hope to conclude positively in relation to the initial hypothesis. (AU)

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