Acta cirurgica brasileira · 2006
The number of podocyte and slit diaphragm is decreased in experimental diabetic nephropathy.
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Lerco Mauro Masson, Macedo Célia Sperandéo, Silva Reinaldo José, Pinheiro Daniela de Oliveira, Spadella César Tadeu
Аннотация
PURPOSE: To determine the number of podocyte, slit diaphragms, slit diaphragm extensions and GBM thickness in diabetic nephropathy.
METHODS: Sixty "Rattus Wistar"of both sexes weighing 200-300 g were divided in two experimental groups: normal group 10 animals, and alloxan diabetic rats--50 animals. Alloxan was administered in a single IV dose of 42 mg/kg body weight. Body weight, water and food intake, diuresis, and blood and urine glucose were determined in both groups before alloxan injection and two weeks, six and twelve months after alloxan injection. Proteinuria was measured at 12 months in both groups. After 12 months animals were sacrificed, and the right kidney processed for electron microscopy.
RESULTS: Clear clinical and laboratory signs of severe diabetes were seen, in all alloxan-diabetic rats at all follow-up times. Glomerular basement membrane (GBM) thickening, podocyte number, and slit diaphragm number and extension were determined. GBM of all diabetic rats was significantly thicker (median=0.29 microm; semi-interquartile range=0.065 microm) than in the normal rats (0.23 microm; 0.035 microm). Diabetic rat podocyte number (8; 1), slit diaphragm number (4; 1), and slit diaphragm extension (0.021 microm; 0.00435 microm) were significantly lower than in normal rats (11; 1) and (7; 1.5), and (0.031 microm; 0.0058 microm). Diabetic rat proteinuria (0.060 mg/24 h; 0.037 mg/24 h) was higher than in normal rats (0.00185 mg/24 h; 0.00055 mg/24 h).
CONCLUSION: Experimental diabetes is associated with significant (p<0.05) changes in podocyte foot process, slit number, slit diaphragm extension, and GBM thickness.
METHODS: Sixty "Rattus Wistar"of both sexes weighing 200-300 g were divided in two experimental groups: normal group 10 animals, and alloxan diabetic rats--50 animals. Alloxan was administered in a single IV dose of 42 mg/kg body weight. Body weight, water and food intake, diuresis, and blood and urine glucose were determined in both groups before alloxan injection and two weeks, six and twelve months after alloxan injection. Proteinuria was measured at 12 months in both groups. After 12 months animals were sacrificed, and the right kidney processed for electron microscopy.
RESULTS: Clear clinical and laboratory signs of severe diabetes were seen, in all alloxan-diabetic rats at all follow-up times. Glomerular basement membrane (GBM) thickening, podocyte number, and slit diaphragm number and extension were determined. GBM of all diabetic rats was significantly thicker (median=0.29 microm; semi-interquartile range=0.065 microm) than in the normal rats (0.23 microm; 0.035 microm). Diabetic rat podocyte number (8; 1), slit diaphragm number (4; 1), and slit diaphragm extension (0.021 microm; 0.00435 microm) were significantly lower than in normal rats (11; 1) and (7; 1.5), and (0.031 microm; 0.0058 microm). Diabetic rat proteinuria (0.060 mg/24 h; 0.037 mg/24 h) was higher than in normal rats (0.00185 mg/24 h; 0.00055 mg/24 h).
CONCLUSION: Experimental diabetes is associated with significant (p<0.05) changes in podocyte foot process, slit number, slit diaphragm extension, and GBM thickness.