Glomerular Sclerosis
Mostrando 13-24 de 43 artigos, teses e dissertações.
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13. Endothelial cell injury initiates glomerular sclerosis in the rat remnant kidney.
The development of progressive glomerulosclerosis in the renal ablation model has been ascribed to a number of humoral and hemodynamic events, including the peptide growth factor, transforming growth factor-beta 1 (TGF-beta 1). An important role has also been attributed to angiotensin II (AII), which, in addition to its hemodynamic effects, can stimulate tra
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14. Glomerulosclerosis is transmitted by bone marrow–derived mesangial cell progenitors
We found that ROP Os/+ (Os/+) mice had diffuse glomerulosclerosis and glomerular hypertrophy and that their mesangial cells (the vascular smooth muscle cells of the glomerulus) displayed an apparent sclerosing phenotype. Since mesangial cells are the major source of scar tissue in glomerulosclerosis, we postulated that the sclerosis phenotype was carried by
American Society for Clinical Investigation.
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15. Anemia lessens and its prevention with recombinant human erythropoietin worsens glomerular injury and hypertension in rats with reduced renal mass.
Chronic renal disease is frequently characterized by anemia, which may modify systemic and renal hemodynamics. In adult Munich-Wistar rats, the mild anemia (hematocrit, approximately equal to 42 vol/dl) that accompanies five-sixths nephrectomy was either made more severe (approximately equal to 30 vol/dl) by feeding a low iron diet or prevented (approximatel
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16. Essential role of Gas6 for glomerular injury in nephrotoxic nephritis
Growth-arrest specific gene 6 (Gas6) is a vitamin K–dependent growth factor for mesangial and epithelial cells. To investigate whether Gas6 is essential for progressive glomerular injury, we constructed Gas6–/– mice and examined the role of Gas6 in accelerated nephrotoxic nephritis (NTN), a model of progressive glomerulonephritis. We found less mortali
American Society for Clinical Investigation.
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17. Microcephaly and congenital nephrotic syndrome owing to diffuse mesangial sclerosis: an autosomal recessive syndrome.
Three sibs born to consanguineous parents had congenital nephrotic syndrome, microcephaly, and psychomotor retardation. Pathology of the kidneys showed diffuse mesangial sclerosis with deposits of IgG and C3 in the mesangium and glomerular basement membranes. All three children died before the age of 3 years. Of 19 published cases of children with the associ
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18. Angiotensin converting enzyme inhibition ameliorates glomerular filtration of macromolecules and water and lessens glomerular injury in the rat.
The effect of enalapril on glomerular hemodynamics and permselectivity and on subsequent sclerosis was studied in male MWF/Ztm rats which spontaneously develop proteinuria and glomerular structural damage. Untreated group 1 and enalapril-treated group 2 (50 mg/liter, in the drinking water) underwent micropuncture studies after 2 mo of observation. After the
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19. Glomerular nodules and long-spacing collagen in kidneys of patients with multiple myeloma
Light microscopic examination of the kidneys in 170 patients with multiple myeloma revealed three from patients without diabetes with glomerular nodules that were indistinguishable from those of diabetic glomerular sclerosis. Electron microscopic studies showed the nodules to be deposits of fine-grained material that corresponded to precipitations of protein
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20. The Immunohistopathology of Glomerular Antigens THE GLOMERULAR BASEMENT MEMBRANE, COLLAGEN, AND ACTOMYOSIN ANTIGENS IN NORMAL AND DISEASED KIDNEYS
The immunofluorescent localization of antisera to human glomerular basement membrane (GBM), collagen, and smooth muscle actomyosin was examined in 15 specimens of normal renal tissue and 98 specimens from patients with renal disease. The anti-GBM and anticollagen antisera normally localize to GBM, while antiactomyosin localizes to the mesangium. Diabetic nep
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21. Podocyte loss and progressive glomerular injury in type II diabetes.
Kidney biopsies from Pima Indians with type II diabetes were analyzed. Subjects were classified clinically as having early diabetes (n = 10), microalbuminuria (n = 17), normoalbuminuria, despite a duration of diabetes equal to that of the subjects with microalbuminuria (n = 12), or clinical nephropathy (n = 12). Subjects with microalbuminuria exhibited moder
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22. Control of glomerular hypertension limits glomerular injury in rats with reduced renal mass.
Micropuncture and morphologic studies were performed in four groups of male Munich-Wistar rats after removal of the right kidney and segmental infarction of two-thirds of the left kidney. Groups 1 and 3 received no specific therapy. Groups 2 and 4 were treated with the angiotensin I converting enzyme inhibitor, enalapril, 50 mg/liter of which was put in thei
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23. Glomerular injury in uninephrectomized spontaneously hypertensive rats. A consequence of glomerular capillary hypertension.
Micropuncture and/or morphologic studies were performed in intact Wistar-Kyoto rats (WKY) (group 0), intact spontaneously hypertensive rats (SHR) (groups 1 and 5), uninephrectomized (UNX) WKY (groups 2 and 6), and UNX SHR (groups 3 and 4, 7 and 8). UNX was performed when rats were 5 wk of age. Groups 0-4 were observed for 34 wk after which whole kidney clear
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24. Outcome of the acute glomerular injury in proliferative lupus nephritis.
Treatment with total lymphoid irradiation (TLI) and corticosteroids markedly reduced activity of systemic lupus erythematosis in 10 patients with diffuse proliferative lupus nephritis (DPLN) complicated by a nephrotic syndrome. Physiologic and morphometric techniques were used serially before, and 12 and 36 mo post-TLI to characterize the course of glomerula