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- W2014558605 abstract "F OLLOWING LOSS of functional renal mass, the residual renal tissue undergoes progressive hypertrophy and hyperplasia. Single nephron glomerular filtration rate (SNGFR) increases dramatically and this enhancement of SNGFR in remnant units has generally been considered a beneficial response in that the animal's total fall in GFR is thereby mitigated. However, evidence has been developed which suggests that single nephron hyperfiltration may have maladaptive and eventually injurious consequences. For nearly 50 yr it has been recognized that removal of approximately 3,4 or more of the renal mass in the rat, either by surgical resection, infarction, or a combination of these maneuvers, results in a syndrome of progressive azotemia, proteinuria and arterial hypertension. 1.2 Furthermore, striking structural alterations appear in these initially normal residual glomeruli during the course of this process of adaptation, eventuating ultimately in glomerulosclerosis. Shimamura and Morrison 3 carefully documented the progression of glomerular damage in adult rats subjected to surgical resection of approximately 5/6 of their total renal mass. They described an increase in glomerular size within the first 3 mo of nephrectomy. This hypertrophy was accompanied by ultrastructural alterations, including vacuolization of glomerular epithelial cells, deposition of osmophilic droplets within these cells, and fusion of foot processes. By about 6 mo, expansion of mesangial matrix became evident along with denudation of cells from areas of glomerular basement membrane. These ultrastructural alterations heralded progressive hyalinization and ultimately sclerosis of these remnant glomeruli. Studies employing unilateral nephrectomy and 3/5 infarction of the remaining kidney" @default.
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- W2014558605 title "Compensatory Renal Hemodynamic Injury: A Final Common Pathway of Residual Nephron Destruction" @default.
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- W2014558605 doi "https://doi.org/10.1016/s0272-6386(82)80032-2" @default.
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