Causes of Progression of Renal Disease

  • S. Klahr
  • K. Harris
Part of the Topics in Renal Medicine book series (TIRM, volume 7)


In kidney diseases characterized by irreversible injury, it appears that once a critical level of renal functional deterioration is reached, progression to end-stage disease occurs frequently, even if the initiating event or condition is resolved or eradicated. The immunologic mechanisms and the mediators of kidney tissue damage that they induce may be responsible for initiating most renal diseases, but certain clinical and experimental observations suggest that the rate of progression of these diseases is influenced by several non-immuno-logical factors. Studies on the mechanisms underlying the progression of renal disease have utilized experimental animal models. The most widely used experimental model has utilized the ablation of renal mass in rats. Animals with subtotal renal ablation develop proteinuria, hypertension, and glomerulosclerosis in the viable portion of the remnant kidney. The pathogenesis of these abnormalities has not been completely elucidated. Hypertrophy of the residual renal mass occurs after ablation. This hypertrophy, as mentioned, is accompanied by a marked increase in plasma flow per nephron and in single-nephron glomerular filtration rate (SNGFR). Structural alterations occur in all three glomerular cell types. Three weeks after renal ablation, adhesion of epithelial cells to Bowman’s capsule may be seen in severely involved glomeruli. In some areas, epithelial cells are detached from their underlying basement membrane. There is a prominent increase in mesangial cells and mesangial matrix.


Mesangial Cell Mesangial Matrix Alternative Complement Pathway Remnant Kidney Intraglomerular Pressure 
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© Kluwer Academic Publishers, Boston 1989

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  • S. Klahr
  • K. Harris

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