Abstract
Clinical and experimental data have indicated that heavy proteinuria in renal glomerular diseases is associated with the formation of tubulointerstitial fibrosis and contributes to the progression of renal failure. In recent years studies have focused on the possibility that albumin and other proteins that accumulate in the lumen of proximal tubular cells as a consequence of glomerular permeability dysfunction, are a direct cause of tubular cell injury. Specific proteins that have been shown to be cytotoxic are transferrin/iron, lipoproteins and complement components, all of which appear in the urine in proteinuric states. As an additional pathway of injury one may consider the effects of lipids bound to albumin and lipoproteins, including oxidized low density lipoproteins, which, by inducing an oxidative stress to tubular cells, are potent cytotoxic molecules. Moreover, reabsorption of high molecular weight proteins activates proximal tubular cells to produce matrix proteins, cytokines, chemoattractants and vasoactive mediators that may converge in stimulating interstitial inflammation and scarring. Given the functional toxicity of filtered proteins on the kidney, pharmacological and dietary manipulations aimed at reducing glomerular protein traffic may have a beneficial impact on the deterioration of renal function in progressive nephropathies.
| Original language | English |
|---|---|
| Journal | Kidney international. Supplement |
| Volume | 51 |
| Issue number | 62 |
| Publication status | Published - 1997 |
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Keywords
- Proteinuria
- Proximal tubular cells
- Renal failure
- Tubulointerstitial fibrosis
ASJC Scopus subject areas
- Nephrology
Cite this
Role of increased glomerular protein traffic in the progression of renal failure. / Bruzzi, I.; Benigni, A.; Remuzzi, G.
In: Kidney international. Supplement, Vol. 51, No. 62, 1997.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of increased glomerular protein traffic in the progression of renal failure
AU - Bruzzi, I.
AU - Benigni, A.
AU - Remuzzi, G.
PY - 1997
Y1 - 1997
N2 - Clinical and experimental data have indicated that heavy proteinuria in renal glomerular diseases is associated with the formation of tubulointerstitial fibrosis and contributes to the progression of renal failure. In recent years studies have focused on the possibility that albumin and other proteins that accumulate in the lumen of proximal tubular cells as a consequence of glomerular permeability dysfunction, are a direct cause of tubular cell injury. Specific proteins that have been shown to be cytotoxic are transferrin/iron, lipoproteins and complement components, all of which appear in the urine in proteinuric states. As an additional pathway of injury one may consider the effects of lipids bound to albumin and lipoproteins, including oxidized low density lipoproteins, which, by inducing an oxidative stress to tubular cells, are potent cytotoxic molecules. Moreover, reabsorption of high molecular weight proteins activates proximal tubular cells to produce matrix proteins, cytokines, chemoattractants and vasoactive mediators that may converge in stimulating interstitial inflammation and scarring. Given the functional toxicity of filtered proteins on the kidney, pharmacological and dietary manipulations aimed at reducing glomerular protein traffic may have a beneficial impact on the deterioration of renal function in progressive nephropathies.
AB - Clinical and experimental data have indicated that heavy proteinuria in renal glomerular diseases is associated with the formation of tubulointerstitial fibrosis and contributes to the progression of renal failure. In recent years studies have focused on the possibility that albumin and other proteins that accumulate in the lumen of proximal tubular cells as a consequence of glomerular permeability dysfunction, are a direct cause of tubular cell injury. Specific proteins that have been shown to be cytotoxic are transferrin/iron, lipoproteins and complement components, all of which appear in the urine in proteinuric states. As an additional pathway of injury one may consider the effects of lipids bound to albumin and lipoproteins, including oxidized low density lipoproteins, which, by inducing an oxidative stress to tubular cells, are potent cytotoxic molecules. Moreover, reabsorption of high molecular weight proteins activates proximal tubular cells to produce matrix proteins, cytokines, chemoattractants and vasoactive mediators that may converge in stimulating interstitial inflammation and scarring. Given the functional toxicity of filtered proteins on the kidney, pharmacological and dietary manipulations aimed at reducing glomerular protein traffic may have a beneficial impact on the deterioration of renal function in progressive nephropathies.
KW - Proteinuria
KW - Proximal tubular cells
KW - Renal failure
KW - Tubulointerstitial fibrosis
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M3 - Article
C2 - 9350674
AN - SCOPUS:0030710211
VL - 51
JO - Kidney International, Supplement
JF - Kidney International, Supplement
SN - 0098-6577
IS - 62
ER -