Abstract
Experimental and human studies indicate that altered glomerular permeability to proteins correlates with tubulointerstitial injury and subsequent glomerular scarring. Maneuvers that restore the selectivity of glomerular barrier to macromolecules limit renal injury in progressive nephropathies. The abnormal traffic of proteins through the glomerular capillary has an intrinsic renal toxicity linked to the process of over- reabsorption by proximal tubular cells. Excessive protein reabsorption induces functional alterations of tubular cells that overexpress inflammatory and vasoactive molecules, as indicated by in vitro or in vivo studies. Thus monocyte chemoattractant protein-1 and osteopontin may attract inflammatory cells into renal interstitium. Enhanced tubular endothelin-1 secretion, mainly toward the basolateral membrane of the cell, may stimulate interstitial macrophage infiltration and in addition may promote interstitial fibroblast proliferation and extracellular matrix synthesis, thus amplifying tubulointerstitial inflammation and injury.
| Original language | English |
|---|---|
| Pages (from-to) | 151-159 |
| Number of pages | 9 |
| Journal | Seminars in Nephrology |
| Volume | 16 |
| Issue number | 3 |
| Publication status | Published - 1996 |
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ASJC Scopus subject areas
- Nephrology
Cite this
Glomerular protein trafficking and progression of renal disease to terminal uremia. / Benigni, Ariela; Remuzzi, Giuseppe.
In: Seminars in Nephrology, Vol. 16, No. 3, 1996, p. 151-159.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Glomerular protein trafficking and progression of renal disease to terminal uremia
AU - Benigni, Ariela
AU - Remuzzi, Giuseppe
PY - 1996
Y1 - 1996
N2 - Experimental and human studies indicate that altered glomerular permeability to proteins correlates with tubulointerstitial injury and subsequent glomerular scarring. Maneuvers that restore the selectivity of glomerular barrier to macromolecules limit renal injury in progressive nephropathies. The abnormal traffic of proteins through the glomerular capillary has an intrinsic renal toxicity linked to the process of over- reabsorption by proximal tubular cells. Excessive protein reabsorption induces functional alterations of tubular cells that overexpress inflammatory and vasoactive molecules, as indicated by in vitro or in vivo studies. Thus monocyte chemoattractant protein-1 and osteopontin may attract inflammatory cells into renal interstitium. Enhanced tubular endothelin-1 secretion, mainly toward the basolateral membrane of the cell, may stimulate interstitial macrophage infiltration and in addition may promote interstitial fibroblast proliferation and extracellular matrix synthesis, thus amplifying tubulointerstitial inflammation and injury.
AB - Experimental and human studies indicate that altered glomerular permeability to proteins correlates with tubulointerstitial injury and subsequent glomerular scarring. Maneuvers that restore the selectivity of glomerular barrier to macromolecules limit renal injury in progressive nephropathies. The abnormal traffic of proteins through the glomerular capillary has an intrinsic renal toxicity linked to the process of over- reabsorption by proximal tubular cells. Excessive protein reabsorption induces functional alterations of tubular cells that overexpress inflammatory and vasoactive molecules, as indicated by in vitro or in vivo studies. Thus monocyte chemoattractant protein-1 and osteopontin may attract inflammatory cells into renal interstitium. Enhanced tubular endothelin-1 secretion, mainly toward the basolateral membrane of the cell, may stimulate interstitial macrophage infiltration and in addition may promote interstitial fibroblast proliferation and extracellular matrix synthesis, thus amplifying tubulointerstitial inflammation and injury.
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UR - http://www.scopus.com/inward/citedby.url?scp=0029985360&partnerID=8YFLogxK
M3 - Article
C2 - 8734458
AN - SCOPUS:0029985360
VL - 16
SP - 151
EP - 159
JO - Seminars in Nephrology
JF - Seminars in Nephrology
SN - 0270-9295
IS - 3
ER -