Glomerular protein trafficking and progression of renal disease to terminal uremia

Research output: Contribution to journalArticle

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 languageEnglish
Pages (from-to)151-159
Number of pages9
JournalSeminars in Nephrology
Volume16
Issue number3
Publication statusPublished - 1996

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Uremia
Protein Transport
Disease Progression
Kidney
Wounds and Injuries
Proteins
Osteopontin
Chemokine CCL2
Endothelin-1
Cicatrix
Extracellular Matrix
Permeability
Fibroblasts
Macrophages
Cell Membrane
Inflammation

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 journalArticle

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