Burton CJ, Walls J, Harris KPJ
Tubular MCP-1 production, a mechanism for proteinuria-
induced interstitial inflammation
33rd Congress of the Eur Dial Transplant Assoc
Nephrol Dial Transplant
(Jun) 11:A56 1996
Recently an increasing interest has been focused on the role of
tubular cells in the pathogenesis of interstitial damage. These cells
have always been considered the main target of the deleterious
effects of proteinuria.
In this work, Burton et al
demonstrate a link between the interaction of proteinuria with tubular
cells and the development of interstitial inflammation. Indeed, they
show, in an interesting in vitro system, that the exposure of the
apical surface of tubular cells to serum proteins results in the
secretion of MCP-1 at the apical and basolateral level. The release of
this chemokine in the peritubular space would explain the influx of
macrophage into the interstitium and the consequent interstitial
damage in proteinuric renal diseases. (Loreto Gesualdo, M.D.,
University of Bari, Italy)
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33rd Congress of the Eur Dial Transplant Assoc
Proteinuria/Hematuria :
Mechanisms of renal injury
Nephrotic Syndrome :
Pathogenesis, complications, RVT