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01.12.2010 | Review | Ausgabe 1/2010 Open Access

Journal of Inflammation 1/2010

Role of inflammation in túbulo-interstitial damage associated to obstructive nephropathy

Zeitschrift:
Journal of Inflammation > Ausgabe 1/2010
Autoren:
María T Grande, Fernando Pérez-Barriocanal, José M López-Novoa
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1476-9255-7-19) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

MTG and JML-N designed the review. MTG drafted the manuscript, FP-B and JML-N have rewritten the manuscript and MTG, FP-B and JML-N have completed the final version of the manuscript. All authors read and approved the final manuscript

Abstract

Obstructive nephropathy is characterized by an inflammatory state in the kidney, that is promoted by cytokines and growth factors produced by damaged tubular cells, infiltrated macrophages and accumulated myofibroblasts. This inflammatory state contributes to tubular atrophy and interstitial fibrosis characteristic of obstructive nephropathy. Accumulation of leukocytes, especially macrophages and T lymphocytes, in the renal interstitium is strongly associated to the progression of renal injury. Proinflammatory cytokines, NF-κB activation, adhesion molecules, chemokines, growth factors, NO and oxidative stress contribute in different ways to progressive renal damage induced by obstructive nephropathy, as they induce leukocytes recruitment, tubular cell apoptosis and interstitial fibrosis. Increased angiotensin II production, increased oxidative stress and high levels of proinflammatory cytokines contribute to NF-κB activation which in turn induce the expression of adhesion molecules and chemokines responsible for leukocyte recruitment and iNOS and cytokines overexpression, which aggravates the inflammatory response in the damaged kidney. In this manuscript we revise the different events and regulatory mechanisms involved in inflammation associated to obstructive nephropathy.
Zusatzmaterial
Authors’ original file for figure 1
12950_2009_138_MOESM1_ESM.pdf
Authors’ original file for figure 2
12950_2009_138_MOESM2_ESM.pdf
Authors’ original file for figure 3
12950_2009_138_MOESM3_ESM.ppt
Literatur
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