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Renal angiotensin II up-regulation and myofibroblast activation in human membranous nephropathy

Sergio A Mezzano1, Claudio A Aros, Alejandra Droguett

  • 1Division of Nephrology, School of Medicine, Universidad Austral, Valdivia, Chile. smezzano@uach.cl

Kidney International. Supplement
|September 13, 2003
PubMed
Abstract

Insights

The renin-angiotensin system (RAS) is activated in progressive idiopathic membranous nephropathy (MN), contributing to kidney injury. This study shows angiotensin II (Ang II) may drive fibrosis and disease progression in MN.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathology

Background:

  • The molecular basis of renal injury and fibrosis in proteinuric nephropathies, such as idiopathic membranous nephropathy (MN), remains incompletely understood.
  • The renin-angiotensin system (RAS) is implicated in these processes, and MN can lead to kidney failure.

Purpose of the Study:

  • To investigate the localization of RAS components in MN kidney biopsies.
  • To correlate RAS component expression with profibrotic markers and indicators of renal injury.

Main Methods:

  • Immunohistochemistry was used to assess angiotensin-converting enzyme (ACE) and angiotensin II (Ang II) expression in 20 MN patient biopsies.
  • In situ hybridization detected transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF)-BB mRNA, while alpha-smooth muscle actin (alpha-SMA) staining identified myofibroblast transdifferentiation.

Main Results:

  • Elevated ACE and Ang II levels were observed in tubular and interstitial cells, particularly in progressive MN cases.
  • TGF-beta and PDGF mRNA were upregulated in tubular epithelial cells in progressive MN and correlated with myofibroblast activation (alpha-SMA).
  • Overexpression of ACE and Ang II was associated with tubular profibrotic factor expression and interstitial myofibroblast activation.

Conclusions:

  • The intrarenal RAS is selectively activated in progressive MN.
  • De novo ACE expression suggests in situ Ang II generation contributes to TGF-beta upregulation, epithelial-myofibroblast transdifferentiation, and disease progression.
  • Angiotensin II plays a novel role in human tubulointerstitial injury in MN.

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