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Urinary tract obstruction.

S Klahr1

  • 1Department of Medicine, Barnes-Jewish Hospital at Washington University School of Medicine, St. Louis, MO 63110-1092, USA. sklahr@imgate.wustl.edu

Seminars in Nephrology
|March 14, 2001
PubMed
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Angiotensin II promotes kidney disease progression, increasing factors like TGF-beta1 and NF-kappaB, leading to fibrosis and apoptosis. ACE inhibitors and other therapies show promise in treating obstructive nephropathy.

Area of Science:

  • Nephrology
  • Renal Pathophysiology
  • Molecular Biology

Background:

  • Angiotensin II is a key factor in the progression of renal diseases, particularly obstructive nephropathy.
  • Obstructive nephropathy leads to increased expression of pro-fibrotic and pro-inflammatory factors, including TGF-beta1, TNF-alpha, and NF-kappaB.
  • Renal fibrosis is mediated by local TGF-beta production and endothelin, exacerbated by oxidative stress.

Purpose of the Study:

  • To elucidate the role of Angiotensin II in the molecular mechanisms of obstructive nephropathy.
  • To review factors contributing to renal fibrosis, apoptosis, and interstitial expansion in obstructive nephropathy.
  • To discuss potential therapeutic interventions for ameliorating renal damage in urinary tract obstruction.

Main Methods:

Related Experiment Videos

  • Review of literature on molecular pathways involved in renal disease progression.
  • Analysis of factors upregulated by Angiotensin II in obstructive nephropathy.
  • Examination of the effects of pharmacological interventions on renal pathology markers.

    • Main Results:

    • Angiotensin II upregulates numerous factors (TGF-beta1, TNF-alpha, NF-kappaB, etc.) contributing to renal damage.
    • TGF-beta activation stimulates endothelin production, a potent fibrogenic stimulus.
    • Angiotensin-converting enzyme (ACE) inhibitors reduce NF-kappaB activation; EGF and IGF-1 administration show protective effects.

    Conclusions:

    • Obstructive nephropathy involves complex molecular pathways including TGF-beta, oxidative stress, and NF-kappaB activation.
    • Pharmacological interventions like ACE inhibitors, EGF, and IGF-1 show potential in mitigating renal fibrosis and apoptosis.
    • Future advances in genetic manipulation and drug therapies may offer novel strategies to prevent fibrosis in urinary tract obstruction.