Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Antibody and complement reduce renal hemodynamic function in isolated perfused rat kidney

T Jocks1, G Zahner, U Helmchen

  • 1Department of Medicine, University of Hamburg, Germany.

The American Journal of Physiology
|January 1, 1996
PubMed
Summary

Antibody and rat serum cause kidney damage by increasing thromboxane (Tx) production, leading to altered renal hemodynamics. Inhibiting Tx synthesis or blocking its receptors can mitigate these harmful effects.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

[Membranous nephropathy--crucial developments for diagnostic and treatment].

Deutsche medizinische Wochenschrift (1946)·2014
Same author

[Tubulointerstitial nephritis with uveitis (TINU) syndrome. A relatively rare rheumatological differential diagnosis with unexplained uveitis].

Zeitschrift fur Rheumatologie·2013
Same author

[From mice to men - insights from the hantavirus epidemic in 2010].

Deutsche medizinische Wochenschrift (1946)·2012
Same author

[Membranous glomerulonephritis: better therapy with autoantibody monitoring?].

Deutsche medizinische Wochenschrift (1946)·2011
Same author

A new role for the neuronal ubiquitin C-terminal hydrolase-L1 (UCH-L1) in podocyte process formation and podocyte injury in human glomerulopathies.

The Journal of pathology·2008
Same author

[A 42 year old patient with bilateral loss of sight and hypertension. Gemcitabine-associated thrombotic microangiopathy (TMA)].

Der Internist·2008

Area of Science:

  • Nephrology
  • Immunology
  • Pharmacology

Background:

  • Antibody and complement activation can lead to glomerular injury.
  • Renal hemodynamic alterations are a key feature of kidney damage.
  • The role of thromboxane in antibody-mediated kidney injury requires further elucidation.

Purpose of the Study:

  • To investigate the impact of antibody and complement on renal hemodynamics.
  • To determine the involvement of thromboxane in antibody-induced renal hemodynamic changes.
  • To assess the therapeutic potential of thromboxane inhibitors in this model.

Main Methods:

  • Isolated perfused rat kidneys were subjected to injury using anti-thymocyte antibody (ATS) and rat serum (RS).
  • Glomerular filtration rate (GFR), renal vascular resistance (RVR), and renal perfusate flow (RPF) were measured.

Related Experiment Videos

  • Thromboxane (Tx) synthesis inhibitor (UK-38485) and Tx receptor blocker (daltroban) were used to test the role of Tx.
  • Main Results:

    • ATS and RS significantly reduced GFR and RPF, while markedly increasing RVR.
    • These hemodynamic changes were ameliorated by pretreatment with daltroban and UK-38485.
    • Glomerular Tx formation was significantly increased in kidneys perfused with ATS and RS.

    Conclusions:

    • Antibody and rat serum induce significant impairment of renal hemodynamics.
    • Increased thromboxane formation mediates these antibody-induced renal hemodynamic alterations.
    • Targeting thromboxane pathways offers a potential therapeutic strategy for antibody-mediated kidney injury.