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

Autologous immune complex glomerulonephritis induces abnormal embryonic development.

C C Leung1, C L Yan, B Cheewatrakoolpong

  • 1Department of Anatomy, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark 07103.

Journal of Reproductive Immunology
|April 1, 1990
PubMed
Summary

Maternal immune complex glomerulonephritis in rats led to significant congenital malformations and fetal growth issues in offspring. The exact cause of these adverse embryonic and fetal effects remains unclear.

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

Changes in the epidemiology and clinical manifestations of human immunodeficiency virus-associated tuberculosis in Hong Kong.

Hong Kong medical journal = Xianggang yi xue za zhi·2024
Same author

[Analysis on epidemiological characteristics of allergens with allergic skin diseases in a hospital in Beijing City from 2017 to 2021].

Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]·2024
Same author

Combating the tridemic: new guidelines, masking and altruism.

The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease·2023
Same author

Grave impact of undetected rpoB I572F mutation on clinical course of multidrug-resistant tuberculosis: a case report.

Hong Kong medical journal = Xianggang yi xue za zhi·2023
Same author

[Incidence and cause of abnormal cholesterol in children aged 2-18 years in a single center].

Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences·2022
Same author

Clinical standards for the assessment, management and rehabilitation of post-TB lung disease.

The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease·2021

Area of Science:

  • Nephrology
  • Immunology
  • Developmental Biology

Background:

  • Chronic autologous immune complex glomerulonephritis (Heymann nephritis) in rats serves as a model for human idiopathic membranous glomerulonephritis.
  • Understanding the impact of maternal kidney disease on fetal development is crucial for both human and animal health.

Purpose of the Study:

  • To investigate the effects of induced chronic immune complex glomerulonephritis in female rats on their offspring.
  • To characterize the types and incidence of congenital malformations and fetal growth abnormalities in the progeny of nephritic mothers.

Main Methods:

  • Induction of Heymann nephritis in Wistar rats via immunization with homologous renal brush border membranes.
  • Mating of nephritic female rats to assess reproductive outcomes and offspring development.

Related Experiment Videos

  • Detailed examination of offspring for congenital malformations and growth retardation.
  • Immunofluorescent studies to detect the presence of rat IgG and complement C3 in extraembryonic membranes, embryos, and fetuses.
  • Main Results:

    • Immunized rats developed Heymann nephritis, mirroring human membranous glomerulonephritis.
    • Offspring of nephritic mothers exhibited high rates of embryonic/fetal resorptions.
    • Observed congenital malformations included microphthalmia, cleft palate, and omphalocele, with ocular anomalies being most frequent.
    • Absence of rat IgG and complement C3 in extraembryonic membranes, embryos, and fetuses was confirmed.

    Conclusions:

    • Maternal immune complex glomerulonephritis in rats causes significant embryonic and fetal developmental abnormalities.
    • The observed teratogenic effects occur despite the apparent absence of maternal antibody or complement transfer to the conceptus.
    • The underlying pathophysiological mechanism for these deleterious embryonic/fetal effects requires further investigation.