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 Concept Videos

Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of fluid...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Cytomegalovirus Disease01:27

Cytomegalovirus Disease

Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

You might also read

Related Articles

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

Sort by
Same author

World kidney day 2011: protect your kidneys, save your heart.

International journal of organ transplantation medicine·2014
Same author

World Kidney Day 2011: protect your kidneys, save your heart.

Internal medicine journal·2012
Same author

Meeting report on the Bellagio Conference 'prevention of vascular diseases in the emerging world: An approach to global health equity'.

Kidney international·2006
Same author

Abnormal development of glomerular endothelial and mesangial cells in mice with targeted disruption of the lama3 gene.

Kidney international·2006
Same author

Endothelial chylomicron binding is altered by interaction with high-density lipoprotein in Heymann's nephritis.

American journal of kidney diseases : the official journal of the National Kidney Foundation·2001
Same author

Intravenous immunoglobulin protects against experimental thrombotic microangiopathy.

Kidney international·2001

Related Experiment Video

Updated: May 11, 2026

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
06:39

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation

Published on: August 19, 2020

Pathogenesis of membranous nephropathy.

W G Couser1, C K Abrass

  • 1Department of Medicine, University of Washington, Seattle.

Annual Review of Medicine
|January 1, 1988
PubMed
Summary

Membranous nephropathy, a leading cause of adult nephrotic syndrome, involves glomerular immune deposits. New research highlights cell surface antigens and complement

Area of Science:

  • Nephrology
  • Immunology
  • Pathogenesis of glomerular diseases

Background:

  • Membranous nephropathy (MN) is the primary cause of idiopathic nephrotic syndrome in adults.
  • Subepithelial glomerular immune deposits characterize MN.
  • Recent research has elucidated novel pathogenic mechanisms.

Purpose of the Study:

  • To explore the mechanisms of subepithelial glomerular immune deposit formation in MN.
  • To document the role of the complement system's membrane attack complex (C5b-9) in renal injury.
  • To understand the broader implications for immune-mediated diseases and therapeutic strategies.

Main Methods:

  • Analysis of recent studies on MN pathogenesis.
  • Investigation of cell surface antigens in immune deposit formation.

More Related Videos

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Optimizing Isolation and Purification of Murine Glomerular Mesangial Cells
04:46

Optimizing Isolation and Purification of Murine Glomerular Mesangial Cells

Published on: March 7, 2025

Related Experiment Videos

Last Updated: May 11, 2026

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
06:39

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation

Published on: August 19, 2020

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Optimizing Isolation and Purification of Murine Glomerular Mesangial Cells
04:46

Optimizing Isolation and Purification of Murine Glomerular Mesangial Cells

Published on: March 7, 2025

  • Documentation of the C5b-9 membrane attack complex's role in renal injury.

    • Main Results:

    • Identified new mechanisms of glomerular immune deposit formation involving cell surface antigens.
    • Confirmed the role of the C5b-9 membrane attack complex in mediating renal injury in MN.
    • Provided insights into the pathogenesis of immune-mediated diseases.

    Conclusions:

    • Understanding MN pathogenesis offers insights into other immune-mediated diseases.
    • The C5b-9 complex is a key mediator of renal injury in MN.
    • These findings have implications for developing novel therapeutic interventions for MN.