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

Hyperfiltration and glomerulosclerosis.

Thomas H Hostetter1

  • 1National Institutes of Health, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, MD, USA. HostetterT@extra.niddk.nih.gov

Seminars in Nephrology
|April 22, 2003
PubMed
Summary
This summary is machine-generated.

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

For-Profit Dialysis and Academic Neglect Are Undermining Dialysis Research in the United States.

Journal of the American Society of Nephrology : JASN·2026
Same author

A Metabolomics Approach to Identify Metabolites Associated With Mortality in Patients Receiving Maintenance Hemodialysis.

Kidney international reports·2024
Same author

Association of urine and plasma ADMA with atherosclerotic risk in DKD cardiovascular disease risk in diabetic kidney disease: findings from the Chronic Renal Insufficiency Cohort (CRIC) study.

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association·2023
Same author

Type 2 diabetes affects arsenic metabolism via transporters in arsenic trioxide treated acute promyelocytic leukemia patients.

Environmental toxicology and pharmacology·2023
Same author

Efficacy, Safety, and Tolerability of Oral Furosemide Among Patients Receiving Hemodialysis: A Pilot Study.

Kidney international reports·2022
Same author

Effect of Furosemide on Proximal Tubular Secretion of Organic Solutes in Patients Receiving Hemodialysis.

Clinical journal of the American Society of Nephrology : CJASN·2022
Same journal

Current Options for Kidney Protection: Are Renin-Angiotensin System Inhibitors Still Relevant?

Seminars in nephrology·2026
Same journal

Proposed Role for Quantitative Podocyturia as a Clinical Marker of Systemic Endothelial Injury: Implications for Cardiovascular Disease and Longevity.

Seminars in nephrology·2026
Same journal

Kidney Protection Options in 2025: Are Renin-Angiotensin System Inhibitors Still Needed?

Seminars in nephrology·2026
Same journal

From Nephron Number to Global Health.

Seminars in nephrology·2026
Same journal

Chronic Kidney Disease Progression Mechanisms: Why They Matter in an Era of Novel Kidney Protective Therapies.

Seminars in nephrology·2026
Same journal

Of Diuretics, Transporters, and Mechanisms of Hypertension.

Seminars in nephrology·2026
See all related articles

Reduced kidney mass leads to glomerular injury due to increased glomerular pressure. The renin-angiotensin-aldosterone system contributes to this pressure, driving pathological changes in residual nephrons.

Area of Science:

  • Nephrology
  • Pathology
  • Physiology

Background:

  • The link between reduced renal mass and glomerular injury is known.
  • Pathologic changes are attributed to adaptive hemodynamic shifts in remaining nephrons.
  • This phenomenon is observed in both animal models and humans.

Purpose of the Study:

  • To explore the hemodynamic mechanisms underlying glomerular injury after renal mass reduction.
  • To elucidate the role of the renin-angiotensin-aldosterone system in this process.
  • To understand the cellular and matrix changes contributing to glomerulosclerosis.

Main Methods:

  • Review of established literature on renal mass reduction and glomerular injury.
  • Analysis of hemodynamic alterations in residual nephrons.

Related Experiment Videos

  • Examination of the renin-angiotensin-aldosterone system's involvement.
  • Investigation of mesangial, podocyte, and endothelial cell responses.
  • Main Results:

    • Increased glomerular pressure is a key factor in generating pathological changes.
    • The renin-angiotensin-aldosterone system significantly contributes to elevated intrarenal pressure.
    • Glomerular hypertension induces mesangial expansion (increased cell number and matrix volume).
    • Interactions between high pressure, capillary volume, and fixed podocyte number promote sclerosis.

    Conclusions:

    • Elevated glomerular pressure, exacerbated by the renin-angiotensin-aldosterone system, is central to nephron injury following renal mass reduction.
    • Mesangial cell and matrix changes are critical components of the sclerotic process.
    • While endothelial cells are affected, their role in sclerosis is less defined than that of mesangial and glomerular epithelial cells.