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

How does proteinuria cause progressive renal damage?

Mauro Abbate1, Carla Zoja, Giuseppe Remuzzi

  • 1Mario Negri Institute for Pharmacological Research, Bergamo, Italy.

Journal of the American Society of Nephrology : JASN
|October 13, 2006
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

Cardiovascular risk assessment in low-resource settings: a consensus document of the European Society of Hypertension Working Group on Hypertension and Cardiovascular Risk in Low Resource Settings.

Journal of hypertension·2014
Same author

Stamina therapies: Time to call a halt.

Nature·2014
Same author

Hemolytic uremic syndrome.

Seminars in immunopathology·2014
Same author

Rituximab in steroid-dependent or frequently relapsing idiopathic nephrotic syndrome.

Journal of the American Society of Nephrology : JASN·2014
Same author

CD133+ renal stem cells always co-express CD24 in adult human kidney tissue.

Stem cell research·2014
Same author

Cardiovascular complications in atypical haemolytic uraemic syndrome.

Nature reviews. Nephrology·2014
Same journal

Variants to Functions to Therapeutic Strategies Toward Genomically Informed Care for Autosomal Dominant Polycystic Kidney Disease.

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

Personalizing Cardio-Kidney-Metabolic Therapy: Closer But Not There Yet.

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

Autosomal Dominant Tubulointerstitial Kidney Disease: My Kingdom for a Biomarker.

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

Beyond the Margin: Improving Noninferiority Trials of Kidney Transplant Immunosuppression.

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

Parathyroid Hormone Receptor 1 Facilitates Cyst Growth in Genetic Models of Autosomal Dominant Polycystic Kidney Disease.

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

Alanyl-tRNA Synthetase 1 and Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.

Journal of the American Society of Nephrology : JASN·2026
See all related articles

Proteinuria accelerates kidney disease progression through inflammation and fibrosis. Targeting inflammatory pathways and complement activation offers potential therapeutic strategies for chronic kidney disease.

Area of Science:

  • Nephrology
  • Immunology
  • Pathology

Background:

  • Proteinuria is increasingly recognized as a driver of chronic kidney disease (CKD) progression.
  • Multiple pathways link proteinuria to renal injury, including inflammation and fibrosis.
  • Macrophages play a critical role in mediating interstitial inflammation and renal fibrosis.

Purpose of the Study:

  • To review the evidence linking proteinuria to kidney disease progression.
  • To elucidate the molecular mechanisms involved in proteinuria-induced renal injury.
  • To identify potential therapeutic targets for mitigating kidney disease progression.

Main Methods:

  • Review of experimental and clinical studies on proteinuria and kidney disease.
  • Analysis of pathways involving tubular chemokine expression, complement activation, and inflammatory cell infiltration.

Related Experiment Videos

  • Investigation of the role of macrophages in renal injury progression.
  • Examination of NF-kappaB signaling pathways in proximal tubular cells.

    • Main Results:

    • Proteinuria induces inflammatory cell infiltration and fibrosis in the kidney interstitium.
    • Macrophages are key mediators of renal injury, with their numbers predicting renal survival.
    • Excess protein load activates proximal tubular cells via NF-kappaB-dependent and independent pathways.
    • Experimental studies show benefits from inhibiting NF-kappaB activation or chemokine receptors.

    Conclusions:

    • Proteinuria accelerates kidney disease progression to end-stage renal failure.
    • Therapeutic strategies targeting inflammatory mediators, complement activation, and NF-kappaB signaling show promise.
    • Understanding proximal tubular cell responses to protein overload is crucial for developing novel treatments.