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

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...
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...
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...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Chronic Kidney Disease I: Introduction01:25

Chronic Kidney Disease I: Introduction

Chronic Kidney Disease (CKD) arises when the kidneys progressively lose their ability to function, ultimately leading to end-stage renal disease. At this advanced stage, the kidneys can no longer filter waste or maintain essential body functions, requiring renal replacement therapy (RRT) through dialysis or a kidney transplant for survival.Early-stage chronic kidney disease and detection challengesIn CKD's early stages, symptoms often remain absent because healthy nephrons compensate for...

You might also read

Related Articles

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

Sort by
Same author

<i>Fosl2</i> regulates the transition from parietal epithelial cells to myofibroblasts in the kidney.

bioRxiv : the preprint server for biology·2025
Same author

Podocyte-Specific Deletion of STAT3 in Krüppel-Like Factor 4-Related Experimental Podocytopathy.

Journal of the American Society of Nephrology : JASN·2025
Same author

Non-enzymatic modification of aminophospholipids induces angiogenesis, inflammation, and insulin signaling dysregulation in human renal glomerular endothelial cells in vitro.

Free radical biology & medicine·2025
Same author

Author Correction: LILRB3 genetic variation is associated with kidney transplant failure in African American recipients.

Nature medicine·2025
Same author

LILRB3 genetic variation is associated with kidney transplant failure in African American recipients.

Nature medicine·2025
Same author

Small Molecule Allosteric Inhibitor of HIPK2 as a Novel Therapy against Kidney Fibrosis.

Journal of the American Society of Nephrology : JASN·2024
Same journal

Sex differences in renal acid-base regulation.

Current opinion in nephrology and hypertension·2026
Same journal

Primary prevention of chronic kidney disease in type 2 diabetes mellitus with sodium-glucose cotransporter 2 inhibitors.

Current opinion in nephrology and hypertension·2026
Same journal

Financial and policy challenges of delivering kidney replacement therapies in resource-limited settings.

Current opinion in nephrology and hypertension·2026
Same journal

The role of kir4.1/Kir5.1 in mediating the effect of angiotensin-II on Na-Cl-cotransporter.

Current opinion in nephrology and hypertension·2026
Same journal

Role of the calcium-sensing receptor in regulating calcium transport in the thick ascending limb.

Current opinion in nephrology and hypertension·2026
Same journal

Social determinants of chronic kidney disease: from association to clinical and population action.

Current opinion in nephrology and hypertension·2026
See all related articles

Related Experiment Video

Updated: Jun 4, 2026

Peptide-based Identification of Functional Motifs and their Binding Partners
14:28

Peptide-based Identification of Functional Motifs and their Binding Partners

Published on: June 30, 2013

HIV-associated nephropathy: pathogenesis.

Raj K Medapalli1, John C He, Paul E Klotman

  • 1Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA.

Current Opinion in Nephrology and Hypertension
|March 2, 2011
PubMed
Summary
This summary is machine-generated.

HIV-associated nephropathy (HIVAN) arises from HIV-1 infection of kidney cells, particularly in individuals with specific genetic risks. Viral genes like Nef and Vpr drive kidney damage through podocyte dysfunction and apoptosis.

More Related Videos

Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis
10:12

Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis

Published on: September 11, 2019

Related Experiment Videos

Last Updated: Jun 4, 2026

Peptide-based Identification of Functional Motifs and their Binding Partners
14:28

Peptide-based Identification of Functional Motifs and their Binding Partners

Published on: June 30, 2013

Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis
10:12

Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis

Published on: September 11, 2019

Area of Science:

  • Nephrology
  • Virology
  • Genetics

Background:

  • HIV-associated nephropathy (HIVAN) presents as collapsing focal segmental glomerulosclerosis (FSGS), tubular dilation, and fibrosis.
  • Understanding HIVAN pathogenesis is crucial for managing kidney disease in HIV patients.

Purpose of the Study:

  • To review current knowledge on the mechanisms driving HIVAN pathogenesis.
  • To elucidate the roles of host genetics and viral factors in HIVAN.

Main Methods:

  • Review of in-vivo and in-vitro studies on HIVAN.
  • Analysis of genetic susceptibility factors and key viral proteins.

Main Results:

  • Apolipoprotein L 1 (ApoL1) gene variants are major risk factors for FSGS and end-stage renal disease in Black populations.
  • HIV infects renal tubular epithelial cells, with Nef and Vpr identified as key viral mediators.
  • Nef induces podocyte dysfunction, while Vpr causes renal tubular epithelial cell apoptosis.

Conclusions:

  • HIVAN results from HIV-1 infection and viral gene expression (Nef, Vpr) in genetically susceptible individuals.
  • Renal epithelium serves as a distinct viral reservoir, promoting viral evolution.
  • Host cellular pathways, including cell cycle and apoptosis, are dysregulated, leading to HIVAN's characteristic pathology.