Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Diabetic Nephropathy

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...

Nephrotic Syndrome I : Introduction

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...

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...

Nephrons

Nephrons

The kidneys are intricate organs with millions of working units known as nephrons. Each nephron features two major structures: the renal corpuscle, which facilitates blood plasma filtration, and the renal tubule, which handles the glomerular filtrate. Blood supply is directly linked to the nephrons. The renal corpuscle consists of the glomerulus, a capillary network, and the Bowman's capsule, a double-walled epithelial structure that encases the glomerulus. The filtering of blood plasma happens...

Acute Kidney Injury II: Pathophysiology

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...

Retrovirus Life Cycles

Retrovirus Life Cycles

Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...

You might also read

Related Articles

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

Sort by

Same author

Acute Kidney Injury, Fever, and Dark Urine in a Kidney Transplant Recipient.

Kidney360·2026

Same author

Genetic Testing for APOL1 in Adults With Hypertension: The GUARDD-US Randomized Clinical Trial.

JAMA network open·2026

Same author

HIV-associated kidney diseases: progress, gaps, and future directions.

Clinical microbiology reviews·2025

Same author

Women and kidney health: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.

Kidney international·2025

Same author

Paratesticular Endometrial Stromal Sarcoma-Like Sarcoma With EPC1-SUZ12 Fusion.

Genes, chromosomes & cancer·2025

Same author

Second Trimester Kidney Function and Adverse Pregnancy Outcomes among Patients with Lupus.

Kidney360·2025

Search research articles

Related Experiment Video

Updated: Jul 6, 2026

Peptide-based Identification of Functional Motifs and their Binding Partners

Peptide-based Identification of Functional Motifs and their Binding Partners

Published on: June 30, 2013

HIV-associated nephropathy.

Christina M Wyatt¹, Paul E Rosenstiel, Paul E Klotman

¹Department of Medicine, Mount Sinai School of Medicine, New York, N.Y., USA.

Contributions to Nephrology

|April 9, 2008

Summary

HIV-associated nephropathy (HIVAN) is a kidney disease caused by HIV infection, particularly involving Nef and Vpr genes. Host genetics also contribute, necessitating combined antiretroviral and targeted therapies for HIVAN management.

Area of Science:

Nephrology
Virology
Genetics

Background:

HIV-associated nephropathy (HIVAN) is a severe kidney disease linked to advanced HIV infection.
It presents as a unique form of collapsing focal segmental glomerulosclerosis.
HIVAN pathogenesis involves direct viral infection and gene expression within kidney cells.

Purpose of the Study:

To elucidate the pathogenesis of HIVAN.
To identify key viral and host genetic factors involved in HIVAN.
To explore therapeutic strategies for HIVAN.

Main Methods:

Analysis of HIV infection and gene expression in renal epithelial cells.
Investigation of specific HIV genes (Nef, Vpr) in disease development.
Examination of host genetic factors and differential gene expression in HIVAN.

More Related Videos

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

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

Published on: September 11, 2019

Related Experiment Videos

Last Updated: Jul 6, 2026

Peptide-based Identification of Functional Motifs and their Binding Partners

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

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

Published on: September 11, 2019

Main Results:

HIVAN pathogenesis is driven by direct HIV infection and expression of specific viral genes, notably Nef and Vpr.
Host genetic factors play a significant role, evidenced by the disproportionate burden in certain populations.
Differential gene expression in renal cells during HIV infection was observed.

Conclusions:

HIVAN is a complex disease influenced by viral genes (Nef, Vpr) and host genetic susceptibility.
Current management combines antiretroviral therapy with agents targeting downstream effects.
Future therapies may target viral replication, gene expression, or cellular pathways.