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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...
Renal Corpuscle01:20

Renal Corpuscle

The glomerulus and Bowman's capsule are two essential components of the nephron, which is the functional unit of the kidney. These microscopic structures play a critical role in the process of blood filtration to produce urine.
Glomerulus: Structure and Function
The glomerulus is a tiny, intricate network of capillaries located at the beginning of the nephron. It's enveloped by the Bowman's capsule and receives its blood supply from an afferent arteriole, which divides into numerous capillaries...
Nephrotic Syndrome II : Assessment and Medical Management01:26

Nephrotic Syndrome II : Assessment and Medical Management

IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document any history...
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...

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Related Experiment Video

Updated: Jun 26, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Glomerular transcriptome changes associated with lipopolysaccharide-induced proteinuria.

Ying Sun1, Liqun He, Minoru Takemoto

  • 1Department of Medical Biochemistry and Biophysics, Division of Matrix Biology, Karolinska Institutet, Stockholm, Sweden.

American Journal of Nephrology
|January 13, 2009
PubMed
Summary
This summary is machine-generated.

Lipopolysaccharide (LPS) causes significant gene expression changes in mouse glomeruli, impacting podocyte survival and glomerular structure. These alterations may serve as early markers for glomerular injury and proteinuria.

Related Experiment Videos

Last Updated: Jun 26, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Area of Science:

  • Nephrology
  • Molecular Biology
  • Genomics

Background:

  • Global gene expression in normal glomeruli is known.
  • Gene expression changes in glomerular disease are poorly understood.

Purpose of the Study:

  • To map global glomerular gene expression changes in lipopolysaccharide (LPS)-induced proteinuria in mice.
  • To identify potential biomarkers for early glomerular injury.

Main Methods:

  • Induction of proteinuria using lipopolysaccharide (LPS) in mice.
  • Global gene expression profiling of glomeruli.
  • Bioinformatic analysis of transcriptional changes.
  • Construction of protein-protein interaction networks.

Main Results:

  • LPS induced dramatic transcriptional reprogramming in glomeruli (20% of all genes).
  • Significant changes were observed in genes regulating adherence junctions, actin cytoskeleton, and podocyte survival.
  • Downregulation of podocyte number and upregulation of immature glomerular matrix proteins (collagen IV, laminin alpha5) were noted.
  • Gene expression dysregulation occurred in endothelial, mesangial, and podocyte cells.

Conclusions:

  • Detected glomerular gene expression changes and protein interactions offer potential early markers for transient glomerular injury.
  • These findings enhance understanding of molecular mechanisms underlying proteinuria.