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Related Concept Videos

Type IV Collagen of Basal Lamina01:05

Type IV Collagen of Basal Lamina

Type IV collagen is a 400 nm long, network-forming collagen that acts as a barrier between the epithelial and endothelial cells. Type IV collagen  forms the backbone of the basement membrane by scaffolding with laminin, entactin, proteoglycans, and fibronectin. Apart from rendering structural support to the basement membrane, it also helps entail signaling potentials necessary for both pathological and physiological functions.
A type IV collagen molecule has six alpha chains which can exist in...
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
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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...
Glucose Transporters01:27

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
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Glomerular Filtration01:15

Glomerular Filtration

The filtration membrane in the renal system is a highly specialized structure essential for filtering blood. It consists of glomerular capillaries and podocytes, forming a selective barrier that permits the passage of water and small solutes while restricting most plasma proteins and blood cells.
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Nephrons

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Related Experiment Video

Updated: Jun 9, 2026

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
06:39

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation

Published on: August 19, 2020

Thin Glomerular Basement Membrane Phenotypes With No Identified Pathogenic COL4A3/A4/A5 Variant.

Cristian V Riella1, Dan A Colombo1, Helmut G Rennke2

  • 1Division of Nephrology and Hypertension, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.

Kidney International Reports
|June 8, 2026
PubMed
Summary

Genetic testing for COL4A3/A4/A5 variants has limited diagnostic yield in thin glomerular basement membrane (GBM) disease. Most patients with thin GBM lack COL4A variants, underscoring the continued need for kidney biopsy in diagnosis.

Keywords:
Alport syndromegenetic kidney diseasegenetic testingglomerular basement membranehistopathologythin glomerular basement membrane nephropathy

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Last Updated: Jun 9, 2026

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
06:39

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09:40

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Published on: June 20, 2018

Area of Science:

  • Nephrology
  • Genetics
  • Pathology

Background:

  • Pathogenic variants in COL4A3/A4/A5 genes are associated with thin glomerular basement membrane (GBM) and Alport syndrome.
  • The diagnostic utility of genetic testing for these conditions is not fully established.

Purpose of the Study:

  • To evaluate the diagnostic yield of genetic testing in patients with thin GBM.
  • To correlate genotype with GBM thickness and other clinical parameters.

Main Methods:

  • Retrospective analysis of 115 patients with kidney biopsy and genetic testing on a 385-gene panel.
  • Correlation of GBM ultrastructure, estimated glomerular filtration rate, proteinuria, and hematuria with genetic findings.

Main Results:

  • Nine patients (19.1%) with ultrastructural GBM abnormalities had pathogenic/likely pathogenic COL4A variants; nine additional patients had variants of uncertain significance (VUS).
  • Thirty-one patients (66%) with thin GBM were wildtype for COL4A genes, with some harboring variants in other kidney disease genes.
  • COL4A variants correlated with GBM thickness but not other clinical parameters.

Conclusions:

  • Two-thirds of patients with thin GBM lack COL4A variants, indicating limited diagnostic yield for genetic testing alone.
  • Kidney biopsy remains essential for diagnosing thin GBM and related kidney diseases, even with genetic testing availability.