Related Experiment Video

Updated: Aug 11, 2026

Detection of MicroRNA Expression in the Kidneys of Immunoglobulin A Nephropathic Mice
05:39

Detection of MicroRNA Expression in the Kidneys of Immunoglobulin A Nephropathic Mice

Published on: July 8, 2020

Glomerular immune deposits in experimental IgA nephropathy. A continuum of circulating and in situ formed immune

A Chen1, S S Wong, A Rifai

  • 1Department of Pathology and Laboratory Medicine, University of Texas Health Science Center at Houston.

The American Journal of Pathology
|January 1, 1988
PubMed

Studies were undertaken to elucidate the primary pathogenetic mechanisms responsible for immunoglobulin (Ig) A immune complexes formation and glomerular deposition in vivo. Monomeric (mIgA) and polymeric IgA (pIgA) anti-dinitrophenyl (DNP) were purified from MOPC 315 myeloma. A DNP-conjugated Ficoll was used as an antigen. For simulation of natural conditions of in vivo immune complex formation, 131I-DNP-Ficoll and 125I-IgA were administered through the intravenous and intraperitoneal routes, respectively. The kinetics half-life (t1/2) of the antigen (2.9 hours) and either the pIgA (7.2 hours) or mIgA (6.3 hours) in the experimental groups was not significantly different from the control. Glomerular IgA immune deposits were detectable only in mice that received pIgA and DNP-Ficoll. Plasma samples analyzed by gradient polyacrylamide gel electrophoresis revealed formation of large- and intermediate-sized pIgA complexes in circulation prior to glomerular deposition. Although mIgA failed to interact with such complexes in the circulation, it did bind to the pIgA immune deposits in the glomerulus. These results indicate that glomerular IgA immune deposits evolve from the localization of preformed circulating pIgA complexes that eventuates an in situ mIgA-mediated complex formation.

More Related Videos

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice09:43

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

Published on: June 8, 2022

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro14:18

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro

Published on: October 13, 2023

Related Concept Videos

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 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...
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...
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
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...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...