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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...
Nephrons01:10

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...
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...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Nephrotic Syndrome III : Nursing Management01:24

Nephrotic Syndrome III : Nursing Management

Nursing management for nephrotic syndrome adapts as the disease progresses, with strategies evolving to address advancing symptoms and complications.Early-Stage Management In the early stages, nursing interventions for nephrotic syndrome resemble those used in managing acute glomerulonephritis, focusing on symptom monitoring, fluid balance, and managing mild to moderate edema.Vital Signs: Regularly monitor blood pressure, pulse, respiratory rate, and temperature to promptly identify...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...

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Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
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Published on: June 26, 2018

Cytokines expression in SLE nephritis.

A Gigante1, M L Gasperini, A Afeltra

  • 1Department of Clinical Medicine, "Sapienza" University, Rome, Italy. antonietta_gigante@yahoo.it

European Review for Medical and Pharmacological Sciences
|March 9, 2011
PubMed
Summary
This summary is machine-generated.

Systemic lupus erythematosus (SLE) nephritis involves immune deposits and inflammation, with elevated cytokines correlating to disease activity. Targeting these cytokines shows promise for reducing proteinuria and improving kidney function in SLE patients.

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Area of Science:

  • Immunology
  • Nephrology
  • Rheumatology

Background:

  • Renal involvement, or lupus nephritis, is a frequent complication of systemic lupus erythematosus (SLE).
  • Glomerular injury in SLE nephritis stems from in situ immune deposit formation, primarily involving anti-double-stranded DNA (anti-dsDNA) and anti-C1q antibodies.
  • Immune complex deposition triggers inflammation via endothelial adhesion molecule activation, recruiting pro-inflammatory leukocytes to the kidney.

Purpose of the Study:

  • To elucidate the role of cytokines in the pathogenesis of lupus nephritis.
  • To investigate the correlation between serum and urinary cytokine levels and disease activity in SLE patients.
  • To explore the therapeutic potential of cytokine blockade in managing lupus nephritis.

Main Methods:

  • Analysis of immune deposit formation and inflammatory cell infiltration in SLE nephritis.
  • Quantification of serum and urinary cytokine concentrations (e.g., IL-6, IL-17, IL-10, INF-gamma, TNF-alpha) in SLE patients.
  • Correlation of cytokine levels with clinical disease activity indices, such as the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI).

Main Results:

  • Elevated serum levels of IL-6, IL-17, IL-12, INF-gamma, IL-18, IL-10, and TNF-alpha were observed in SLE patients compared to healthy individuals.
  • Increased serum cytokine concentrations correlated with SLE disease activity.
  • Urinary cytokine levels (IL-6, IL-10, INF-gamma, TGF-beta) also showed a correlation with disease activity, and SLEDAI scores correlated with the overexpression of specific cytokines like IL-17, IL-10, TNF-alpha, and the INF-gamma/IL-12 axis.

Conclusions:

  • Cytokines play a critical role as inflammatory mediators in extending renal injury in lupus nephritis.
  • Elevated cytokine levels serve as potential biomarkers for SLE disease activity.
  • Cytokine blockade therapy presents a promising therapeutic strategy for reducing proteinuria and improving renal function in SLE patients.