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Related Concept Videos

Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

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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...
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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...
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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...
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Canonical Wnt Signaling Pathway02:54

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Cytoplasmic Localization of WT1 and Decrease of miRNA-16-1 in Nephrotic Syndrome.

Pablo Zapata-Benavides1, Mariela Arellano-Rodríguez2, Juan José Bollain-Y-Goytia3

  • 1Departamento de Microbiología e Inmunología, Facultad de Ciencias Biológicas, Universidad Autónoma de Nuevo León (UANL), 66450 San Nicolás de los Garza, NL, Mexico.

Biomed Research International
|March 17, 2017
PubMed
Summary

Steroid-resistant nephrotic syndrome (SRNS) involves decreased Wilms tumor 1 (WT1) expression and podocyte loss. While serum miR-16-1 levels were significantly lower in NS patients, specific miRNAs did not appear to modulate WT1 protein levels.

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Genetics

Background:

  • Nephrotic syndrome (NS) is a kidney disorder characterized by proteinuria, hypoalbuminemia, hyperlipidemia, and edema.
  • Steroid-resistant NS (SRNS) presents a therapeutic challenge due to poor response to corticosteroids and is linked to reduced Wilms tumor 1 (WT1) expression in podocytes.
  • MicroRNAs (miRNAs) are implicated in regulating WT1 expression.

Purpose of the Study:

  • To investigate the expression and localization of WT1 protein in patients with idiopathic NS.
  • To quantify serum levels of miR-15a, miR-16-1, and miR-193a in NS patients and healthy controls.
  • To explore the association between serum miRNA levels and WT1 protein modulation in NS.

Main Methods:

  • Kidney biopsies from 21 idiopathic NS patients (68.75% SSNS, 31.25% SRNS) and 10 controls were analyzed for podocyte number and WT1 localization via immunofluorescence.
  • Serum samples were analyzed for miR-15a, miR-16-1, and miR-193a expression using quantitative reverse transcription polymerase chain reaction (RT-qPCR).

Main Results:

  • SRNS patients exhibited low WT1 expression and cytoplasmic delocalization, while SSNS patients showed both nuclear and cytoplasmic WT1 localization.
  • NS patients displayed reduced serum levels of miR-15a and miR-16-1 compared to controls, with a statistically significant decrease observed for miR-16-1 (p=0.019).
  • Serum miR-193a levels showed a slight increase in NS patients.

Conclusions:

  • Reduced WT1 expression and altered localization in NS contribute to podocyte loss.
  • The analyzed serum miRNAs (miR-15a, miR-16-1, miR-193a) do not appear to be significantly associated with WT1 protein modulation in the sera of NS patients.