ReviewMediators of inflammation2022
The Role of Cytokines in Nephrotic Syndrome.
Review in Mediators of inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Advances in SRNS Gene Research: From Precision Classification to Precision Diagnosis and Treatment.Biomedicines · 2026Review
- Dysregulated Bone Marrow Contributes to Glomerular Injury through Soluble Factors.Journal of the American Society of Nephrology : JASN · 2026Article
- Short interference RNAs in glomerulonephritis: A mini review.BioImpacts : BI · 2026Review
- [Effect of rituximab combined with short-course glucocorticoid therapy on cellular immunity and cytokines in children with new-onset nephrotic syndrome].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- Risk factors for relapse of pediatric PNS based on oral health problems: a prediction model.BMC oral health · 2025Article
- Immune mechanisms and immunomodulatory therapies in steroid-resistant nephrotic syndrome.Renal failure · 2025Review
- Systemic inflammation accelerates the development of focal segmental glomerulosclerosis in a mouse model of adriamycin induced nephrosis.Scientific reports · 2025Article
- Curcumin as a protective agent against chromium and ammonia toxicity using molecular and biochemical approaches in fish.Scientific reports · 2025Article
- Urinary interleukin 13 level in steroid sensitive and resistant nephrotic syndrome: a cross-sectional single center study.Scientific reports · 2025Article
- Detailed Pathophysiology of Minimal Change Disease: Insights into Podocyte Dysfunction, Immune Dysregulation, and Genetic Susceptibility.International journal of molecular sciences · 2024Review
- Association of ABCB1(Rs10276036, C/T) Gene, IL-18, and TNFα as Risk Factors for Nephrotic Syndrome Incidence.Reports of biochemistry & molecular biology · 2024Article
- The Role of TNF-α in the Pathogenesis of Idiopathic Nephrotic Syndrome and Its Usefulness as a Marker of the Disease Course.Journal of clinical medicine · 2024Article
- Manganese nutrient mitigates ammonia, arsenic toxicity and high temperature stress using gene regulation via NFkB mechanism in fish.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic nephrotic syndrome (INS) is an important primary glomerular disease characterized by severe proteinuria. Evidence supports a role for T cell dysfunction in the pathogenesis of INS. Glucocorticoids are the primary therapy for INS; however, steroid-resistant NS (SRNS) patients are at a higher risk of drug-induced side effects and harbor poor prognosis. Although the exact mechanism of the resistance is unknown, the imbalances of T helper subtype 1 (Th1), Th2, and regulatory T cells (Tregs) and their cytokines may be involved in the pathogenesis of glucocorticoid responsiveness. Up to now, no confirmed biomarkers have been able to predict SRNS; however, a panel of cytokines may predict responsiveness and identify SRNS patients. Thus, the introduction of distinctive cytokines as novel biomarkers of SRNS enables both preventions of drug-related toxicity and earlier switch to more effective therapies. This review highlights the impacts of T cell population imbalances and their downstream cytokines on response to glucocorticoid responsiveness state in INS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.