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Purpose of Review <p>Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are primarily attributed to glomerular diseases in a worldwide perspective. Increasing evidence suggests that inflammatory cytokines and their associated genetic polymorphisms play critical roles in disease susceptibility, progression, and therapeutic response. This review summarizes current knowledge regarding cytokine-mediated mechanisms involved in glomerular injury and evaluates the clinical significance of cytokine gene variants in glomerular diseases.</p> Recent Findings <p>Experimental and clinical evidence suggests that the following pro inflammatory cytokines can cause podocyte injury, mesangial cell proliferation, recruitment of leukocytes to the glomerulus and create glomerular inflammation. <i>IL-6</i> (Interleukin 6), <i>IL-1</i> (Interleukin 1 βeta), <i>TNF-alpha</i> (Tumor Necrosis Factor), <i>IL</i> -8 (Interleukin 8). Conversely, <i>TGF-β</i> (Transforming Growth Factor) and <i>IL-13</i> (Interleukin 13) lead to accumulation of extracellular matrix and renal fibrosis ultimately resulting in progression of renal disease. Additionally Polymorphisms in cytokine-related genes, including <i>IL1B</i>,<i> IL1RN</i>,<i> IL10</i>,<i> TNF</i>, and <i>TGFB1</i>, are associated with altered cytokine expression, disease susceptibility, steroid responsiveness, and renal outcomes. Emerging evidence supports cytokine biomarkers and molecular profiling for risk stratification and therapeutic monitoring.</p> Summary <p>Inflammatory cytokines act as central mediators linking immune dysregulation to structural and functional renal damage in glomerular diseases. Cytokine gene polymorphisms may serve as valuable biomarkers for disease prediction and therapeutic stratification. Cytokine targeting therapy and precision medical therapy are newly emerging therapies that present an opportunity to improve outcomes for patients suffering from nephrotic syndrome (NS), lupus nephritis, IgA nephropathy, FSGS and diabetic nephropathy.</p>

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Investigating the Role of Inflammatory Cytokine Genes in Glomerular Disease

  • 期刊论文

  • 发表日期：

    2026年7月31日

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  • Raghul Priyadharson S.,
  • Sangeetha G.,
  • Sudha Ekambaram,
  • Thendral Hepsibha B.,
  • Sneha Grace Mathews,
  • Mohana Priya C. D.

摘要

Purpose of Review

Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are primarily attributed to glomerular diseases in a worldwide perspective. Increasing evidence suggests that inflammatory cytokines and their associated genetic polymorphisms play critical roles in disease susceptibility, progression, and therapeutic response. This review summarizes current knowledge regarding cytokine-mediated mechanisms involved in glomerular injury and evaluates the clinical significance of cytokine gene variants in glomerular diseases.

Recent Findings

Experimental and clinical evidence suggests that the following pro inflammatory cytokines can cause podocyte injury, mesangial cell proliferation, recruitment of leukocytes to the glomerulus and create glomerular inflammation. IL-6 (Interleukin 6), IL-1 (Interleukin 1 βeta), TNF-alpha (Tumor Necrosis Factor), IL -8 (Interleukin 8). Conversely, TGF-β (Transforming Growth Factor) and IL-13 (Interleukin 13) lead to accumulation of extracellular matrix and renal fibrosis ultimately resulting in progression of renal disease. Additionally Polymorphisms in cytokine-related genes, including IL1B, IL1RN, IL10, TNF, and TGFB1, are associated with altered cytokine expression, disease susceptibility, steroid responsiveness, and renal outcomes. Emerging evidence supports cytokine biomarkers and molecular profiling for risk stratification and therapeutic monitoring.

Summary

Inflammatory cytokines act as central mediators linking immune dysregulation to structural and functional renal damage in glomerular diseases. Cytokine gene polymorphisms may serve as valuable biomarkers for disease prediction and therapeutic stratification. Cytokine targeting therapy and precision medical therapy are newly emerging therapies that present an opportunity to improve outcomes for patients suffering from nephrotic syndrome (NS), lupus nephritis, IgA nephropathy, FSGS and diabetic nephropathy.