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<p>Diabetic nephropathy (DN) is a severe microvascular complication of type 2 diabetes mellitus (T2DM), driven by complex interactions between metabolic, hemodynamic, and inflammatory pathways. Prolonged inflammation has been linked to tissue damage and fibrotic lesions in certain diseases. Genetic variations in inflammatory cytokines such as interleukin-6 (IL-6) and interleukin-8 (IL-8) may influence individual susceptibility to DN. This case–control study investigated the association between two functional promoter polymorphisms-IL-6&#xa0;rs1800795 (-174G &gt; C) and&#xa0;IL-8&#xa0;rs4073 (-251&#xa0;T &gt; A)-and the risk of diabetic nephropathy in patients with type 2 diabetes mellitus. We enrolled 100 T2DM patients with DN and 100 T2DM controls without nephropathy. Genotyping was performed using ARMS-PCR, and clinical/biochemical profiles were assessed. The results demonstrated that the&#xa0;IL-6&#xa0;C allele and&#xa0;IL-8&#xa0;A allele were significantly more frequent in the DN group and exhibited a clear gene-dose effect on DN risk. Carriers of these risk alleles presented with a more severe clinical phenotype, including significantly worse renal function (lower eGFR, higher creatinine), a higher prevalence of hypertension, and an adverse metabolic profile marked by dyslipidemia. These findings elevate pro-inflammatory cytokines IL-6/ IL-8 from a mere inflammatory mediator to a potential genetic fulcrum in a pathogenic network that integrates inflammatory, hemodynamic, and metabolic axes in diabetic nephropathy.</p>

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Association of Functional IL-6 (-174G > C) and IL-8 (-251 T > A) Promoter Variants with Genetic Susceptibility and Aggressive Clinical Phenotype in Diabetic Nephropathy: A Case–Control Study

  • 期刊论文

  • 发表日期：

    2026年3月19日

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  • Mohammad Fahad Ullah,
  • Rashid Mir,
  • Khalid Salman Albalawi,
  • Yazeed Ahmed Alshehri,
  • Rayan Khalil Alahmadi,
  • Yousef Ali Alshamrani,
  • Jamsheed Javid,
  • Mohammed M. Jalal,
  • Malik A. Altayar,
  • Imadeldin Elfaki

摘要

Diabetic nephropathy (DN) is a severe microvascular complication of type 2 diabetes mellitus (T2DM), driven by complex interactions between metabolic, hemodynamic, and inflammatory pathways. Prolonged inflammation has been linked to tissue damage and fibrotic lesions in certain diseases. Genetic variations in inflammatory cytokines such as interleukin-6 (IL-6) and interleukin-8 (IL-8) may influence individual susceptibility to DN. This case–control study investigated the association between two functional promoter polymorphisms-IL-6 rs1800795 (-174G > C) and IL-8 rs4073 (-251 T > A)-and the risk of diabetic nephropathy in patients with type 2 diabetes mellitus. We enrolled 100 T2DM patients with DN and 100 T2DM controls without nephropathy. Genotyping was performed using ARMS-PCR, and clinical/biochemical profiles were assessed. The results demonstrated that the IL-6 C allele and IL-8 A allele were significantly more frequent in the DN group and exhibited a clear gene-dose effect on DN risk. Carriers of these risk alleles presented with a more severe clinical phenotype, including significantly worse renal function (lower eGFR, higher creatinine), a higher prevalence of hypertension, and an adverse metabolic profile marked by dyslipidemia. These findings elevate pro-inflammatory cytokines IL-6/ IL-8 from a mere inflammatory mediator to a potential genetic fulcrum in a pathogenic network that integrates inflammatory, hemodynamic, and metabolic axes in diabetic nephropathy.