Diabetic type 2 patients compared to nondiabetic patients exhibit an increased risk of developing diabetic kidney disease (DKD), the leading cause of end-stage renal disease. Hyperglycemia, hypertension, oxidative stress (OS), and genetic background are some of the mechanisms and pathways implicated in DKD pathogenesis. However, data on OS pathway susceptibility genes show limited success and conflicting or inconclusive results. Our study is aimed at exploring OS pathway genes and variants which could be associated with DKD. We recruited 121 diabetes mellitus type 2 (DM2) patients with DKD (cases) and 220 DM2, non-DKD patients (control) of Greek origin and performed a case-control association study using genome-wide association data. PLINK and EIGENSOFT were used to analyze the data. Our results indicate 43 single nucleotide polymorphisms with their 21 corresponding genes on the OS pathway possibly contributing or protecting from DKD: SPP1, TPO, TTN, SGO2, NOS3, PDLIM1, CLU, CCS, GPX4, TXNRD2, EPHX2, MTL5, EPX, GPX3, ALOX12, IPCEF1, GSTA, OXR1, GPX6, AOX1, and PRNP. Therefore, a genetic OS background might underlie the complex pathogenesis of DKD in DM2 patients.

中文翻译：

---

2型糖尿病中的氧化应激基因：与糖尿病肾病的关系

与非糖尿病患者相比，2 型糖尿病患者患糖尿病肾病 (DKD) 的风险增加，这是导致终末期肾病的主要原因。高血糖、高血压、氧化应激 (OS) 和遗传背景是与 DKD 发病机制有关的一些机制和途径。然而，关于 OS 通路易感基因的数据显示成功有限，结果相互矛盾或不确定。我们的研究旨在探索可能与 DKD 相关的 OS 通路基因和变体。我们招募了 121 名患有 DKD 的 2 型糖尿病 (DM2) 患者（病例）和 220 名 DM2、希腊血统的非 DKD 患者（对照），并使用全基因组关联数据进行了病例对照关联研究。PLINK 和 EIGENSOFT 用于分析数据。我们的结果表明 43 个单核苷酸多态性及其 21 个相应基因在 OS 通路上可能有助于或保护 DKD：SPP1、TPO、TTN、SGO2、NOS3、PDLIM1、CLU、CCS、GPX4、TXNRD2、EPHX2、MTL5、EPX、GPX3 、ALOX12、IPCEF1、GSTA、OXR1、GPX6、AOX1 和 PRNP。因此，遗传性 OS 背景可能是 DM2 患者 DKD 复杂发病机制的基础。