Department of Biology, North Carolina A&T State University, Greensboro, NC 27411, USA.
Cone Health Community Health and Wellness Center, Greensboro, NC 27401, USA.
J Diabetes Res. 2019 Feb 5;2019:5359635. doi: 10.1155/2019/5359635. eCollection 2019.
African Americans are disproportionately burdened by diabetic kidney disease (DKD). However, little is known about the cellular and molecular mechanisms underlying the onset and progression of DKD in this population. The goal of the current study was to determine the association between specific inflammation markers and kidney injury in diabetic African American men. To this end, we recruited diabetic patients either with ( = 20) or without ( = 87) diagnosed kidney disease along with age-matched nondiabetic controls ( = 81). Urinary albumin-to-creatinine ratios (UACRs) and estimated glomerular filtration rates (eGFR) were used for biochemical assessment of kidney function. We then measured plasma and urinary levels of seven inflammatory markers, including adiponectin, C-reactive protein (CRP), tumor necrosis factor- (TNF-), TNF receptor 1 (TNFR1), TNF receptor 2 (TNFR2), interleukin-6 (IL-6), and intercellular cell adhesion molecule-1 (ICAM-1). Plasma levels of TNF-, TNFR1, and TNFR2 were significantly higher in diabetics with macroalbuminuria compared to nondiabetic controls and diabetics with normoalbuminuria or microalbuminuria. Likewise, urinary levels of ICAM-1 were higher in diabetics with macroalbuminuria compared to the other groups. Indeed, urinary ICAM-1, plasma TNF-, and adiponectin had moderate positive correlations with UACR while plasma TNFR1 and TNFR2 levels were strongly correlated with kidney injury, indicated by multiple biomarkers of kidney injury. In contrast, though plasma CRP was elevated in diabetic subjects relative to nondiabetic controls, its levels did not correlate with kidney injury. Together, these data suggest that inflammation, particularly that mediated by the TNF-/NF-B signaling axis, may play a role in the pathogenesis of DKD in African American men.
非裔美国人患有糖尿病肾病(DKD)的比例不成比例。然而,对于这一人群中 DKD 的发生和进展的细胞和分子机制知之甚少。本研究的目的是确定特定炎症标志物与糖尿病非裔美国男性肾脏损伤之间的关联。为此,我们招募了患有(n=20)或未患有(n=87)诊断性肾病的糖尿病患者以及年龄匹配的非糖尿病对照者(n=81)。尿白蛋白与肌酐比值(UACR)和估计肾小球滤过率(eGFR)用于评估肾功能的生化指标。然后,我们测量了七种炎症标志物的血浆和尿液水平,包括脂联素、C 反应蛋白(CRP)、肿瘤坏死因子-(TNF-)、TNF 受体 1(TNFR1)、TNF 受体 2(TNFR2)、白细胞介素-6(IL-6)和细胞间黏附分子-1(ICAM-1)。与非糖尿病对照者和 UACR 正常或微量白蛋白尿的糖尿病患者相比,大量白蛋白尿的糖尿病患者的血浆 TNF-、TNFR1 和 TNFR2 水平明显更高。同样,大量白蛋白尿的糖尿病患者的尿液 ICAM-1 水平也高于其他组。事实上,尿 ICAM-1、血浆 TNF-和脂联素与 UACR 呈中度正相关,而血浆 TNFR1 和 TNFR2 水平与肾脏损伤强烈相关,由肾脏损伤的多个生物标志物表明。相比之下,虽然与非糖尿病对照组相比,糖尿病患者的血浆 CRP 水平升高,但与肾脏损伤无相关性。总的来说,这些数据表明炎症,特别是 TNF-/NF-B 信号轴介导的炎症,可能在非裔美国男性 DKD 的发病机制中发挥作用。