Nephrology unit, Internal Medicine Department, Faculty of Medicine, Zagazig University, Egypt.
Clinical Pathology Department, Faculty of Medicine, Zagazig University, Egypt.
Cytokine. 2024 Dec;184:156772. doi: 10.1016/j.cyto.2024.156772. Epub 2024 Oct 3.
Chronic inflammation has been increasingly recognized as an essential pathogenic mechanism for the development and progression of diabetic kidney disease (DKD). Chemerin is an adipokine which has been suggested to be related to inflammation and has been correlated with the development of diabetic complications. We aimed to explore the potential links between chemerin, TNF - α, as a marker of systemic inflammation, and the level of albuminuria in patients with type 2 diabetes mellitus (T2DM).
The study included 84 patients with T2DM and 10 normoalbuminuric non-diabetic controls. Demographic, clinical and laboratory data including chemerin and TNF-α levels were collected.
A total of 84 diabetic patients were enrolled, 32 males (38.1 %), with mean age 57.9 ± 10.7 years. They were divided into 3 groups: A1: 14 with normalbuminuria, A2: 27 with microalbuminuria, and A3: 43 with macroalbuminuria (uACR < 30, 30-300 and > 300 mg/gm respectively). Chemerin and TNF-α levels increased with the progress of albuminuria (control: 21.3 (14.7 -77), A1: 794 (683-925), A2: 1150 (962.9 - 1221.5) and A3: 1466 (1197.5 - 2002.5) ng/ml; p < 0.001) and (control: 77.9 (59 - 96.8), A1: 85.2 (71-116.3), A2: 87.3 (81 - 97.5) and A3: 99 (85.1 - 142.5) pg/ml; p = 0.009) respectively. Among the diabetics, a significant association was evident between serum chemerin and serum TNF-α (r = 0.53; p < 0.001). On linear stepwise regression analysis, chemerin was significantly associated with TNF-α and HbA1c (unstandardized β 10.881 and 272.68 respectively, p < 0.001); and TNF-α was significantly correlated with chemerin, uACR (unstandardized β 0.059 and 0.004 respectively, p < 0.001) and HbA1c (unstandardized β -13.699, p = 0.014).
Our findings suggest a potential role of chemerin and TNF-α in the development and progression of DKD, and thus support the role of the inflammatory pathway. Larger follow up studies are warranted to further explore the potential links between chemerin, inflammation and DKD.
慢性炎症已被越来越多地认为是糖尿病肾病（DKD）发展和进展的重要发病机制。趋化素是一种脂肪因子，据报道与炎症有关，并与糖尿病并发症的发展相关。我们旨在探讨趋化素、TNF-α（一种全身性炎症的标志物）与 2 型糖尿病（T2DM）患者蛋白尿水平之间的潜在联系。
本研究纳入了 84 名 T2DM 患者和 10 名非糖尿病的正常白蛋白尿对照者。收集了人口统计学、临床和实验室数据，包括趋化素和 TNF-α 水平。
共纳入 84 例糖尿病患者，男性 32 例（38.1%），平均年龄 57.9±10.7 岁。他们分为 3 组：A1：14 例为正常白蛋白尿，A2：27 例为微量白蛋白尿，A3：43 例为大量白蛋白尿（uACR＜30、30-300 和＞300mg/gm）。趋化素和 TNF-α 水平随白蛋白尿的进展而升高（对照组：21.3（14.7-77）、A1：794（683-925）、A2：1150（962.9-1221.5）和 A3：1466（1197.5-2002.5）ng/ml；p＜0.001）和（对照组：77.9（59-96.8）、A1：85.2（71-116.3）、A2：87.3（81-97.5）和 A3：99（85.1-142.5）pg/ml；p=0.009）。在糖尿病患者中，血清趋化素与血清 TNF-α之间存在显著相关性（r=0.53；p＜0.001）。线性逐步回归分析显示，趋化素与 TNF-α和 HbA1c 显著相关（标准化β分别为 10.881 和 272.68，p＜0.001）；TNF-α与趋化素、uACR（标准化β分别为 0.059 和 0.004，p＜0.001）和 HbA1c（标准化β为-13.699，p=0.014）显著相关。
我们的研究结果表明，趋化素和 TNF-α在 DKD 的发生和发展中可能发挥作用，因此支持炎症途径的作用。需要进行更大规模的随访研究来进一步探讨趋化素、炎症与 DKD 之间的潜在联系。
