2型糖尿病患者血清同种异体移植炎症因子-1浓度及其与糖尿病肾病发病进展的关系

Yahia Zakareya, Fatma Al-zahraa Sayed Bukhary, El-Ghaffar Mohamad, Khaled M Othman, Osama Abdel Shakoor
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The patients' group was classified according to the Urinary Albumin Excretion (UAE) level into the following: group IA (normoalbuminuria group), which included 30 patients with UAE less than 30 mg/g of creatinine (mg/g Cr); group IIA (microalbuminuria group), which comprised 25 patients with UAE from 30 to 300 mg/g Cr; and group IIIA (macroalbuminuria group), which included 25 patients with UAE greater than 300 mg/g Cr. All patients were subjected to further classification according to estimated glomerular filtration rate (eGFR) into the following: group IB, which included 31 patients with eGFR less than or equal to 60 ml/min/1.73 m2; and group IIB, which included 49 patients with eGFR greater than 60 ml/min/1.73 m2. Results AIF-1 was significantly raised in all patients compared with controls (P = 0.001), and in both group IIA and group IIIA than in group IA (P = 0.001). 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引用次数: 0

摘要

目的炎症机制可能在糖尿病肾病(DN)中起关键作用。同种异体移植炎症因子-1 (AIF-1)是活化巨噬细胞的标志物,可能在DN的进展中起作用。目的探讨血清AIF-1浓度与DN参数的关系。患者与方法本研究共纳入80例2型糖尿病患者和20例健康志愿者(对照组)。排除肾功能不全或有炎症的患者。对患者和对照组进行了临床和实验室检查。根据尿白蛋白排泄(UAE)水平将患者组分为:IA组(正常尿白蛋白组),其中30例UAE低于30 mg/g肌酐(mg/g Cr);IIA组(微量白蛋白尿组),包括25例Cr含量为30至300 mg/g的UAE患者;IIIA组(巨白蛋白尿组),包括25例大于300mg /g Cr的UAE患者。所有患者根据估计的肾小球滤过率(eGFR)进一步分类如下:IB组,包括31例eGFR小于或等于60ml /min/1.73 m2的患者;IIB组包括49例eGFR大于60 ml/min/1.73 m2的患者。结果所有患者的AIF-1水平均显著高于对照组(P = 0.001), IIA组和IIIA组的AIF-1水平均显著高于IA组(P = 0.001)。AIF-1与年龄、糖尿病病程、UAE、对数尿白蛋白肌酐(A/C)比、尿素、肌酐、空腹血糖(FBS)呈正相关(P < 0.001)。AIF-1浓度与eGFR呈负相关。IB组血清AIF-1(112.35±26.8)明显高于IIB组(83.41±26.23)(P < 0.001)。单纯性和增生性糖尿病视网膜病变组的血清AIF-1均显著高于非糖尿病视网膜病变组(P = 0.001)。结论AIF-1在2型糖尿病患者、DN患者和视网膜病变患者中显著升高,可能为炎症过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Serum allograft inflammatory factor-1 concentration in type 2 diabetes mellitus and its relation to the pathogenesis and progression of diabetic nephropathy
Objective Inflammatory mechanisms may play a pivotal role in diabetic nephropathy (DN). Allograft inflammatory factor-1 (AIF-1), a marker of activated macrophage, may have a role in the progression of DN. Aim The aim of the present study was to examine the relationship between serum AIF-1 concentration and parameters of DN. Patients and methods A total of 80 type 2 diabetes patients and 20 healthy volunteers (control group) were included in the present study. Patients with renal dysfunction or inflammatory conditions were excluded. Clinical and laboratory tests for patients and controls were carried out. The patients' group was classified according to the Urinary Albumin Excretion (UAE) level into the following: group IA (normoalbuminuria group), which included 30 patients with UAE less than 30 mg/g of creatinine (mg/g Cr); group IIA (microalbuminuria group), which comprised 25 patients with UAE from 30 to 300 mg/g Cr; and group IIIA (macroalbuminuria group), which included 25 patients with UAE greater than 300 mg/g Cr. All patients were subjected to further classification according to estimated glomerular filtration rate (eGFR) into the following: group IB, which included 31 patients with eGFR less than or equal to 60 ml/min/1.73 m2; and group IIB, which included 49 patients with eGFR greater than 60 ml/min/1.73 m2. Results AIF-1 was significantly raised in all patients compared with controls (P = 0.001), and in both group IIA and group IIIA than in group IA (P = 0.001). AIF-1 had significant positive correlation with age, diabetes duration, UAE, log urinary albumin creatinine (A/C) ratio, urea, creatinine, and Fasting Blood Sugar (FBS) (P < 0.001). AIF-1 concentration was inversely correlated with eGFR. Serum AIF-1 was significantly raised in group IB (112.35 ± 26.8) compared with group IIB (83.41 ± 26.23) (P < 0.001). Serum AIF-1 was significantly raised in both groups of simple and proliferative diabetic retinopathy than in the group of nondiabetic retinopathy (P = 0.001). Conclusion AIF-1 was significantly raised in type 2 diabetic patients and in those with DN and retinopathy, which may raise a possibility of their pathogenesis as an inflammatory process.
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