METHODS: The study sample included patients with type 2 DM referred for elective PCI who had poor blood pressure (BP) control according to 24-hour BP monitoring (24-BPM) (mean daily systolic BP ≥130 mmHg, mean daily diastolic BP ≥80 mmHg). The data were collected from 2018 through 2020. A total of 75 patients was included and distributed by simple randomization into two groups: group 1 (main, n=37) received azilsartan medoxomil as an antihypertensive drug at a dose of 40 mg/day (previously prescribed angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers (ARB) were discontinued); group 2 (control, n=38) continued on their previous antihypertensive therapy. The follow-up period was 6 months. During each of 5 consecutive follow-up visits, the patient was examined, 24-BPM was recorded, and urinary markers of renal dysfunction (glomerular filtration rate, GFR; neutrophil gelatinase-associated lipocalin, NGAL; urine albumin-creatinine ratio, UACR; kidney injury molecule, KIM-1; and interleukin-18, IL-18) were measured.
RESULTS: During the azilsartan treatment, GFR decreased by 7.4%, while in the control group, it decreased by 18.9% (p<0.001). For 6 months of follow-up, no changes in the NGAL concentration were found in the main group, while the NGAL concentration in the control group increased by 12.9%. With azilsartan, there was a decrease in the urinary concentration of IL-18 (16.9%), while in patients of the control group, IL-18 increased (7.14%). Proteinuria progressed in both groups, which was expectable given the presence of DM; however, in patients receiving azilsartan, the UACR value increased by 37.5%, while in patients of the control group, it increased by 96.15%. These differences were statistically significant. No statistically significant differences were found in the concentrations of cystatin C and KIM-1.
CONCLUSIONS: This study demonstrated two important facts: the possibility for diagnosing contrast-induced acute kidney injury (CI-AKI) using new, more sensitive markers of kidney damage, which is important for assessing the effectiveness of prevention, and the possibility of using ARBs, in particular azilsartan, for the prevention of CI-AKI in patients with IHD in combination with AH and DM.
方法:研究样本包括接受择期PCI治疗的2型糖尿病患者,根据24小时血压监测(24-BPM)(平均每日收缩压≥130mmHg,血压(BP)控制不佳,平均每日舒张压≥80mmHg)。这些数据是从2018年到2020年收集的。共纳入75例患者,通过简单随机分为两组:第1组(主要,n=37)接受阿齐沙坦酯作为抗高血压药物,剂量为40毫克/天(先前处方的血管紧张素转换酶抑制剂或血管紧张素II受体阻滞剂(ARB)停用);第2组(对照,n=38)继续进行先前的抗高血压治疗。随访期为6个月。在连续的5次随访中,病人接受了检查,记录了24-BPM,和肾功能不全的尿标志物(肾小球滤过率,GFR;中性粒细胞明胶酶相关脂质运载蛋白,NGAL;尿白蛋白-肌酐比值,UACR;肾损伤分子,测量KIM-1;和白介素-18,IL-18)。
结果:在阿齐沙坦治疗期间,GFR下降7.4%,而在对照组中,下降了18.9%(p<0.001)。6个月的随访,在主要组中没有发现NGAL浓度的变化,而对照组的NGAL浓度增加了12.9%。阿齐沙坦,尿中IL-18浓度下降(16.9%),而在对照组的患者中,IL-18增加(7.14%)。两组蛋白尿均有进展,考虑到DM的存在,这是可以预期的;然而,在接受阿齐沙坦的患者中,UACR值增加了37.5%,而在对照组的患者中,增长96.15%。这些差异具有统计学意义。胱抑素C和KIM-1的浓度无统计学差异。
结论:这项研究证明了两个重要事实:使用新的造影剂引起的急性肾损伤(CI-AKI)诊断的可能性,更敏感的肾损伤标志物,这对于评估预防的有效性很重要,以及使用ARB的可能性,特别是阿齐沙坦,用于预防IHD合并AH和DM患者的CI-AKI。