n randomized, controlled, blinded, imitation-controlled study the neph的简体中文翻译

n randomized, controlled, blinded,

n randomized, controlled, blinded, imitation-controlled study the nephroprotective effect of RIPC in CHD patients with low-moderate CIN risk was investigated. As a result, 26 patients were randomizedfor RIPC and 25 for sRIPC. It is considered, that CIN develops in 9% of cases when iodinated contrast agent is injected [18], and in 20–30% among those with a baseline creatinine >2 mg/dl [2]. In our study, CIN developed in 28% of cases in sRIPC group, and in RIPC – only in 3.8%. The resultsUncorrected Author Proof approximately correspond to the data by Er et al. [9] who indicated 28% CIN reduction after RIPC,given the fact that in the above-referred study the GFR baseline threshold for inclusion in the studywas higher –≤60 mL/min/1,73 m2 in contrast to the present one (≤80 mL/min/1,73m2 173 ). Menting etal. [25] not noted the effect of RIPC on CIN occurrence in patients with moderate CIN risk, but in the high risk ones (≥11 points according to the Mehran score). Our data corresponds also with study of Igarashi et al. [17], who used more RIPC cycles (4 versus 3 in our study) and estimated another kidney-sensitive marker – liver-type fatty acid-binding protein (L-FABR) in patients with moderate CKD. As a result, CIN incidence decreased from 26.9% to 7.7% in compare to sham and L-FABRdeclined (p = 0,003), due to, as proposed by the authors, oxidative stress modification.As it is known, NGAL and cystatin-C have higher sensitivity and specificity of the predictive power in identification of AKI compared to creatinine and urea [7, 19]. For instance, creatinine increases in case of 50% of kidney tissue damage [15]. NGAL has proved as an early, sensitive, specific and predictive biomarker of AKI after contrast agent administration [32]. When the concentration of cystatin-C increases by 10%, it also shows itself to be a CIN marker which is 100% sensitive and 30% specificity[27, 32]. If in RIPC group there was a downward trend for all the four biomarkers after CAG, in the sRIPC group – they tended to increase, for creatinine and urea was significant. The comparison of changes between the sRIPC/RIPC groups before/after CAG was also significant.Thus in the study RIPC showed nephroprotective effect and considerably prevented CIN in patients with CHD and low-moderate GFR decline.This study has certain limitations. In particular, the sampling size is rather small; patients widely varied in kidney failure and GFR degree. However, the comparison of the obtained data with the findings of other studies allows us to suggest that the achieved results are reliable.
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在一项随机,对照,盲法,仿对照研究中,研究了RIPC对<br>低中度CIN风险的冠心病患者的肾脏保护作用。结果,随机分配<br>了26例RIPC 患者和25例sRIPC患者。据认为,注射碘化造影剂的病例中有9%发生CIN [18],基线肌酐> 2 mg / dl的病例中有20-30%发生CIN [2]。在我们的研究中,sRIPC组中有28%的病例发展为CIN,而RIPC组中只有3.8%。未<br>校正的作者证明的结果大约与Er等人的数据相对应。[9]指出RIPC后CIN降低28%,原因是上述研究中纳入研究的GFR基线阈值<br>与目前的相比(≤80mL / min / 1,73m2 173)更高–≤60mL / min / 1,73 m2。门庭等。[25]没有注意到在中度CIN风险患者中RIPC对CIN发生的影响,但在<br>高风险患者中(根据Mehran评分≥11分)。我们的数据也与Igarashi等人的研究相对应。[17],他们使用了更多的RIPC周期(在我们的研究中为4比3),并估计了中度CKD患者的另一种肾脏敏感标记物-肝型脂肪酸结合蛋白(L-FABR)。结果,与假手术相比,CIN发生率从26.9%下降到7.7%,L-FABR <br>下降(p = 0,003),这是由于作者提出的氧化应激修饰。<br>众所周知,与肌酐和尿素相比,NGAL和半胱氨酸蛋白酶抑制剂C在预测AKI方面具有更高的灵敏度和特异性[7,19]。例如,在50%的肾脏组织受损的情况下,肌酐会增加[15]。服用造影剂后,NGAL已被证明是AKI的早期,敏感,特异性和可预测的生物标志物[32]。当胱抑素-C的浓度增加10%时,它也表明自己是CIN标记,具有100%的敏感性和30%的特异性[27,32]。如果在RIPC组中,CAG后所有四个生物标志物都有下降的趋势,那么在sRIPC组中,它们的趋势会增加,因为肌酐和尿素含量很高。在CAG前后,sRIPC / RIPC组之间的变化比较也很有意义。<br>这项研究有一定的局限性。特别是,采样量很小。患者的肾功能衰竭和肾小球滤过率程度差异很大。但是,将获得的数据与其他研究的结果进行比较可以使我们建议所获得的结果是可靠的。
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结果 (简体中文) 2:[复制]
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n randomized, controlled, blinded, imitation-controlled study the nephroprotective effect of RIPC in<br> CHD patients with low-moderate CIN risk was investigated. As a result, 26 patients were randomized<br>for RIPC and 25 for sRIPC. It is considered, that CIN develops in 9% of cases when iodinated contrast agent is injected [18], and in 20–30% among those with a baseline creatinine >2 mg/dl [2]. In our study, CIN developed in 28% of cases in sRIPC group, and in RIPC – only in 3.8%. The results<br>Uncorrected Author Proof approximately correspond to the data by Er et al. [9] who indicated 28% CIN reduction after RIPC,given the fact that in the above-referred study the GFR baseline threshold for inclusion in the study<br>was higher –≤60 mL/min/1,73 m2 in contrast to the present one (≤80 mL/min/1,73m2 173 ). Menting etal. [25] not noted the effect of RIPC on CIN occurrence in patients with moderate CIN risk, but in<br> the high risk ones (≥11 points according to the Mehran score). Our data corresponds also with study of Igarashi et al. [17], who used more RIPC cycles (4 versus 3 in our study) and estimated another kidney-sensitive marker – liver-type fatty acid-binding protein (L-FABR) in patients with moderate CKD. As a result, CIN incidence decreased from 26.9% to 7.7% in compare to sham and L-FABR<br>declined (p = 0,003), due to, as proposed by the authors, oxidative stress modification.<br>As it is known, NGAL and cystatin-C have higher sensitivity and specificity of the predictive power in identification of AKI compared to creatinine and urea [7, 19]. For instance, creatinine increases in case of 50% of kidney tissue damage [15]. NGAL has proved as an early, sensitive, specific and predictive biomarker of AKI after contrast agent administration [32]. When the concentration of cystatin-C increases by 10%, it also shows itself to be a CIN marker which is 100% sensitive and 30% specificity[27, 32]. If in RIPC group there was a downward trend for all the four biomarkers after CAG, in the sRIPC group – they tended to increase, for creatinine and urea was significant. The comparison of changes between the sRIPC/RIPC groups before/after CAG was also significant.Thus in the study RIPC showed nephroprotective effect and considerably prevented CIN in patients with CHD and low-moderate GFR decline.<br>This study has certain limitations. In particular, the sampling size is rather small; patients widely varied in kidney failure and GFR degree. However, the comparison of the obtained data with the findings of other studies allows us to suggest that the achieved results are reliable.
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结果 (简体中文) 3:[复制]
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随机、对照、盲法、模拟对照研究肾保护作用<br>对冠心病患者进行中、低CIN风险调查。结果,26名患者被随机分为两组<br>RIPC为25,sRIPC为25。据认为,注射碘化造影剂时,9%的病例会发生CIN[18],而在基线肌酐>2 mg/dl的病例中,有20-30%的病例发生CIN[2]。在我们的研究中,sRIPC组28%的病例发生CIN,RIPC组仅3.8%发生CIN。结果<br>未经修正的作者证明与Er等人的数据基本一致。[9] 世卫组织表示,RIPC后CIN降低了28%,因为在上述研究中,GFR基线阈值可纳入研究<br>与目前的(≤80 mL/min/1,73m2)相比,≤60 mL/min/1,73 m2 173。门汀等。[25]未注意到RIPC对中度CIN风险患者CIN发生的影响,但是<br>高危组(Mehran评分≥11分)。我们的数据也与Igarashi等人的研究一致。[17] 他使用了更多的RIPC周期(在我们的研究中是4个,而不是3个),并估计了另一个肾敏感标志物-肝型脂肪酸结合蛋白(L-FABR)在中度CKD患者中的应用。结果,与sham和L-FABR相比,CIN的发生率从26.9%下降到7.7%<br>下降(p=0003),这是由于作者提出的氧化应激修饰。<br>众所周知,与肌酐和尿素相比,NGAL和cystatin-C在识别AKI方面具有更高的敏感性和特异性[7,19]。例如,在50%的肾组织损伤的情况下,肌酐增加[15]。NGAL已被证明是一种早期、敏感、特异、可预测的AKI生物标志物。当cystatin-C浓度增加10%时,它也显示出它是一个100%敏感和30%特异性的CIN标记物[27,32]。如果在RIPC组,CAG后所有四个生物标志物都有下降趋势,在sRIPC组,它们趋于增加,肌酐和尿素显著。比较sRIPC/RIPC组CAG前后的变化很重要。因此在这项研究中,RIPC对CHD患者具有肾保护作用,并可显著预防CIN和低-中度GFR下降。<br>这项研究有一定的局限性。特别是样本量较小,肾功能衰竭和GFR程度差异很大。然而,将所获得的数据与其他研究的结果进行比较,我们可以认为所取得的结果是可靠的。<br>
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