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Decreased renal perfusion during acute kidney injury in critical COVID-19 assessed by magnetic resonance imaging: a prospective case control study
Critical Care ( IF 15.1 ) Pub Date : 2022-09-01 , DOI: 10.1186/s13054-022-04132-8
Tomas Luther 1 , Per Eckerbom 2 , Eleanor Cox 3, 4 , Miklos Lipcsey 1, 5 , Sara Bülow 1 , Michael Hultström 1, 6 , Francisco Martinez Torrente 1 , Jan Weis 7 , Fredrik Palm 6 , Susan Francis 3, 4 , Robert Frithiof 1 , Per Liss 2
Affiliation  

Renal hypoperfusion has been suggested to contribute to the development of acute kidney injury (AKI) in critical COVID-19. However, limited data exist to support this. We aim to investigate the differences in renal perfusion, oxygenation and water diffusion using multiparametric magnetic resonance imaging in critically ill COVID-19 patients with and without AKI. A prospective case–control study where patients without prior kidney disease treated in intensive care for respiratory failure due to COVID-19 were examined. Kidney Disease: Improving Global Outcomes Creatinine criteria were used for group allocation. Main comparisons were tested using Mann–Whitney U test. Nineteen patients were examined, ten with AKI and nine without AKI. Patients with AKI were examined in median 1 [0–2] day after criteria fulfillment. Age and baseline Plasma-Creatinine were similar in both groups. Total renal blood flow was lower in patients with AKI compared with patients without (median 645 quartile range [423–753] vs. 859 [746–920] ml/min, p = 0.037). Regional perfusion was reduced in both cortex (76 [51–112] vs. 146 [123–169] ml/100 g/min, p = 0.015) and medulla (28 [18–47] vs. 47 [38–73] ml/100 g/min, p = 0.03). Renal venous saturation was similar in both groups (72% [64–75] vs. 72% [63–84], ns.), as was regional oxygenation (R2*) in cortex (17 [16–19] vs. 17 [16–18] 1/s, ns.) and medulla (29 [24–39] vs. 27 [23–29] 1/s, ns.). In critically ill COVID-19 patients with AKI, the total, cortical and medullary renal blood flows were reduced compared with similar patients without AKI, whereas no differences in renal oxygenation were demonstrable in this setting. Trial registration ClinicalTrials ID: NCT02765191 , registered May 6 2014 and updated May 7 2020.

中文翻译:

通过磁共振成像评估重症 COVID-19 急性肾损伤期间肾灌注减少:一项前瞻性病例对照研究

有人认为,肾脏灌注不足会导致重症 COVID-19 患者发生急性肾损伤 (AKI)。但是,支持这一点的数据有限。我们旨在使用多参数磁共振成像研究合并和不合并 AKI 的危重 COVID-19 患者的肾脏灌注、氧合和水扩散的差异。一项前瞻性病例对照研究,对因 COVID-19 导致呼吸衰竭而接受重症监护治疗且既往没有肾脏疾病的患者进行了检查。肾脏疾病:改善全球结果 肌酐标准用于组分配。主要比较使用 Mann–Whitney U 检验进行测试。对 19 名患者进行了检查,其中 10 名患有 AKI,9 名未患 AKI。AKI 患者在达到标准后的中位数 1 [0-2] 天接受检查。两组的年龄和基线血浆肌酐相似。与没有 AKI 的患者相比,AKI 患者的总肾血流量较低(中位数 645 四分位范围 [423-753] 对比 859 [746-920] ml/min,p = 0.037)。皮质(76 [51–112] 对比 146 [123–169] ml/100 g/min,p = 0.015)和髓质(28 [18–47] 对比 47 [38–73])的区域灌注减少毫升/100 克/分钟,p = 0.03)。两组的肾静脉饱和度相似(72% [64-75] vs. 72% [63-84],ns.),皮质区域氧合(R2*)也是如此(17 [16-19] vs. 17 [16–18] 1/s,ns.)和髓质(29 [24–39] 与 27 [23–29] 1/s,ns.)。在患有 AKI 的危重 COVID-19 患者中,与没有 AKI 的类似患者相比,总肾血流量、皮质肾血流量和髓质肾血流量减少,而在这种情况下,肾氧合没有差异。
更新日期:2022-09-01
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