Reduced renal perfusion has been implicated in the development of septic AKI. However, the relative contributions of macro- and microcirculatory blood flow and the extent to which impaired perfusion is an intrinsic renal phenomenon or part of a wider systemic shock state remains unclear. Single-centre prospective longitudinal observational study was carried out. Assessments were made at Day 0, 1, 2 and 4 after ICU admission of renal cortical perfusion in 50 patients with septic shock and ten healthy volunteers using contrast-enhanced ultrasound (CEUS). Contemporaneous measurements were made using transthoracic echocardiography of cardiac output. Renal artery blood flow was calculated using velocity time integral and vessel diameter. Assessment of the sublingual microcirculation was made using handheld video microscopy. Patients were classified based on the degree of AKI: severe = KDIGO 3 v non-severe = KDIGO 0–2. At study enrolment, patients with severe AKI (37/50) had prolonged CEUS mean transit time (mTT) (10.2 vs. 5.5 s, p < 0.05), and reduced wash-in rate (WiR) (409 vs. 1203 au, p < 0.05) and perfusion index (PI) (485 vs. 1758 au, p < 0.05); differences persisted throughout the entire study. Conversely, there were no differences in either cardiac index, renal blood flow or renal resistive index. Sublingual microcirculatory variables were not significantly different between groups at study enrolment or at any subsequent time point. Although lactate was higher in the severe AKI group at study enrolment, these differences did not persist, and there were no differences in either ScvO2 or ScvCO2-SaCO2 between groups. Patients with severe AKI received higher doses of noradrenaline (0.34 vs. 0.21mcg/kg/min, p < 0.05). Linear regression analysis showed no correlation between mTT and cardiac index (R-0.18) or microcirculatory flow index (R-0.16). Renal cortical hypoperfusion is a persistent feature in critically ill septic patients who develop AKI and does not appear to be caused by reductions in macrovascular renal blood flow or cardiac output. Cortical hypoperfusion appears not be associated with changes in the sublingual microcirculation, raising the possibility of a specific renal pathogenesis that may be amenable to therapeutic intervention. Trial Registration Clinical Trials.gov NCT03713307 , 19 Oct 2018.

中文翻译：

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肾皮质灌注减少与感染性休克患者急性肾损伤的严重程度相关，与肾血流变化和舌下微循环障碍无关

肾灌注减少与脓毒性 AKI 的发展有关。然而，宏观和微循环血流的相对贡献以及灌注受损的程度是一种内在的肾脏现象还是更广泛的全身性休克状态的一部分仍不清楚。进行了单中心前瞻性纵向观察研究。在 ICU 入院后第 0、1、2 和 4 天，使用对比增强超声 (CEUS) 对 50 名感染性休克患者和 10 名健康志愿者进行肾皮质灌注评估。使用经胸超声心动图对心输出量进行同期测量。使用速度时间积分和血管直径计算肾动脉血流量。使用手持视频显微镜对舌下微循环进行评估。根据 AKI 的程度对患者进行分类：严重 = KDIGO 3 v 非严重 = KDIGO 0-2。入组研究时，严重 AKI (37/50) 患者的 CEUS 平均通过时间 (mTT) 延长（10.2 vs. 5.5 s，p < 0.05），洗入率 (WiR) 降低（409 vs. 1203 au， p < 0.05) 和灌注指数 (PI) (485 vs. 1758 au, p < 0.05)；在整个研究过程中始终存在差异。相反，心脏指数、肾血流量或肾阻力指数均无差异。在研究登记或任何后续时间点，各组之间的舌下微循环变量没有显着差异。尽管在研究入组时重度 AKI 组的乳酸较高，但这些差异并未持续存在，并且组间 ScvO2 或 ScvCO2-SaCO2 没有差异。严重 AKI 患者接受更高剂量的去甲肾上腺素（0.34 vs. 0.21mcg/kg/min，p < 0.05）。线性回归分析显示 mTT 与心脏指数 (R-0.18) 或微循环流量指数 (R-0.16) 之间没有相关性。肾皮质低灌注是发生 AKI 的危重脓毒症患者的持续特征，并且似乎不是由大血管肾血流量或心输出量减少引起的。皮质低灌注似乎与舌下微循环的变化无关，这增加了可能适合治疗干预的特定肾脏发病机制的可能性。试验注册 Clinical Trials.gov NCT03713307，2018 年 10 月 19 日。18）或微循环流量指数（R-0.16）。肾皮质低灌注是发生 AKI 的危重脓毒症患者的持续特征，并且似乎不是由大血管肾血流量或心输出量减少引起的。皮质低灌注似乎与舌下微循环的变化无关，这增加了可能适合治疗干预的特定肾脏发病机制的可能性。试验注册 Clinical Trials.gov NCT03713307，2018 年 10 月 19 日。18）或微循环流量指数（R-0.16）。肾皮质低灌注是发生 AKI 的危重脓毒症患者的持续特征，并且似乎不是由大血管肾血流量或心输出量减少引起的。皮质低灌注似乎与舌下微循环的变化无关，这增加了可能适合治疗干预的特定肾脏发病机制的可能性。试验注册 Clinical Trials.gov NCT03713307，2018 年 10 月 19 日。皮质低灌注似乎与舌下微循环的变化无关，这增加了可能适合治疗干预的特定肾脏发病机制的可能性。试验注册 Clinical Trials.gov NCT03713307，2018 年 10 月 19 日。皮质低灌注似乎与舌下微循环的变化无关，这增加了可能适合治疗干预的特定肾脏发病机制的可能性。试验注册 Clinical Trials.gov NCT03713307，2018 年 10 月 19 日。