Fig. 4

Emergence of acute kidney injury and volume requirement. A Volume need was observed by significantly increase of the SVV from baseline (8.8 ± 1.2%) to shock (22.7 ± 2.7%). n = 10, paired t test. B Onset of acute kidney injury shown by significant decrease of urine output (BL 2.4 ± 0.39 to S 0.18 ± 0.56 mL/kg). n = 10, Wilcoxon matched-pairs signed rank test. C AKI was accompanied by significant hyperkalaemia (BL 4.7 ± 0.14 mmol/L, S 6.1 ± 0.16 mmol/L). n = 10, Wilcoxon matched-pairs signed rank test. D Significant increase of creatinine from baseline (1.29 ± 0.08 mg/dL) to shock (2.06 ± 0.09 mg/dL), meeting the KDIGO criteria of AKI. n = 10, paired t test. mean ± SEM. E–J Histopathological changes in hematoxylin–eosin-stained kidney sections, top: control, below: sepsis. Scale bars indicate 100 µm. E–H Representative micrographs of tubular integrity. I–J Representative micrographs of glomerular integrity. K Quantitative summary of acute tubular injury in HE-stained kidney sections in sepsis (score 3.4 ± 0.3) with significant increase compared to healthy control (score 0.4 ± 0.2). n = 10 sepsis, n = 5 control, Mann–Whitney test. L Quantitative summary of collapsed glomeruli in HE-stained kidney sections with significant impaired glomerular integrity in 25–50% of the glomeruli in sepsis (score 2.5 ± 0.5) compared to healthy control (score 0.2 ± 0.2). n = 10 sepsis, n = 5 control, Mann–Whitney test. *P < 0.05, **P < 0.01, ***P < 0.001. BL = baseline, S = shock