Correction to: Urine cell cycle arrest biomarkers distinguish poorly between transient and persistent AKI in early septic shock: a prospective, multicenter study.

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Urine cell cycle arrest biomarkers distinguish poorly between transient and persistent AKI in early septic shock: a prospective, multicenter study.

BACKGROUND: The urine biomarkers tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) have been validated for predicting and stratifying AKI. In this study, we analyzed the utility of these biomarkers for distinguishing between transient and persistent AKI in the early phase of septic shock. METHODS: We performed a prospective, multicenter study in 11 French ICUs. Patients presenting septic shock, with the development of AKI within the first 6 h, were included. Urine [TIMP-2]*[IGFBP7] was determined at inclusion (0 h), 6 h, 12 h, and 24 h. AKI was considered transient if it resolved within 3 days. Discriminative power was evaluated by receiver operating characteristic (ROC) curve analysis. RESULTS: We included 184 patients, within a median [IQR] time of 1.0 [0.0-3.0] h after norepinephrine (NE) initiation; 100 (54%) patients presented transient and 84 (46%) presented persistent AKI. Median [IQR] baseline urine [TIMP-2]*[IGFBP7] was higher in the persistent AKI group (2.21 [0.81-4.90] (ng/ml)2/1000) than in the transient AKI group (0.75 [0.20-2.12] (ng/ml)2/1000; p < 0.001). Baseline urine [TIMP-2]*[IGFBP7] was poorly discriminant, with an AUROC [95% CI] of 0.67 [0.59-0.73]. The clinical prediction model combining baseline serum creatinine concentration, baseline urine output, baseline NE dose, and baseline extrarenal SOFA performed well for the prediction of persistent AKI, with an AUROC [95% CI] of 0.81 [0.74-0.86]. The addition of urine [TIMP-2]*[IGFBP7] to this model did not improve the predictive performance. CONCLUSIONS: Urine [TIMP-2]*[IGFBP7] measurements in the early phase of septic shock discriminate poorly between transient and persistent AKI and do not improve clinical prediction over that achieved with the usual variables. TRIAL REGISTRATION: NCT02812784.

Global end-diastolic volume as an indicator of cardiac preload in patients with septic shock.

STUDY OBJECTIVE: To assess the value of the global end-diastolic volume (GEDV) evaluated by transpulmonary thermodilution as an indicator of cardiac preload. DESIGN: Prospective clinical study. SETTING: Medical ICU of a university hospital (20 beds). PATIENTS: Thirty-six patients with septic shock. INTERVENTIONS: Volume loading and dobutamine infusion. MEASUREMENTS AND RESULTS: Hemodynamic parameters were evaluated in triplicate by the transpulmonary thermodilution technique: (1) before and after 66 fluid challenges in 27 patients, and (2) before and after 28 increases in dobutamine infusion rate in 9 patients. Volume loading induced a significant (p < 0.001) increase in central venous pressure (CVP) from 10 +/- 4 to 13 +/- 4 mm Hg, in GEDV index from 711 +/- 164 to 769 +/- 144 mL/m(2), in stroke volume index (SVI) from 36 +/- 12 to 42 +/- 12 mL/m(2), and in cardiac index (CI) from 3.4 +/- 1.1 to 3.9 +/- 1.2 L/min/m(2) (mean +/- SD). Changes in GEDV index were correlated (r = 0.72, p < 0.001) with changes in SVI, while changes in CVP were not. The increase in SVI was > 15% in 32 of 66 instances (positive response). The preinfusion GEDV index was lower (637 +/- 134 mL/m(2) vs 781 +/- 161 mL/m(2), p < 0.001) in the cases of positive response, and was negatively correlated with the percentage increase in GEDV index (r = - 0.65, p < 0.001) and in SVI (r = - 0.5, p < 0.001). Dobutamine infusion induced an increase in SVI (32 +/- 11 mL/m(2) vs 35 +/- 12 mL/m(2), p < 0.05) and in CI (2.8 +/- 0.6 L/min/m(2) vs 3.2 +/- 0.6 L/min/m(2), p < 0.001) but no significant change in CVP (13 +/- 3 mm Hg vs 13 +/- 3 mm Hg) and in GEDV index (823 +/- 221 mL/m(2) vs 817 +/- 202 mL/m(2)). CONCLUSION: In patients with septic shock, our findings demonstrate that, in contrast to CVP, the transpulmonary thermodilution GEDV index behaves as an indicator of cardiac preload.