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Abstract Background We aimed to study the incidence of acute kidney injury (AKI) in out-of-hospital cardiac arrest (OHCA) patients treated according to low-normal or high-normal mean arterial pressure (MAP) targets. Methods A post hoc analysis of the COMACARE (NCT02698917) and Neuroprotect (NCT02541591) trials that randomized patients to lower or higher targets for the first 36 h of intensive care. Kidney function was defined using the Kidney Disease Improving Global Outcome (KDIGO) classification. We used Cox regression analysis to identify factors associated with AKI after OHCA. Results A total of 227 patients were included: 115 in the high-normal MAP group and 112 in the low-normal MAP group. Eighty-six (38%) patients developed AKI during the first five days; 40 in the high-normal MAP group and 46 in the low-normal MAP group (p = 0.51). The median creatinine and daily urine output were 85 μmol/l and 1730 mL/day in the high-normal MAP group and 87 μmol/l and 1560 mL/day in the low-normal MAP group. In a Cox regression model, independent AKI predictors were no bystander cardiopulmonary resuscitation (p

Background: We aimed to study the incidence of acute kidney injury (AKI) in out-of-hospital cardiac arrest (OHCA) patients treated according to low-normal or high-normal mean arterial pressure (MAP) targets. Methods: A post hoc analysis of the COMACARE (NCT02698917) and Neuroprotect (NCT02541591) trials that randomized patients to lower or higher targets for the first 36 h of intensive care. Kidney function was defined using the Kidney Disease Improving Global Outcome (KDIGO) classification. We used Cox regression analysis to identify factors associated with AKI after OHCA. Results: A total of 227 patients were included: 115 in the high-normal MAP group and 112 in the low-normal MAP group. Eighty-six (38%) patients developed AKI during the first five days; 40 in the high-normal MAP group and 46 in the low-normal MAP group (p = 0.51). The median creatinine and daily urine output were 85 μmol/l and 1730 mL/day in the high-normal MAP group and 87 μmol/l and 1560 mL/day in the low-normal MAP group. In a Cox regression model, independent AKI predictors were no bystander cardiopulmonary resuscitation (p < 0.01), non-shockable rhythm (p < 0.01), chronic hypertension (p = 0.03), and time to the return of spontaneous circulation (p < 0.01), whereas MAP target was not an independent predictor (p = 0.29). Conclusion: Any AKI occurred in four out of ten OHCA patients. We found no difference in the incidence of AKI between the patients treated with lower and those treated with higher MAP after CA. Higher age, non-shockable initial rhythm, and longer time to ROSC were associated with shorter time to AKI. Clinical trial registration: COMACARE (NCT02698917), NEUROPROTECT (NCT02541591). [ABSTRACT FROM AUTHOR]

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Background: Contrast-associated acute kidney injury (CAAKI) is defined as acute kidney injury (AKI) occurring within 72 hours of administration of contrast media (CM) and is linked to adverse outcomes including longer hospital stay, increased hospital mortality, and a higher risk of chronic kidney disease in later life. Risk factors for the development of CAAKI in the Zambian pediatric population have not been well studied., Objectives: The objective of this study was to assess the burden of CAAKI, ascertain its risk factors, and describe short-term outcomes in hospitalized children at the University Teaching Hospitals (UTH) undergoing contrast-enhanced radiological investigations., Methods: This was a prospective observational study of in-patients undergoing contrast-enhanced radiological procedures, between September 2020 and September 2021. The participants were recruited from the Children's Hospital, the Cancer Diseases Hospital, and the Pediatric Surgical Ward at the University Teaching Hospital in Lusaka, Zambia. The primary outcome variable was occurrence of AKI at 48 hours post CM administration. We used 2 criteria to define CAAKI in our study-the European Society of Urogenital Radiology (ESUR) and the Kidney Disease Improving Global Outcomes (KDIGO) 2012 criteria. Multivariable logistic regression models were formulated to assess for risk factors of CAAKI., Results: Of the 201 enrolled participants, 123 (61.2%) were male and the median age of the participants was 5 years (interquartile range [IQR] = 3-10). The mean hemoglobin was 103 g/L (standard deviation [SD] = 26), median creatinine was 30.9 µmol/l (IQR = 22.6-43), and the glomerular filtration rate (GFR) was 102.5 mL/min/1.73 m 2 (IQR = 76.2-129.4). Forty-six (22.9%) developed CAAKI using the ESUR compared with 4.5% (9/201) using the KDIGO criteria. Independent risk factors of CAAKI were receiving a higher dose of CM (adjusted odds ratio [aOR] = 2.54; 95% confidence interval [CI] = [1.12-5.74]), prematurity (aOR = 4.6; 95% CI = [1.05-16.7]), and a higher eGFR (aOR= 1.01; 95% CI = [1.01-1.02]). Females had higher odds of CAAKI (aOR = 2.48; 95% CI = [1.18-5.18]) when compared with males. One CAAKI participant (2.2%) died; none of the participants who developed CAAKI and survived required dialysis and most of them (90%) were discharged before day 7. Day 7 eGFR results had returned to or near baseline values for those whose creatinine results were available., Conclusions: Using the ESUR criteria, a significant proportion (22.9%) of children undergoing contrast-enhanced computed tomography (CT) scans at the UTH developed CAAKI. In contrast, using the KDIGO criteria only 4.5% had CAAKI. Being born as a preterm baby, being female, having a higher eGFR at baseline, and receiving a higher dose of CM were found to be independent risk factors for CAAKI development in Zambian children. Most of the cases of CAAKI in children were transient and of little clinical significance as only a minority of patients developing CAAKI required kidney replacement therapy and all resolved by day 7 post administration of CM., Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2023.)

Background: The exact definition of Acute kidney injury (AKI) for patients with traumatic brain injury (TBI) is unknown., Aim: To compare the power of the "Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease" (RIFLE), Acute Kidney Injury Network (AKIN), Creatinine kinetics (CK), and Kidney Disease Improving Global Outcomes (KDIGO) to determine AKI incidence/stage and their association with the in-hospital mortality rate of patients with TBI., Methods: This retrospective study collected the data of patients admitted to the intensive care unit for neurotrauma from 2001 to 2012, and 1648 patients were included. The subjects in this study were assessed for the presence and stage of AKI using RIFLE, AKIN, CK, and KDIGO. In addition, the propensity score matching method was used., Results: Among the 1648 patients, 291 (17.7%) had AKI, according to KDIGO. The highest incidence of AKI was found by KDIGO (17.7%), followed by AKIN (17.1%), RIFLE (12.7%), and CK (11.5%) ( P = 0.97). Concordance between KDIGO and RIFLE/AKIN/CK was 99.3%/99.1%/99.3% for stage 0, 36.0%/91.5%/44.5% for stage 1, 35.9%/90.6%/11.3% for stage 2, and 47.4%/89.5%/36.8% for stage 3. The in-hospital mortality rates increased with the AKI stage in all four definitions. The severity of AKI by all definitions and stages was not associated with in-hospital mortality in the multivariable analyses (all P > 0.05)., Conclusion: Differences are seen in AKI diagnosis and in-hospital mortality among the four AKI definitions or stages. This study revealed that KDIGO is the best method to define AKI in patients with TBI., Competing Interests: Conflict-of-interest statement: The authors declare that they have no conflict of interest., (©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.)