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Background: Cardiac surgery with cardiopulmonary bypass (CPB) is known to contribute towards the incidence of acute kidney injury (AKI) and peri-operative morbidity and mortality. There are several patient, anaesthetic and surgical factors that contribute to its occurrence. It is imperative to know the profile of a patient who is likely to develop this complication to mitigate for modifiable risks. This study aimed at describing a profile of AKI in an adult patient (over the age of 18 years) following cardiac surgery on CPB. Factors associated with the development of cardiac surgery-associated acute kidney injury (CSA-AKI) are described, as well as the relationship between CSA-AKI and in-hospital mortality., Methods: This was a contextual, descriptive and retrospective single-centre study with data of 476 adult patients admitted post cardiac surgery between January 2016 and December 2017. Data were collected from Charlotte Maxeke Johannesburg Academic Hospital (CMJAH) in South Africa. All adult patients who presented for elective cardiac surgery (coronary artery bypass graft), valvular, aortic and other cardiac surgery on CPB were included. Peri-operative factors such as patient demographics, baseline renal function, co-morbid factors, length of CPB and aortic cross-clamp time, degree of hypothermia, use of assist devices, and post-operative serum creatinine (SCr) levels were collected. Incomplete essential peri-operative data and data for patients who presented on renal replacement therapy (RRT) already were excluded. AKI was defined by Kidney Disease Improving Global Outcomes (KDIGO) criteria., Results: One hundred and thirty-five (28%) patients developed CSA-AKI and 20, 5 and 3% were in KDIGO 1, 2 and 3, respectively. Older age ( p = 0.024), female gender ( p = 0.015), higher serum creatinine level ( p = 0.025), and lower estimated glomerular filtration rate (eGFR) ( p = 0.025) were associated with the development of CSA-AKI, while a history of hypertension was predictive. Forty-six of the 476 patients died. Mortality rates were significantly higher in those with AKI compared to those without [28 (21%) vs 18 (5%), respectively ( p = 0.001)]. The incidence was significantly worse in those with severe kidney injury, as evidenced by mortality rates of 44 versus 5% between KDIGO 3 and KDIGO 1 ( p < 0.001). Pre-operative eGFR and CSA-AKI requiring RRT were significantly associated with mortality, while pre-operative eGFR was an independent predictor of mortality (hazard ratio 0.99, 95% confidence interval: 0.97-0.99, p = 0.019)., Conclusions: A history of hypertension was predictive of the development of CSA-AKI, and pre-operative eGFR was an independent predictor of mortality in this cohort. Both factors are modifiable.

Background: Acute kidney injury (AKI) and chronic kidney disease (CKD) are considered common complications after allogeneic hematopoietic stem cell transplantation (allo-HSCT)., Objectives and Method: In this study, 114 patients who had undergone allo-HSCT were retrospectively analyzed to investigate the risk factors for onset of posttransplant AKI and CKD as defined by the new Kidney Disease Improving Global Outcomes criteria., Results: Seventy-four patients (64.9%) developed AKI and 25 (21.9%) developed CKD. The multivariate analysis showed that the risk factors for developing stage 1 or higher AKI were age ≥46 years at the time of transplant (p = 0.001) and use of ≥3 nephrotoxic drugs (p = 0.036). For CKD, the associated risk factors were disease status other than complete remission at the time of transplantation (p = 0.018) and onset of AKI after transplant (p = 0.035). The 5-year overall survival (OS) was significantly reduced by development of AKI (p < 0.001), but not CKD. Posttransplant AKI significantly increased the 5-year nonrelapse mortality (p < 0.001), whereas posttransplant CKD showed an increasing tendency, but the difference was not significant., Conclusions: Posttransplant AKI impacts OS, significantly increases the risk of CKD, and is significantly associated with disseminated intravascular coagulation and use of ˃3 nephrotoxic drugs., (© 2019 S. Karger AG, Basel.)

Background: Levels of the biomarkers presepsin and procalcitonin are affected by renal function. We evaluated the accuracies of presepsin and procalcitonin levels for diagnosing sepsis in patients with and without acute kidney injury (AKI)., Methods: We evaluated patients with presepsin and procalcitonin data, and classified them into AKI and non-AKI groups based on the Kidney Disease Improving Global Outcomes criteria. Each group was then subdivided according to sepsis status for each stage of AKI. Receiver operating characteristic curve analyses were used to investigate the accuracies of biomarker levels for diagnosing sepsis., Results: In the non-AKI group, the area under the curves (AUCs) for procalcitonin and presepsin levels were 0.897 and 0.880, respectively (p = .525) and optimal cut-off values were 0.10 ng/ml (sensitivity: 85.1%, specificity: 79.1%) and 240 pg/ml (sensitivity: 80.9%, specificity: 83.2%), respectively. In the stage 3 subgroup, the AUC for procalcitonin (0.946) was significantly higher than that for presepsin (0.768, p < .001). The optimal cut-off values for diagnosing sepsis were 4.07 ng/ml (sensitivity: 87.2%, specificity: 93.5%) for procalcitonin and 500 pg/ml (sensitivity: 89.7%, specificity: 59.7%) for presepsin., Conclusions: In patients with severe AKI, the accuracy of the diagnosis of sepsis with procalcitonin was significantly higher than with presepsin., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: Acute kidney injury (AKI) is a strong predictor of morbidity and mortality after cardiac surgery. Lack of valid early biomarkers for predicting AKI has hampered the ability to take therapeutic measures for preventive cause. Hyperphosphatemia that occurs in AKI due to renal excretion defect was not studied in this context and could be simple marker of AKI. Therefore, we tested role of serum phosphorus in prediction of AKI as a biomarker after cardiac surgery in children., Methodology: We prospectively evaluated 51 children aged between 3 weeks and 12 years undergoing elective cardiac surgery. Serum creatinine and phosphorus were measured preoperatively and postoperatively at 24 and 48 h. As per the Kidney Disease Improving Global Outcomes criteria, patients were grouped into AKI and non-AKI on the basis of the development of AKI within 48 h postsurgery. The postoperative diagnostic performance of phosphorus thresholds was analyzed by the area under receiver operating characteristic curves (AUC-ROC)., Results: From 51 children included, 10 developed AKI. In AKI group, serum phosphorus increased significantly from 4.47 ± 0.43 baseline to 6.29 ± 0.32 at 24 h postsurgery (P = 0.01) while serum creatinine increased from baseline 0.33 (0.24-0.46) to 0.49 (0.26-0.91) at 24 h which is statistically insignificant (P = 0.16). ROC analysis showed that serum phosphorus at 24 h, the AUC was 0.84 with sensitivity 0.75 and specificity 0.93 for a cutoff value of 6.4 mg/dl. Whereas serum phosphorus at 48 h, the AUC was 0.86 with sensitivity 66.67% and specificity 97.62% for a cutoff value of 5.4 mg/dl., Conclusion: Serum phosphorus can be an alternative biomarker as early as 24 h for early prediction of AKI in pediatric cardiac surgery., Competing Interests: There are no conflicts of interest

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: Acute kidney injury (AKI) is a strong predictor of morbidity and mortality after cardiac surgery. Lack of valid early biomarkers for predicting AKI has hampered the ability to take therapeutic measures for preventive cause. Hyperphosphatemia that occurs in AKI due to renal excretion defect was not studied in this context and could be simple marker of AKI. Therefore, we tested role of serum phosphorus in prediction of AKI as a biomarker after cardiac surgery in children. Methodology: We prospectively evaluated 51 children aged between 3 weeks and 12 years undergoing elective cardiac surgery. Serum creatinine and phosphorus were measured preoperatively and postoperatively at 24 and 48 h. As per the Kidney Disease Improving Global Outcomes criteria, patients were grouped into AKI and non-AKI on the basis of the development of AKI within 48 h postsurgery. The postoperative diagnostic performance of phosphorus thresholds was analyzed by the area under receiver operating characteristic curves (AUC-ROC). Results: From 51 children included, 10 developed AKI. In AKI group, serum phosphorus increased significantly from 4.47 ± 0.43 baseline to 6.29 ± 0.32 at 24 h postsurgery (P = 0.01) while serum creatinine increased from baseline 0.33 (0.24–0.46) to 0.49 (0.26–0.91) at 24 h which is statistically insignificant (P = 0.16). ROC analysis showed that serum phosphorus at 24 h, the AUC was 0.84 with sensitivity 0.75 and specificity 0.93 for a cutoff value of 6.4 mg/dl. Whereas serum phosphorus at 48 h, the AUC was 0.86 with sensitivity 66.67% and specificity 97.62% for a cutoff value of 5.4 mg/dl. Conclusion: Serum phosphorus can be an alternative biomarker as early as 24 h for early prediction of AKI in pediatric cardiac surgery.

Acute kidney injury (AKI) can be a devastating diagnosis for any patient and can increase mortality during hospitalization. There can be long-term consequences for those who survive the initial insult. This article discusses AKI and its implications for nurses. [ABSTRACT FROM AUTHOR]